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The Labor Market Experience of Workers with Disabilities The ADA and Beyond This Page Intentionally Left Blank The Labor Market Experience of Workers with Disabilities The ADA and Beyond Julie L. Hotchkiss 2003 W.E. Upjohn Institute for Employment Research Kalamazoo, Michigan Library of Congress Cataloging-in-Publication Data Hotchkiss, Julie L. The labor market experience of workers with disabilities / Julie L. Hotchkiss. p. cm. ISBN 0-88099-251-4 (pbk. : alk. paper)—ISBN 0-88099-252-2 (hardcover : alk. paper) 1. Handicapped—Employment—United States. 2. Handicapped—Employment—Government policy—United States. 3. Labor market—United States. 4. Discrimination in employment—Law and legislation—United States. 5. Handicapped—Legal status, laws, etc.—United States. 6. United States. Americans with Disabilities Act of 1990. I. Title. HD7256.U5 H68 2002 331.590973—dc21 2002151811 2003 W.E. Upjohn Institute for Employment Research 300 S. Westnedge Avenue Kalamazoo, Michigan 49007-4686 The facts presented in this study and the observations and viewpoints expressed are the sole responsibility of the authors. They do not necessarily represent positions of the W.E. Upjohn Institute for Employment Research. Cover design by J.R. Underhill. Index prepared by Nancy Humphreys. Printed in the United States of America. Contents List of Figures vi List of Tables viii Acknowledgment xi Preface xiii 1 Introduction 1 Disability Legislation in the United States 1 Policy Issues 3 Focus and Strategy of Analyses 5 Disabled Americans 12 Survey of Income and Program Participation (SIPP) 15 Notes 18 2 Employment 21 Unconditional and Joint Probabilities 23 Explaining the Decline in Labor Force Participation Rates 27 Pooled, Cross-Sectional Analysis 30 Evidence from the SIPP 34 Employment Probability and Firm Size 37 Conclusions 43 Notes 44 3 Compensation: Wages and Benefits 49 Wage Levels 50 Differences in Wages Over Time 51 Wage Decomposition 61 Benefit Analysis 66 Conclusions 70 Notes 72 4 Hours of Work, Distribution, and Representation 75 Hours of Work 76 Distribution of Workers 90 Representation of Workers 95 Conclusions 99 Notes 101 5 Separation, Unemployment, and Job Search 105 Separation 106 Unemployment 111 v Job Search 115 Conclusions 120 Notes 121 6 State versus Federal Legislation 125 Impact on Employment 129 Impact on Wages 133 Impact on Hours 137 Conclusions 138 Notes 140 7 Conclusions and Policy Implications 141 Employment Incentives 143 Education, Training, and Job Characteristics 147 Screening and Matching 151 The ADA and Beyond 152 Notes 154 Appendix A: CPS Sample Construction 157 Appendix B: SIPP Sample Construction 159 Appendix C: Supplemental Tables 163 Appendix D: State Disability Legislation 179 References 209 The Author 217 Index 219 About the Institute 229 Figures 1.1 Percentage of Sample and of Workers in the CPS Data Set Indicating a Work-Limiting Disability, 1981–2000 12 1.2 Average Weekly Hours of Disabled and Nondisabled Workers, CPS, 1981–2000 15 1.3 Percentage of Sample and of Workers in the SIPP Data Set Indicating a Work-Limiting Disability, 1986–1997 17 1.4 Distribution of Disabled Individuals across Disability Type, SIPP, 1986–1997 17 vi 2.1 Percentage Employed of Disabled and Nondisabled Individuals, CPS, 1981–2000 22 2.2 Impact of Disability on Joint Labor Force Participation and Employment Probabilities, CPS, 1981–2000 25 2.3 Separate Predictions of Employment and Labor Force Participation Probabilities for the Disabled, CPS, 1987–2000 26 2.4 Distribution of Disabled and Nondisabled Workers across Firm Size, CPS, 1987–1999 40 2.5 Ratio of Predicted Employment Probabilities for Disabled versus Nondisabled Workers by Firm Size, CPS, 1987–1999 41 3.1 Average Real Hourly Wages, CPS, 1981–2000 50 3.2 Observed and Selectivity-corrected Wage Differentials and the Coefficient Effect as Percentage of Corrected Wage Differential, CPS, 1981–2000 63 3.3 Difference in Proportion of Nondisabled and Disabled Workers Receiving Benefits, CPS, 1980–1999 67 3.4 Marginal Effect of Disability on the Probability of Fringe Benefit Receipt, CPS, 1987–1999 69 4.1 Percentage of Disabled and Nondisabled Workers That Are Employed Part-Time, CPS, 1981–2000 77 4.2 Impact of Having a Disability on Being Employed Part-Time, CPS, 1981–2000 79 4.3 Impact of Having a Disability on Being Voluntarily Employed Part-Time, CPS, 1981–2000 82 4.4 Full-Time/Part-Time Wage Differentials for Disabled and Nondisabled Workers, CPS, 1981–2000 90 4.5 Distribution of Disabled and Nondisabled Workers across Occupations and Industries, CPS, 2000 91 4.6 Duncan Indices of Dissimilarity across Occupations and Industries, Disabled versus Nondisabled and Nonwhite versus White, CPS, 1981–2000 93 4.7 Duncan Indices of Dissimilarity across Occupations and Industries, by Type of Disability, SIPP, 1997 94 4.8 Correlation Coefficients, Concentration of Disabled Workers and Industry/Occupation Wage, CPS, 1981–2000 99 5.1 Weeks Spent Looking for Work by Disability Status, CPS, 1980–1999 106 5.2 Percentage of Job Separations by Type and Disability Status, CPS, 1981–2000 108 5.3 Marginal Effect of Being Disabled on the Probability of Separation Type, CPS, 1981–2000 110 vii 5.4 Probability of Different Types of Unemployment by Disability Status, CPS, 1989–2000 113 5.5 Average Search Spell Length Differential between Unemployed Disabled and Nondisabled Searchers, CPS, 1981–2000 116 5.6 Predicted Expected Search Duration by Disability Status, CPS, 1981–2000 118 5.7 Percentage of Disabled and Nondisabled Searchers Using Each Search Strategy, Averaged over the Period 1981–2000, CPS 119 6.1 Labor Force Participation Rates for the Disabled and the Nondisabled, CPS, 1981–1991 128 6.2 Proportion of Disabled and Nondisabled Labor Force Participants That Are Employed, CPS, 1981–1991 128 6.3 Proportion of Disabled and Nondisabled Workers That Are Employed Part-Time, CPS, 1981–1991 137 Tables 1.1 Sample Sizes for Merged CPS Data Files 10 1.2 Means of Select Demographic Variables for Disabled and Nondisabled Workers over Entire Time Period, CPS, 1981–2000 14 1.3 Sample Sizes for SIPP Data Files 16 2.1 Labor Force Participation and Employment Bivariate Probit with Selection Results, CPS, Combined Years 1981–2000 32 2.2 Change in Marginal Effect of Disability on Labor Force Participation and Employment Probabilities 33 2.3 Labor Force Participation and Employment Bivariate Probit with Selection Results, SIPP Combined Years, 1986–1997 34 2.4 Labor Force Participation and Employment Bivariate Probit with Selection Results by Type of Disability, SIPP Combined Years, 1986–1997 36 2.5 DDD Calculation for Average Predicted Probability of Employment by Firm Size, Disability Status, and across Time, CPS, 1987–1999 42 3.1 OLS Selectivity-Corrected Regression Results for Log Real Wages, across Disability Status and ADA Implementation, CPS, 1984–2000 53 3.2 OLS Selectivity-Corrected DD Regression Results for Log Real Wages, across Disability Status and Type of Disability Status, SIPP, 1986–1997 55 viii 3.3 OLS Selectivity-Corrected Regression Results for Log Real Wages, across Disability Status, Covered Firm Size, and ADA Implementation, CPS 59 3.4 Contribution of Regressors to Log Wage Differentials, Median across Years, CPS, 1981–2000 65 4.1 Employment and Part-Time Employment Bivariate Probit with Selection Results, CPS Combined Years, 1981–2000 80 4.2 Linear Probability, Voluntary Part-Time Employment Results, CPS Combined Years, 1981–2000 83 4.3 Employment and Part-Time Employment Bivariate Probit with Selection and Linear Probability Model for Voluntary Part- Time Employment, SIPP, 1986–1997 86 4.4 Employment Growth Rates for Industry and Occupational Classifications 97 4.5 Marginal Effect of Disability on the Probability of Employment in a ‘‘High Growth’’ Occupation or Industry, CPS 98 6.1 Summary of State-Level Disability Legislation 126 6.2 Labor Force Participation and Employment Bivariate Probit with Selection Results, CPS, 1981–1991 131 6.3 Log Real Wage OLS Estimation with Selection, CPS, 1981–1991 135 6.4 Employment and Part-Time Employment Bivariate Probit with Selection Results, CPS, 1981–1991 139 B.1 SIPP Data Structure 160 B.2 Classification of Disabilities in the SIPP Data Set 162 C.1 Trends in the Percentages of Total Sample and of Workers Indicating a Work-Limiting Disability, CPS Combined Outgoing Rotation Groups, 1981–2000 165 C.2 Percentages of Disabled and Nondisabled Individuals Employed, CPS, 1981–2000 166 C.3 Predicted Joint Probability of Labor Force Participation and Employment and Predicted Unconditional Employment Probability, by Disability Status, CPS, 1981–2000 167 C.4 Relative Predicted Probabilities of Working in Each Firm Size, CPS, 1987–1999 168 C.5 Observed and Selectivity-Corrected Wage Differentials, CPS, 1981–2000 169 C.6 Marginal Effect of Being Disabled on the Probability of Employer-Provided Health Insurance and of Being Included in the Employer’s Pension Plan, CPS 170 C.7 Impact of Being Disabled on the Probability of Part-time and Voluntary Part-Time Employment, CPS, 1981–2000 172 ix C.8 The Duncan Index as a Measure of Dissimilarity in Distribution of Workers across Occupations and Industries, CPS, 1981–2000 173 C.9 Disabled and Nondisabled Job Separators by Reason for Job Separation (%), CPS, 1981–2000 174 C.10 Probability of an Employment Separation Being Voluntary and Involuntary by Disability Status, CPS, 1981–2000 175 C.11 Probability of an Unemployment Spell Being the Result of Losing a Job, Leaving a Job, Reentering the Labor Force, or Newly Entering the Labor Force, by Disability Status, CPS, 1989–2000 176 C.12 Mean Difference in Expected Duration and Predicted Expected Duration across Disability Status, CPS, 1981–2000 177 D.1 State Disability Legislation 181 x Acknowledgments This research would not have been possible without the financial support of the W.E. Upjohn Institute for Employment Research. I also appreciate the assistance and comments of the Upjohn Institute staff economists. Allan Hunt, Kevin Hollenbeck, and Stephen Woodbury were particularly helpful. In addition, I would like to thank the following people who were instrumental in the completion of this project: Jack McNeil and Vic Valdisera of the U.S. Census Bureau, Bob McIntire of the U.S. Bureau of Labor Statistics, David Autor, Christopher Bollinger, Barry Hirsch, Doug Kruse, David Macpherson, Robert Margo, Walter Oi, and my colleagues Robert E. Moore and M. Melinda Pitts. The research assistance and contributions of Ludmila Rovba are without measure. Generosa Kagaruki also provided valuable research help. Lastly, I would like to dedicate this book to my parents, Burt and Nonnie Hotchkiss. xi This Page Intentionally Left Blank Preface As of July 26, 1994, employers with 15 or more employees have been subject to the labor market provisions of the Americans with Disabilities Act (ADA). Employers with 25 or more employees became subject to the provi- sions in 1992. For people with disabilities, the ADA gives civil rights protec- tions similar to those provided to individuals on the basis of race, color, sex, national origin, age, and religion. It guarantees equal opportunity in public accommodations, employment, transportation, state and local government ser- vices, and telecommunications. This book focuses exclusively on the labor market provisions of the ADA. Its goal is to provide a comprehensive analysis of the current labor market experience of American workers with disabilities and an assessment of the impact the ADA has had on that experience. The ADA prohibits discrimination in all employment practices, including job application procedures, hiring, firing, advancement, compensation, train- ing, and other terms, conditions, and privileges of employment. It applies to recruitment, advertising, tenure, layoff, leave, fringe benefits, and all other employment-related activities. It is hoped that, by breaking down the labor market barriers that Americans with disabilities have faced in the past, we will all benefit from an untapped source of productivity, the resulting increase in purchasing power, and a simultaneous savings on disability payments. Most previous studies have either focused on only one dimension of the labor market experience (e.g., wages or employment levels), evaluated that experience at only one point in time, or focused on the labor supply impact of disability policies. However, one’s labor market experience has many dimen- sions; this research explores the labor market experience across those dimen- sions and across time. The result is a more complete picture of what Americans with disabilities can expect as participants in the labor market and of whether this experience has been affected by the passage of the ADA. Given that policies such as the ADA are designed to affect the lives of groups of individuals, the experience of disabled workers as a whole is evaluated rather than the experience of any one person. Much of the earlier research on workers with disabilities relates to issues of labor supply, such as policies that shape workforce participation decisions of the disabled, circumstances that improve the chances of injured workers returning to work, or details of the special needs of the disabled (e.g., access to health care, personal assistance) that might hinder their entrance into the workforce. While the analyses contained in this book do not ignore labor supply issues, the focus is on more direct evidence of the existence of and changes in barriers to a positive labor market experience. Barriers are de- xiii fined here as parts of the labor market experience controlled by the employer, which are the aspects directly addressed by the ADA and can be considered demand-side factors. When a policy such as the ADA finally comes to fruition, there is often a question as to whether |
any observed changes in the experience of those af- fected by the law can be attributed to the law itself or whether changes in experience merely reflect the environment in which the law was passed. If the latter were true, this would not be to say that the ADA was unnecessary, just that it did not have the dramatic impact some opponents probably feared because the changes were already occurring. It is also possible that no change in experience of the disabled will be seen leading up to the passage or follow- ing implementation of the ADA. If this is the case and if the experience of disabled workers in the labor market remains inferior to that of the nondis- abled, then we clearly have to look beyond the ADA to improve that labor market situation. The analyses in this book show that while disabled workers are making progress in some dimensions of their labor market experience, the ADA does not seem to have had a striking impact in either a positive or negative direc- tion. Expanding or strengthening incentives to enter the labor force, providing training focused in high-growth and high-earnings occupations, and assistance in screening and matching workers with appropriate jobs are policies that would capitalize on the recent progress made by disabled workers and move them in the direction of greater labor market gains. xiv 1 Introduction DISABILITY LEGISLATION IN THE UNITED STATES The excitement, fear, and general controversy surrounding the pas- sage of the Americans with Disabilities Act (ADA) in 1990 might lead some to believe that this was the first time the United States had ever confronted the issue of potential discrimination against or differential treatment of people with disabilities. To the contrary, the nation has demonstrated some concern through legislation for individuals with disabilities since the 1920s. Not until the ADA, however, was there as sweeping a mandate, theoretically touching multiple dimensions of a disabled person’s life. The National Civilian Vocational Rehabilitation Act became law in 1920, was amended several times, then became the Vocational Rehabil- itation Act in 1954. Public Law 93-112 transformed it into the Rehabil- itation Act of 1973 (sections 503–504), which prohibits discrimination against the disabled by any program receiving federal assistance and requires federal agencies to take affirmative action to employ handi- capped individuals. In addition, the act dictates that companies having contracts of a certain size with the federal government ($10,000 or more, as of 1998) publicly state that the organization takes affirmative action to employ and accommodate workers with disabilities. Execu- tive Order 12086 in 1978 reassigned enforcement of the act to the U.S. Department of Labor. This strengthened the position of disabled and veteran workers by placing the regulation enforcement in line with protection from discrimination based on race, color, religion, sex, or national origin.1 So, while nondiscrimination against and employment of disabled workers have been of concern for firms doing business with the federal government for some time, it was not until the passage of the ADA that all firms in the United States (employing 15 or more people) would be held to the same standard regarding employment and accommodation of individuals with disabilities. In many ways individual states have taken the lead in providing workplace opportunities for the disabled. By 1990, all states had 1 2 Hotchkiss passed antidiscrimination legislation covering employment by state agencies and often employment by any firm doing business with the state.2 In addition, nearly all states by that time covered private em- ployers in some form or another, and many states covered all employ- ment, including that by very small firms (fewer than 15 workers). Common exclusions from the discrimination legislation included reli- gious organizations, social clubs, family members, American Indian tribes, and farm or domestic workers. Details of when each state passed legislation related to treatment of the disabled in the workplace and the exclusions of those laws are in Appendix D. The Rehabilitation Act of 1973, and the concern already expressed at the state level about the employment opportunities of disabled work- ers, culminated in the passage of the ADA in 1990. This act was unlike others before it, in that it provided for the civil rights of people with disabilities in the same way that all citizens are protected against dis- crimination based on race, color, sex, national origin, age, and religion. The ADA requires that employers treat workers, and potential workers, with disabilities identically to those without disabilities, with regard to hiring, compensation, and other aspects of employment. In addition, employers must make reasonable efforts to accommodate the nature of the worker’s disability in connection with the performance of the work- er’s job. Owners of places of public accommodation are required to provide facilities (e.g., entrances, elevators, bathrooms) fit for the dis- abled, and to provide services in such a way that people with disabili- ties are not restricted from receiving those services (e.g., requiring a driver’s license as the only way to provide proof of identification dis- criminates against the vision impaired). Public accommodation also includes equal access through telecommunication, such as access to the Internet. While admittedly only a small part of the entire legislation, the implications and impact of the labor market provisions (Title I) of the ADA provide the focus of this book. Any interpretation of the effect of the ADA or recommendations for enhancements must take into account policies already in place that may or may not influence a disabled worker’s labor market experience. The Social Security Administration manages two cash payment pro- grams for Americans with disabilities. Such programs are of great concern regarding labor market analyses for two main reasons. First, cash payment programs might crowd out labor market activity, and Introduction 3 second, they may be structured in such a way that labor market partici- pation is discouraged. The Social Security Disability Insurance Pro- gram (SSDI) provides benefits to workers who have been able to make enough contributions through the social security Federal Insurance Contributions Act (FICA) tax paid on their previous earnings. The Supplemental Security Income Program (SSI) is available to disabled Americans who have limited income and resources. The eligibility rules for payments from these two programs differ, but they both re- quire the applicant to be either not working or earning less than some specified amount. Both programs include incentives to get recipients back into the labor force. These incentives include a trial work period where some or all of the payments are retained for a certain period of time; continuation of Medicaid or Medicare even if cash payments have ended because of high earnings; reimbursement of impairment-related work expenses; exclusion of certain income from the earnings test if set aside for future self-sufficiency, such as education or starting a business; and referral and payment for vocational rehabilitation. Many of these incentives were only adopted recently as part of the Ticket to Work and Work Incentives Improvement Act of 1999 (Public Law 106- 170). The goals of the Ticket to Work initiative complement the goals of the ADA. Whereas these work incentive programs are designed to encourage the disabled to seek jobs and become self-sufficient, the ADA is intended to provide an environment in which these efforts are met with support and reasonable assistance. POLICY ISSUES The United States has a history of enacting legislation with strong social content, expressing society’s ethics and morals. Child labor laws and other civil rights legislation fall into this category. One could argue that such laws are grounded in economic concerns. For example, discrimination against workers with disabilities or against African Americans robs our economy of the efficient allocation and use of valuable resources. Also, with the prohibition of child labor, children really have no other option but to attend school, raising the human capital of our economy overall. While these arguments have merit in 4 Hotchkiss fact, it is also true that as a society we support these laws from an emotional and moral level. For example, the 1991 Harris poll on Public Attitudes toward People with Disabilities demonstrated that while most people were not even aware that the ADA had been passed (62 percent), they felt overwhelmingly (95 percent) that ‘‘Given how many difficul- ties disabled people face in their daily lives, the least society can do is make an extra effort to improve things for them.’’3 In addition, 81 percent of those surveyed thought that there should be an affirmative action program for people with disabilities. These are responses not entirely driven by economic concerns. When legislation is propelled by an evolution of ethical and moral concerns, we must face the question of whether it serves as a statement of where we (as a society) are rather than as a prediction of where we are going.4 For example, the establishment of a minimum age for employment (child labor laws) has been shown to have had little impact on the decline of child labor in the early part of the 20th century (Moehling 1999). The implication is that legislation of strong social content, rather than precipitating social change, is often actually a re- sponse to social change. In other words, the ADA might merely serve as a reflection of our moral and ethical beliefs rather than as a tool with which to improve the condition of a segment of society. Some argue that the ADA is ‘‘feel-good legislation that promises more than it deliv- ers’’ (Jay 1990, p. 23). A major criticism is that the ADA is absent of specifics necessary for effective compliance, particularly on the subject of what constitutes ‘‘undue hardship,’’ which serves as the measure of whether a firm must make the physical environment, service, or employment ‘‘accessible.’’ Some interpret the refusal of Congress to tackle the difficult issues that were sure to arise as indication that the ADA’s primary function was merely to be a statement of our morals. In addition, an amendment to the ADA that would have disallowed jury trials and punitive damages for disabled victims of discrimination (an amendment that would have been a clear sign that the ADA was not meant to have any teeth), was only narrowly defeated (Jay 1990). The implication, if the ADA serves merely as a statement of where we are, is that no impact of the law will be detected because, for the most part, we have already adopted the principles and practices laid out by the legislation. This outcome, then, begs the question of whether the ADA or child labor laws are necessary, or whether such Introduction 5 legislation is simply an expensive declaration of our morals. Even though one could argue that these laws might merely be statements of something we already knew, an even stronger argument might be made that public acknowledgment of a collective moral foundation serves an important purpose, one beyond quantification in economic terms.5 These laws strongly proclaim our social values and provide a legal mechanism with which to arrest the activities of those who have not yet adopted those ethics. In order to address whether the ADA merely serves as a statement of where we are rather than as a prediction of where we are headed, the analyses in this book will focus on two basic questions. First, how are disabled workers faring (relative to nondisabled workers) at any given point in time, and is their relative experience in the labor market improving? Second, did the ADA have any discernible impact on the relative experience of disabled workers? These questions will be asked in relation to as many dimensions of the labor market experience as possible. The questioning does not stop with the analyses, however. If it is discovered that the ADA has had or is having a positive impact on the labor market experience of disabled workers, then the ADA is accomp- lishing what it was designed to do. If the ADA has not had a measur- able effect on the relative labor market experience of disabled workers, and if their experience still falls short of that of nondisabled workers, then we may need to look toward additional or different legislation, specifically targeted at improving those dimensions identified as the most lacking. FOCUS AND STRATEGY OF ANALYSES This book is concerned with the labor market implications and impact of the ADA. In addition |
to the multiple dimensions of the potential effect of the ADA on disabled workers, there are at least as many more ways in which the ADA influences the lives of all disabled Americans; these other outcomes are not the subject of the present discussion, but may in fact amount to a much greater overall impact than that felt by the disabled in the labor market. The strategy of analysis followed here for documenting the impact of the ADA on the 6 Hotchkiss labor market experience of disabled workers has been to assemble as much information on as many dimensions of that experience as possi- ble. The major contribution of the analyses that follow is the wide- ranging coverage and synthesis of a massive amount of information in such a way as to make recommendations for policy. The emphasis has not been on developing new ways to examine the labor market experi- ence of the disabled, but to broaden that examination. The focus is on labor demand issues, defining the environment that the disabled might face. As a result, the analyses of employment and wages, for example, will correspond to what a disabled person might encounter upon entering the labor market. The conclusions will not be conditional on the labor supply decisions of the disabled, but will take those decisions into account in presenting unconditional results that apply to the population of the disabled, instead of merely to the sample (of workers) on which the estimates are obtained. Other analyses, such as the incidence of voluntary part-time employment, job separation, or job search experience, will be generalizable only to that population for which the issues are relevant: the part-time employed, the employed only, or the unemployed only. These sample limitations are legitimate and logical given the population for which such questions are relevant. It is important to remember that the purpose of the labor market provisions of the ADA was to break down barriers to the disabled and to improve their experiences in the labor market. Although perhaps expected, the alteration of various voluntary behaviors (such as labor force participation) was not the goal of these provisions. A fair analy- sis of the ADA should only involve an evaluation of what it was de- signed to do. Regardless of its intent, however, any policy can have unintended consequences that should also be addressed. Outline of the Book Chapter 2 explores employment outcomes among the disabled. Both joint labor force and employment and unconditional employment probabilities are examined for the entire sample of disabled individu- als, controlling for selection into the labor force. The availability of firm size and the phased-in nature of the ADA are exploited in a differ- ences-in-differences analysis. Results by type of disability are also presented. The joint labor force participation and employment proba- Introduction 7 bility for disabled persons declined relative to this joint outcome among nondisabled individuals after the ADA was implemented. How- ever, the unconditional (i.e., controlling for selection into the labor market) employment probability did not change post-ADA, relative to the experience of the nondisabled. The source of the deteriorating joint outcome is explored in some depth. In addition, employment among the disabled was found to shift more toward larger firms than did em- ployment among nondisabled workers, suggesting that implementation of the ADA and the financial ability (of larger firms) to accommodate workers’ disabilities mattered in the employment experience of dis- abled workers. Chapter 3 looks at the wages earned by disabled and nondisabled workers. A pooled, cross-sectional analysis suggests that wages among disabled workers fell post-ADA, relative to wages among the nondis- abled. In addition, a standard decomposition of the wage differential observed between disabled and nondisabled workers is performed. The availability of benefits is also explored through a simple probit analy- sis. While the overall compensation experience of disabled workers is found to be deteriorating relative to nondisabled workers (in both wages and availability of employer-sponsored fringe benefits), the de- gree to which discrimination might be used to explain this differential is also declining. It is found, however, that wages of disabled workers explicitly covered by the ADA (based on the size of their employers) have not changed post-ADA, relative to their noncovered counterparts, suggesting the overall lower wages among the disabled are being driven by more than accommodation costs. A number of job quality issues are addressed in Chapter 4. First, hours of work and the incidence of part-time employment and type of part-time employment among disabled and nondisabled workers are explored. Second, the distribution of workers across occupations and industries is compared using a popular distributional index. Third, the representation of disabled workers in high-growth and high-wage jobs is evaluated. This chapter presents evidence that while the incidence of part-time employment is increasing for disabled workers, relative to nondisabled workers, the incidence of voluntary part-time employment is driving that increase, particularly among workers with mental disor- ders. The degree of dissimilarity and the growth in dissimilarity in 8 Hotchkiss occupation and industry distributions of disabled and nondisabled workers over the 1981–2000 period are striking. While showing some improvement since 1992, this is of concern since disabled workers also appear to be concentrated in low-growth, low-wage occupations. Job separation and unemployment experiences of the disabled are explored in Chapter 5. Results from a multinomial logit find that, among individuals who have separated from their job, disabled workers are more likely to have separated voluntarily and less likely to have separated involuntarily than nondisabled workers. A similar analysis then finds that, among the unemployed, disabled workers are more likely to be reentrants and new entrants into the labor market than nondisabled workers. A duration analysis shows that disabled job seekers are searching on average three weeks longer before finding a job than similar nondisabled persons, and that most of the difference in observed search length is explained by differences in individual characteristics. Taken together, these results suggest that while the endowments or characteristics of disabled and nondisabled workers ap- pear to be valued equally, employers may be going to greater lengths to discern the fit of a disabled worker’s skill set with a particular job, thus leading to longer searches, a better match, and less chance that a separation is for involuntary reasons. Chapter 6 explores the impact of state-level legislation on wages, employment, and hours of disabled workers in different states. The analyses in this chapter exploit the differential timing of protective legislation across a number of states. The results are consistent and support the findings from Chapters 2, 3, and 4 on these same issues. Namely, wages decline and overall employment probabilities are un- changed among disabled workers, post-legislation, relative to nondis- abled workers. In addition, part-time employment among disabled workers increases post-legislation. These results suggest that the wage and part-time employment effect of the ADA may have been much greater if the state legislation had not already absorbed some if its potential impact. Chapter 7 synthesizes the results of the previous chapters around policy implications and recommendations. It is suggested that three directions be followed to further enhance the labor market experience of disabled workers: 1) provide incentives to the disabled to enter the labor force and relief to employers for the cost of accommodating these Introduction 9 individuals; 2) expand the support of resources available for disabled workers to increase their general human capital and ability to move into high-paying occupations; and 3) provide mechanisms by which employers and disabled workers can find each other and determine the appropriateness of the employment match. Data Details and Estimation Issues The combined Current Population Survey (CPS) Annual Earnings files for the months of March, April, May, and June, for the years 1981 through 2000, were used to obtain demographic data, employment status, earnings, details related to the respondent’s job, and location information to control for local labor market conditions. These CPS Annual Earnings files were matched with the March CPS survey for each year to obtain data on disability status, other sources of income, and labor market information available for the previous year. This strategy resulted in a sample four times larger than any single month of current labor market statistics, yielding greater confidence in the precision of the results. Some have questioned whether self-reported disability status (as in the CPS) suffers from endogeneity (e.g., Parsons 1980; Haveman and Wolfe 1984). For example, it may be the case that someone less likely to enter the labor market or to be employed is also more likely to report the presence of a disability (i.e., the disability indicator and error term of the regression are not independent). Stern (1989) finds that ‘‘any bias due to potential endogeneity is small’’ (p. 363). Of course, endo- geneity may be more of a concern since the passage of the ADA. As will be addressed in Chapter 2, endogeneity among the population as a whole may be a greater problem than among only labor force partici- pants (also see Kreider 1999). Additional criticism has been lobbed at the use of the traditional ‘‘work disability’’ measure contained in the CPS for drawing conclusions about the overall experience of the dis- abled or the effectiveness of the ADA. Some argue that requiring a disability to be ‘‘work limiting’’ can be too narrow (Kruse and Schur 2002; McNeil 2000). Others contend that not appropriately defining what a work-limiting disability is results in too broad of an inclusion of respondents (Hale 2001 and Kirchner 1996). Yet, others provide evidence supporting the representative nature of the CPS for monitor- 10 Hotchkiss ing outcomes among the disabled (Burkhauser, Daly, and Houtenville 2001). It is because of this controversy that confirmatory evidence of the CPS results is sought from an additional data source. Regardless, the reader should be aware that this book makes use of ‘‘work-limiting disability’’ as the identifier of a disabled person. In addition, it is expected that when focusing on labor market outcomes, those who report a work-limiting disability are the most likely to feel the greatest impacts of the ADA, should they exist. Table 1.1 reports the potential sample sizes for each year obtained from the CPS. Actual sample sizes for each analysis may differ be- cause of missing data or the use of specific subsamples (e.g., the unem- ployed only).6 While the sample sizes vary somewhat from year to year, the proportion of disabled to nondisabled remains fairly constant, and most analyses benefit from roughly 1,500 disabled workers and 50,000 nondisabled workers. Table 1.1 Sample Sizes for Merged CPS Data Files Disabled Nondisabled Labor force Labor force Year Total All participants Employed All participants Employed 1981 100,291 9,818 2,022 1,744 90,473 60,873 56,656 1982 94,351 9,617 1,962 1,661 84,734 57,006 52,015 1983 93,720 9,119 1,788 1,490 84,601 56,606 51,114 1984 94,683 9,654 1,922 1,661 85,029 57,591 53,507 1985 95,075 9,832 1,931 1,648 85,243 58,111 54,192 1986 90,341 8,931 1,848 1,581 81,410 55,604 51,935 1987 88,507 8,513 1,805 1,560 79,994 54,829 51,591 1988 85,371 7,811 1,697 1,493 77,560 52,258 49,625 1989 85,224 7,913 1,713 1,533 77,311 53,364 50,789 1990 93,625 8,745 1,919 1,692 84,880 58,896 56,005 1991 92,958 8,681 1,833 1,598 84,277 58,172 54,558 1992 90,520 8,547 1,913 1,614 81,973 56,617 52,779 1993 90,056 8,842 1,950 1,684 81,214 55,926 52,316 1994 88,674 9,709 1,810 1,602 78,965 55,341 52,246 1995 77,674 8,654 1,507 1,336 69,020 48,217 45,775 1996 77,188 8,396 1,535 1,379 68,792 48,356 45,892 1997 78,322 8,418 1,609 1,456 69,904 49,437 47,112 1998 77,583 7,796 1,468 1,332 69,787 49,403 47,370 1999 77,487 7,625 1,392 1,266 69,862 49,406 47,542 2000 79,242 7,917 1,488 1,358 71,325 50,825 48,999 Introduction 11 Since the ADA (and similar legislation) was designed to improve the labor market conditions of a group of workers, the analyses pre- sented here will be almost purely cross-sectional. The result is a com- prehensive comparison of the labor market experiences of one group of workers (the disabled) with that of another group of workers (the nondisabled). When making comparisons across groups of people, there will surely always be exceptions to the norm. It is important to recognize, however, that policy is rarely designed around exceptions. The use of individual data in the analyses does allow for control of identifiable individual characteristics (other than the group-defining characteristic of being disabled) in the determination of workers’ expe- riences. The |
premise, of course, is that identical disabled and nondis- abled workers should have the same labor market experience. This presupposition, which holds in making any comparisons across groups of workers (i.e., men versus women, or blacks versus whites), is more problematic in making comparisons across disability status; there are likely more unobservable characteristics across disability status than, for example, across gender. In addition, since most of the analyses consider the experience of those in the labor market, or at least control for selection into the labor market, no restriction is imposed on age.7 For each of the analyses, it is important to distinguish any changes in outcomes that might have resulted from the enactment of the ADA from any long-term trend. In other words, changes in the labor market experiences of workers with disabilities may reflect an evolving social awareness that culminated in the passage of the ADA, rather than the other way around. Consequently, this book documents labor market outcomes from 1981 through 2000.8 In addition, since a major over- haul of the CPS questionnaire was undertaken in 1994, care is taken to differentiate any ADA impact from a potential statistical artifact (see Polivka 1996). Also, due to the complicated matching across one to four months of the CPS, all analyses have been performed unweighted. According to Wooldridge (1999), ‘‘stratification based on exogenous variables does not cause any problems: estimators that ignore the stratification are consistent and asymptotically normal, and the usual variance matrix estimators are consistent’’ (p. 1386). Since stratification in the CPS sampling design is based on exogenous variables (geographic and de- mographic), and the attrition that results from the matching procedure 12 Hotchkiss is likely unsystematic, weights should be unnecessary (for further evi- dence on this point, see DuMouchel and Duncan 1983; Manski and McFadden 1981). In addition, any effect of stratification on the estima- tion can be accounted for by including indicator variables that corre- spond to the strata (Ginther and Hayes 2001), so demographic variables (such as disability status) should control for any observable effect sam- pling based on those characteristics might have (either initially or through attrition of matching). Any systematic attrition or sample loss due to unobservables will not be accounted for, but also cannot be corrected using weights. DISABLED AMERICANS As a first look at the data used for the analyses in the following chapters, Figure 1.1 depicts the percentage of the sample in each year and the percentage of workers in each year indicating a work-limiting disability.9 The vertical lines correspond to the phase-in years of the ADA. It is of interest to know whether there is any noticeable change Figure 1.1 Percentage of Sample and of Workers in the CPS Data Set Indicating a Work-Limiting Disability, 1981–2000 12 10 % of 8 sample 6 4 2 % of workers 0 1981 1983 1985 1987 1989 1991 1993 1995 1997 1999 (a) (b) (c) (a) ADA Enactment (b) ADA Phase I (c) ADA Phase II Introduction 13 in the reporting of having a work-limiting disability, particularly on the part of workers. Over the time period from 1981 to 2000, an average of 10 percent of the entire sample indicated having a work-limiting disability.10 There is a significant 1 percentage point difference between the aver- ages prior to and including 1991, and 1994 and later.11 Kreider (1999) finds evidence of substantial overreporting of limitations by nonwork- ers, a behavior which may be enhanced in the presence of protective legislation. It has also been found that the passage of the Personal Responsibility and Work Opportunity Reconciliation Act (PRWORA) in 1996, which essentially put a time limit on welfare payments, re- sulted in a movement of qualified recipients from the welfare rolls to SSI (Lewin Group 1999). The Lewin Group found ‘‘a very substantial flow of program participants from AFDC to SSI during the pre-reform period’’ (p. ES-3). The ‘‘pre-reform’’ period would coincide with the rise in the percentage reporting being disabled between 1993 and 1995 in Figure 1.1. However, the percentage has been declining fairly stead- ily since 1995. This issue of increased reporting of a work-limiting disability among the entire population is taken up in greater detail in Chapter 2, and again points to the potential endogeneity problems in- herent in using a self-reported disability classification. The proportion of workers indicating a work-limiting disability has remained fairly constant at about 3 percent across the entire time span; there is no significant difference in the 1981–1991 and 1994–2000 periods. So, while heightened awareness of the ADA and other pro- gram changes may have increased the reporting of work-limiting dis- abilities among the population, the primary individuals of focus for this study, i.e., workers, do not seem to have changed their reporting behavior in a way that might be expected to bias the analysis. In addi- tion, given that the reporting percentage of the population has begun to decline again, and that the share of workers seems unaffected, it is safe to say that CPS survey design changes that occurred in 1994 do not seem to have impacted the reporting of those with work-limiting dis- abilities. Comparing raw averages of disabled and nondisabled workers across the time period, one can see that there are some significant de- mographic differences among these categories of workers. Table 1.2 reports averages across time for a variety of demographics for disabled 14 Hotchkiss Table 1.2 Means of Select Demographic Variables for Disabled and Nondisabled Workers over Entire Time Period, CPS, 1981–2000 Variable Disabled workers Nondisabled workers Hours of work 33.97 38.01 Female 1 0.47 0.48 Single 1 0.48 0.40 Nonwhite 1 0.13 0.13 College degree 1a 0.10 0.18 Midwest 1 0.26 0.25 South 1 0.29 0.30 West 1 0.24 0.22 Norteast 1 0.21 0.23 Age 43.43 37.49 a Coding of education changed substantially in 1992; these averages reflect the average across years 1992–2000. and nondisabled workers. The distribution of workers across occupa- tions and industries is of interest, as well, but that will be explored in great detail in Chapter 4. While females and nonwhites seem to be equally represented among disabled and nondisabled workers, and each group of workers appears to be equally distributed geographically, there are some notable differences in demographics. Disabled workers, on average, work fewer hours, are less likely to have a college degree, are older, and are more likely to be single. While means across time give us some idea of the relative differences between worker catego- ries, they tell us nothing about trends. One trend of particular interest is the change in average hours per week over time among workers. Figure 1.2 depicts the average hours of disabled and nondisabled workers for each year between 1981 and 2000. While the average weekly hours of nondisabled workers rise fairly steadily over this time period from 37.5 in 1981 to 38.7 in 2000, the hours of disabled workers fall from an average of 34.7 in 1981 to 33.8 in 2000. Since a dramatic part of this decline occurred after 1992, one might suggest that the ADA was a factor. Full-time jobs may be less available to disabled workers; the ADA may have induced employ- ers to be more flexible regarding hours of work in accommodating a worker’s disability; or workers with more serious disabilities, unable to work full-time, may have begun to enter the labor market (Kaye Introduction 15 Figure 1.2 Average Weekly Hours of Disabled and Nondisabled Workers, CPS, 1981–2000 40 39 38 Nondisabled workers 37 36 35 34 33 32 31 Disabled workers 30 1981 1983 1985 1987 1989 1991 1993 1995 1997 1999 (a) ADA Enactment (a) (b) (c) (b) ADA Phase I (c) ADA Phase II 2002). Issues related to differences in part-time employment across disability status will be evaluated in greater detail in Chapter 4. SURVEY OF INCOME AND PROGRAM PARTICIPATION (SIPP) Data from the SIPP were used to construct a sample to supplement the analyses from the CPS. The goal in employing the SIPP is twofold. First, it provides validation of the results obtained using the CPS. Sec- ond, given that the SIPP allows identification of the nature of a respon- dent’s disability, some questions regarding the importance of the type of disability can be addressed. The samples from the SIPP have been constructed to match those from the CPS as closely as possible (e.g., regarding variable definitions, etc.).12 While providing more detail re- lated to the respondent’s disability, the SIPP does not provide as long or as large a data set with which to study labor market experience. Table 1.3 provides sample size details for the SIPP samples constructed 16 Hotchkiss Table 1.3 Sample Sizes for SIPP Data Files Disabled Nondisabled Labor force Labor force Year Total All participants Employed All participants Employed 1986 18,290 2,102 759 650 16,188 12,036 11,191 1987 33,884 3,939 1,470 1,297 29,945 22,278 20,932 1988 34,284 3,995 1,476 1,324 30,289 22,623 21,579 1989 16,274 1,826 651 579 14,448 10,949 10,505 1990 34,010 3,788 1,404 1,233 30,222 22,771 21,629 1991 51,140 5,596 1,998 1,755 45,544 34,392 32,328 1992 76,496 8,231 2,936 2,570 68,265 52,105 48,582 1993 73,831 8,112 2,839 2,442 65,719 49,861 46,694 1994 50,384 5,495 1,881 1,680 44,889 34,338 32,529 1995 23,753 2,610 918 829 21,143 16,313 15,550 1996 57,625 5,865 2,049 1,871 51,760 41,158 39,357 1997 46,914 4,706 1,584 1,470 42,208 33,718 32,558 for each year. Due to the sampling structure of the SIPP, the sample sizes varied from just over 16,000 to over 76,000. However, as Figure 1.3 illustrates, the representation of the disabled within the whole sam- ple and within the working subsample has remained consistent, al- though slightly declining over the period.13 In addition, there does not seem to be any shift in the trends during the ADA phase-in period. The percentages of the sample and of workers indicating a work- limiting disability are slightly higher in the SIPP than in the CPS. This occurs for two reasons. SIPP respondents are given two opportunities to answer a disability question positively. In addition, since the sample came from Wave 2 (the second survey within a panel), the respondent is reminded if he or she indicated a disability in Wave 1 (the first sur- vey), increasing the chances for a positive response (also see Kruse and Schur 2002). The percentages reflected in Figure 1.3 are consistent with those found by other researchers using the SIPP (e.g., DeLeire 2000; Kruse and Schur 2002). The nature of a person’s disability is placed into one of 30 different categories (including ‘‘other’’). In order to be able to include controls for type of disability, these categories were combined to correspond to the groupings used by the Social Security Administration.14 Aggrega- tion was necessary due to category size limitations; the four groups included as controls were: 1) musculoskeletal systems and special Introduction 17 Figure 1.3 Percentage of Sample and of Workers in the SIPP Data Set Indicating a Work-Limiting Disability, 1986–1997 14 12 10 8 % of sample 6 4 2 % of workers 0 1986 1987 1988 1989 1990 1991 1992 1993 1994 1995 1996 1997 (a) ADA Enactment (a) (b) (c) (b) ADA Phase I (c) ADA Phase II senses; 2) internal systems; 3) neurological systems and mental disor- ders; and 4) other. Figure 1.4 presents the distribution of all disabled individuals and disabled workers across these categorizations. The largest group by type of disability contains those with musculoskeletal and special senses disabilities; the internal systems category is gener- ally the next largest, followed by neurological and mental disorders (typically), and other. One can observe a slight upward trend in the Figure 1.4 Distribution of Disabled Individuals across Disability Type, SIPP, 1986–1997 50 45 40 Musculoskeletal and special 35 senses (%) 30 Internal systems 25 20 Neurological and mental disorders 15 10 Other 5 0 1986 1987 1988 1989 1990 1991 1992 1993 1994 1995 1996 1997 18 Hotchkiss neurological and mental disorders classification, while the proportion for internal systems has declined slightly, and that for musculoskeletal and special senses has remained fairly consistent over the time period. These four classifications will be used to determine whether the labor market experience varies across type of disability, an important consid- eration when trying to mold policy to impact those most affected. Notes 1. |
Further details of the history and provision of the Rehabilitation Act of 1973 can be found in Ellner and Bender (1980). 2. See Advisory Commission on Intergovernmental Relations (1989). 3. Data provided by the Roper Center for Public Opinion Research, University of Connecticut, Storrs, Connecticut. By 1999, 67 percent of those surveyed by the same polling group had heard of the ADA. 4. This issue has often been raised by historians. For example, see Landes and Solmon (1972). Donohue and Heckman (1991) also empirically address the sub- ject with regard to civil rights legislation. They conclude that federal civil rights legislation did play a major role in the progress of blacks beginning in 1965. 5. Some have even suggested that our analyses of the labor market impact of the ADA are misguided, and that attempts to quantify an impact in the labor market are merely arrogant efforts to justify our assumptions about how the labor market should operate (see Schwochau and Blanck 2000). 6. Appendix A contains additional information pertaining to the matching and merg- ing of the CPS files across months and concerning other details learned in the process. 7. The exceptions are analyses of employment where age is restricted to 15–65 years. 8. Prior to 1981, identification of a disability in the CPS was made only in the context of why a respondent was not working. 9. See Table C.1, in Appendix C, for percentages used to generate Figure 1.1. 10. The percentages of the entire sample that are disabled are slightly higher than those reported by Burkhauser, Daly, and Houtenville (2000, 2001). This is likely the result of the matching technique employed here, allowing for a much larger sample, and thus greater opportunity to be classified as disabled. 11. The Z statistic corresponding to the hypothesis of equal means over these time periods is 3.18, leading to a rejection of the null hypothesis of equality at the 99 percent confidence level. 12. Details of the construction of the SIPP samples are contained in Appendix B. 13. There are two check variables in the topical module used to identify a work- limiting disability for the 1986–1993 panels. The 1996 panel has only one check variable, which may explain the slightly lower incidence of a work-limiting dis- ability in the 1996 and 1997 SIPP samples. Kruse and Schur (2002) make use of Introduction 19 the functional limitations module (rather than the work disability module used here) and note a similar decline in disability percentages in later years due to question placement in that module. These nuances in the survey design among panels are clearly important and raise, once again, the concerns associated with using a self-reported disability indicator. 14. The Social Security Administration’s listing of impairments for disability status purposes can be found on the Internet at http://www.ssa.gov/OP_Home/cfr20/ 404/404-ap09.htm. The mental disorder category does include those classified as mentally retarded. The mentally retarded group is not broken out into a sepa- rate category in order to be consistent with the classification used by the Social Security Administration, to correspond with the groupings used by others (e.g., DeLeire 2000; Kruse and Schur 2002), and to preserve reasonable sample sizes within the categories. The employment and wage analyses were reestimated with mental retardation as a separate category, and none of the results or conclusions changed. This Page Intentionally Left Blank 2 Employment (Co-authored with Ludmila Rovba) Employment levels of the disabled are affected by both labor sup- ply and labor demand issues. Individuals suffering from a functional disability will also experience a larger cost to entering the labor market as, holding all else constant, greater effort or sacrifices must be made relative to nondisabled workers. The net result is that the reservation wage (the wage at which a person is willing to enter the labor market) for disabled individuals will be higher than for the nondisabled, and fewer disabled people will choose to enter the labor market, ceteris paribus. In addition, a person’s functional disability will be more likely to render him or her less productive than an otherwise identical, nondisabled person. Consequently, the disabled worker will be less likely to qualify for a given job and therefore less likely to be hired. Merely a perception of lower productivity or a greater difficulty of predicting a disabled worker’s productivity will reduce the likelihood of the individual being hired. So, for both supply and demand reasons, the employment levels of disabled workers would be expected to be lower than those of nondisabled workers.1 Figure 2.1 presents evidence from the CPS consistent with this prediction.2 The proportion of dis- abled individuals employed in any given year is at least 44 percentage points lower than the share of nondisabled individuals employed in that year. Other observations are worth mentioning in comparing employ- ment percentages. The recession dips of the early 1980s and early 1990s are obvious for the nondisabled, but not nearly as severe (in percentage terms) for the disabled. In addition, the employment per- centage for the nondisabled has made a fairly steady climb over the entire period compared with the relatively stagnant, then declining, em- ployment percentage of the disabled. Legislation that potentially affects the costs of either labor force participation or of hiring a group of workers can be expected to impact the employment levels of that group. The ADA, through its required 21 22 Hotchkiss and Rovba Figure 2.1 Percentage Employed of Disabled and Nondisabled Individuals, CPS, 1981–2000 80 70 Nondisabled 60 50 40 30 20 10 Disabled 0 1981 1983 1985 1987 1989 1991 1993 1995 1997 1999 (a) (b) (c) (a) ADA Enactment (b) ADA Phase I (c) ADA Phase II NOTE: Individuals in this figure refer to all people, regardless of labor force participa- tion status. accommodations, can be anticipated to reduce the cost to a disabled individual of entering the labor force, thus promoting labor force par- ticipation.3 It might also be argued that greater accommodation of a disabled worker’s limitations will result in enhanced productivity of that disabled worker, thus increasing the likelihood of employment. (This will be the case, however, only if employers are able to accurately predict the cost and productivity gains of such accommodations.) If those required accommodations, however, are ‘‘binding’’ in the sense that the employer would not undertake them in the absence of the ADA, it must be the case that increased productivity of the disabled worker does not offset the cost of implementing those accommodations.4 In other words, the value of the productivity gains is not as great as the cost of accommodation. This may result in decreased employment probabilities of disabled workers, since the cost of hiring a disabled worker has increased. Referring back to Figure 2.1, there does not seem to be any noticeable, or permanent, change in the employment Employment 23 percentages for disabled workers around the time of passage of the ADA, although there is a slight drop around the second phase-in period. This chapter explores more fully the employment probabilities of dis- abled and nondisabled workers between 1981 and 2000, controlling for observable individual characteristics and labor force participation. The issue of joint versus unconditional employment differences is explored through estimating a bivariate probit model, controlling for selection into the labor market. This is followed by an examination of how employment has changed across size of firm. The analyses indi- cate that, at worst, employment probabilities of disabled workers have not deteriorated relative to nondisabled workers, and that employment of disabled workers has shifted from medium and small firms to large firms. UNCONDITIONAL AND JOINT PROBABILITIES The labor market provisions of the ADA were motivated by a de- sire to eliminate barriers to disabled individuals that might exist in the labor market. An appropriate assessment of the success of the ADA in this endeavor would involve evaluation of unconditional employment outcomes. In other words, the question to be answered is whether there has been any progress in employment outcomes for the disabled person drawn from random, controlling for the likelihood that he or she is a labor force participant. The resulting probability of interest is an unconditional probability of employment. An alternative question, which has been the source of recent condemnation of the employment impacts of the ADA, is whether there has been any progress in employ- ment among all disabled people. This second question involves evalu- ation of a joint outcome: what is the probability of entering the labor force and being employed? While the impact of the ADA on labor force participation may be of interest from a social, resource, and de- mographic perspective, the unconditional probability will tell us more about the barriers disabled workers face, which is the focus of the employment provisions of the ADA. Consideration of the joint out- come (or, employment among all disabled people) confounds conclu- sions regarding the employment impact of the ADA with labor supply decisions. 24 Hotchkiss and Rovba When considering the unconditional probability, one must control for unobservable characteristics that might both affect the labor force participation decision and the employment outcome. Without control- ling for this potential self-selection, any differences measured in the employment probabilities may actually be confounded by variations between characteristics that affect the labor supply decision of disabled and nondisabled persons. If these characteristics change in a system- atic way over time, the problem is magnified. A bivariate probit model with selection will be estimated in order to obtain information on un- conditional employment outcomes and to control for selection into the labor market at the same time. The bivariate specification allows for the two outcomes (labor force participation and employment) to be impacted by the same unobservable factors (e.g., motivation). The selectivity part of the model is merely a recognition that we do not get to see the employment outcome unless the person is in the labor market to begin with, and that those we observe in the labor market may have systematically different employment outcomes than those not in the labor market. Correcting for selectivity allows us to make inferences for anyone from the population, not just those found in the labor mar- ket; this is what makes the probability unconditional.5 The following model defines the relationship assumed between labor force participation of person i (lfpi), employment (empi), and individual characteristics that are believed to affect the labor force par- ticipation decision (X1i) and the employment outcome (X2i): (2.1) lfpi 1 1X1i 1disablei 1i 1 if person i is in the labor force 0 otherwise (2.2) empi 2 2X2i 2disablei 2i 1 if person i is employed 0 otherwise disablei is equal to 1 if person i is disabled, 0 otherwise, and 1i and 2i are distributed as a bivariate normal with means equal to 0, variances equal to 1, and correlation equal to . In addition, of course, empi is Employment 25 only observed if lfpi 1.6 X1i and X2i both include age; age squared; female, nonwhite, education, and regional dummies; and state unem- ployment rate. The labor force participation equation regressors (X1i) also include nonlabor income, marital status, and a worked-last-year indicator. The employment equation regressors (X2i) also include num- ber of weeks worked last year. The impact of having a work-limiting disability on employment, then, is determined by calculating the proba- bility of interest for each person (using the estimated parameter coeffi- cients, 1, 2, 1, 2, 1, and 2), varying the disability index between 0 and 1, then averaging the difference across the sample.7 The model is estimated for each year separately, and the marginal impact of having a work-limiting disability is calculated.8 The significance of having a work-limiting disability is determined from the significance of the esti- mated coefficient. Figure 2.2 reflects the marginal effect of having a work-limiting disability on the predicted joint probability of labor force participation and employment in each year.9 The impact of having a work-limiting disability on the joint labor force and employment probability intensifies (becomes more negative), rather dramatically, in 1994, corresponding to the second phase of the ADA. The marginal effect increases from an average of 15 per- centage points prior to 1994 to an average of 19 percentage points Figure 2.2 Impact of Disability on Joint Labor Force Participation and Employment Probabilities, |
CPS, 1981–2000 Difference in 0 probability -0.03 -0.06 -0.09 -0.12 -0.15 -0.18 -0.21 1981 1983 1985 1987 1989 1991 1993 1995 1997 1999 (a) ADA Enactment (a) (b) (c) (b) ADA Phase I (c) ADA Phase II 26 Hotchkiss and Rovba between 1994 and 2000. In other words, having a work-limiting dis- ability decreased an individual’s joint probability of being in the labor force and employed by 4 percentage points more after 1994 than it did prior to 1994. This dramatic relative decline in the joint probability for the disabled is the result on which DeLeire (2000) and Acemoglu and Angrist (2001) base their warnings regarding the ADA. Breaking the joint probability into its employment and labor force participation components, it becomes clear that this salient change in 1994 is driven by decreases in labor force participation among the disabled. Figure 2.3 plots the predicted (unconditional) employment and labor force participation probabilities for the disabled alone using the same parameter estimates that generated Figure 2.2. After increas- ing fairly steadily, the predicted labor force participation rate declines in 1994 and stays below 1986 levels. At the same time, and with the exception of the recession years of 1991–1993, the predicted uncondi- tional employment probability among the disabled has increased fairly steadily. Figure 2.3 Separate Predictions of Employment and Labor Force Participation Probabilities for the Disabled, CPS, 1987–2000 Predicted probability 0.90 of employment 0.85 0.80 0.75 0.70 0.65 Predicted probability of labor force participation 0.60 0.55 0.50 1981 1983 1985 1987 1989 1991 1993 1995 1997 1999 (a) ADA Enactment (a) (b) (c) (b) ADA Phase I (c) ADA Phase II Employment 27 Again, in evaluating the barriers facing disabled workers, change in the unconditional employment probability is a more appropriate measure than the change in the joint labor force and employment out- come. Consequently, the condemnation of the employment impact of the ADA by DeLeire (2000) and Acemoglu and Angrist (2001) is misplaced, since both of these analyses confound their evaluation of employment changes with changes in labor supply decisions. The re- sults in Figure 2.3 show that the decline in employment probabilities among all disabled people is labor-supply driven and does not reflect an increase in employment barriers for individuals with disabilities. One may argue that the disabled have decreased their labor supply behavior in response to a real or perceived change in employment prob- abilities (demonstrating a potential ‘‘feedback effect’’), but the pre- dicted unconditional employment probabilities are not consistent with this view.10 It may be the case, however, that the condemnation of the ADA by recent studies should be aimed at its apparent impact on labor force participation. For example, if the ADA resulted in lower wages for the disabled (their employment has now become more expensive through required accommodations), it is possible that the wage would fall below the reservation wage of a significant number of disabled labor force participants, causing them to drop out of the labor market. It may also be the case that the severity of disabilities has been growing over time, resulting in declining labor force participation rates (Kaye 2002). The next section explores this drop in labor force participation rates among the disabled in greater detail. EXPLAINING THE DECLINE IN LABOR FORCE PARTICIPATION RATES Even if the ADA has not had a negative employment impact but has inadvertently discouraged the disabled from seeking employment, there would be a concern worthy of further policy consideration. The disabled and nondisabled populations can be represented in the follow- ing chart: 28 Hotchkiss and Rovba In labor Not in force labor force Nondisabled A B Disabled C D Cells A through D contain a given number of people at any given time period. A decrease in the disabled labor force participation rate (lfprd) corresponds to a decline in the ratio C/(CD). This ratio can decline if C decreases and/or if D increases.11 If C falls, these people must go somewhere; it is most likely that they either go to A (stay in the labor force but change their identification to nondisabled), or go to D (keep their identification as disabled, but leave the labor force). It is this latter possibility that is of potential concern. Although the ADA was not designed as a policy to necessarily increase the labor force partici- pation rate among the disabled, a precipitous drop in such participation, even remotely attributable to the ADA, is considered by many as unde- sirable. The lfprd may also fall, however, as a result of an increase in D. Again, the increase in D must come from somewhere; the most likely candidates are C (disabled leaving the labor force) or B (nondis- abled, nonparticipants in the labor force changing their identity to dis- abled). The latter (movement from B to D) is what might result, for example, from a shift of (nonparticipant) welfare recipients away from welfare programs and into disability programs; this movement follow- ing the reform of welfare has been documented (the Lewin Group 1999; also see Davies, Iams, and Rupp 2000). Greater effort to be classified (and identified) as disabled might also result from increased generosity of the disability programs themselves (see Autor and Dug- gan 2001; Bound and Waidmann 2002).12 This could be consistent with the finding by Kreider (1999) that nonworkers substantially over- report a work limitation. So, the question is, which is it? Are the disabled moving out of the labor force (from C to D) or are more nonparticipants identifying themselves as disabled (from B to D)? One way to get an indication of the movement across these cells is to evaluate the trends in the percentages represented in each cell. These results are depicted in the Employment 29 following chart. The percentage in each cell represents the growth, or decline, experienced within that cell. The cells exhaust the population, so the changes sum to zero.13 In labor Not in force labor force 0.1504** 0.2309** Nondisabled (A) (B) 0.0225** 0.1030* Disabled (C) (D) ** significant at the 95 percent confidence level. * significant at the 90 percent confidence level. The largest net change in the cells was movement of the nondis- abled out of the nonparticipant category (cell B). The coefficient indi- cates that the nondisabled, nonparticipant percentage declined an average of about 0.23 percentage points per year between 1990 and 2000. Even if the entire increase in cell A (nondisabled labor force participants) came from cell B, that still means that the overwhelming bulk of the increase in cell D (disabled nonparticipants) came from cell B as well, not cell C. In fact, the smallest net cell change was among the disabled labor force participants. This result provides strong evi- dence that the observed decline in the lfprd was not the result of the disabled fleeing the labor force but was most likely due to the reidenti- fication of some nonparticipants from nondisabled to disabled (move- ment from B to D). While providing an explanation for the decline in lfprd, this movement from cell B to cell D is a reminder of the criti- cism of using self-reported disability status in statistical analyses. This also suggests that endogeneity will be less of a concern for analyses that focus exclusively on labor force participants in evaluating the labor market experience of the disabled (using a self-reported measure of disability). In other words, there is less movement across disability status among labor market participants than among nonparticipants. In addition, these results indicate that the observed decline in the lfprd should not be considered as casting a shadow on the measured impacts of the ADA on employment. 30 Hotchkiss and Rovba POOLED, CROSS-SECTIONAL ANALYSIS Along with cross-sectional analyses, an analysis across time is per- formed to help quantify any difference in predicted probabilities of employment between disabled and nondisabled individuals after the ADA relative to before the ADA. The strategy used to accomplish this is to estimate a cross-sectional, time-series bivariate probit model with dummy variables representing whether the observation shows up in the data pre-ADA or post-ADA and whether the observation is a disabled or nondisabled person. These dummy variables are also interacted to determine whether being disabled had any greater impact on employ- ment after the ADA than before the ADA, relative to the experience of a nondisabled person.14 While this type of pooled, cross-sectional anal- ysis has been applied by many researchers (for example, Card 1992; Gruber 1994 and 1996; Zveglich and Rodgers 1996; and Hamermesh and Trejo 2000), the technique also has its critics (such as Heckman 1996). The primary criticism of this approach is that it is impossible to control for unobserved changes in the environment that occurred at the same time as the event of interest. For example, the second phase of the ADA occurred in 1994. This was also when the CPS underwent a major overhaul, and there is no way to disentangle these two events. In addition, the economy began its longest-running expansion in recent history at the same time that the ADA was being phased in, which could potentially confound any measurable impact of the ADA through this estimation strategy. One advantage of the analysis here is that the CPS survey changes should not have a differential impact on the dis- abled and nondisabled (as the changes did not affect measurement or classification by disability),15 and general business cycle activity should essentially impact the disabled and nondisabled in relatively the same proportions.16 Nonetheless, the state unemployment rate is included as a regressor in order to capture any general business cycle influences. The empirical model looks just like the bivariate probit with selec- tion estimated in one year, except with the additional time-period dummy variables: (2.3) lfpi 1 1X1i 1disablei 1posti 1disablei posti 1i Employment 31 (2.4) empi 2 2X2i 2disablei 2posti 2disablei posti 2i. Again, lfpi 1 if person i is in the labor force, 0 otherwise, and empi is not observed unless lfpi 1. disablei is equal to 1 if person i is disabled, 0 otherwise; posti is equal to 1 if person i is observed in 1992 or later; X1i and X2i include individual demographic characteristics; and 1i and 2i are distributed as a bivariate normal with means equal to 0, variances equal to 1, and correlation equal to . In this framework, the affected group (the disabled) is controlled for by a dummy variable indicating whether the individual has a work- limiting disability (disable), and the time period is controlled for by a dummy variable indicating whether the ADA had been implemented yet or not (post); 1 and 2 are the estimated parameter coefficients for the time-period dummies. Given the nonlinearity of the bivariate probit estimation procedure, a single parameter coefficient does not tell us the additional impact the ADA had on the difference in employment probabilities between the disabled and nondisabled. The difference in the impact of having a work-limiting disability on employment across the two time periods can be calculated by evaluating the probabilities of interest for each person, varying the disable and post dummy vari- ables, then taking the difference between these probabilities, and aver- aging this difference across the sample.17 The significance of the coefficient on the interacted disable post (1, and 2) will, however, yield significance levels of the calculated marginal effects. The decision of when one would expect the ADA to have its stron- gest impact (i.e., how to define post) is debatable. One might expect some impact when the ADA was enacted (1990). However, employers were not required to respond until 1992 (for employers with 25 or more employees) and 1994 (for employers with 15 or more employees). The year 1992 was chosen for defining post since that is the first year of enforcement of the law. Table 2.1 details the regression results. The coefficients on disable post presented in Table 2.1 are consistent with the conclusions drawn from Figure 2.2. Namely, labor force participation among the disabled declined significantly after im- plementation of the ADA, relative to labor force participation among the nondisabled. In addition, while all other regressors contribute sig- nificantly to explaining employment (all at the 99 percent confidence 32 Hotchkiss and Rovba Table 2.1 Labor |
Force Participation and Employment Bivariate Probit with Selection Results, CPS, Combined Years 1981–2000 Labor force participation Employment Regressor equation equation Intercept 2.9988*** 0.6421*** (0.0152) (0.0215) Age (00) 13.3928*** 1.3265*** (0.0742) (0.1176) Age2 (0000) 16.6844*** 2.2159*** (0.0905) (0.1544) Female1 0.4651*** 0.1811*** (0.0032) (0.0047) Nonwhite1 0.0176*** 0.2393*** (0.0045) (0.0058) High school grad1 0.2094*** 0.0762*** (0.0041) (0.0061) Some college1 0.1127*** 0.2076*** (0.0046) (0.0067) College grad1 0.2754*** 0.3730*** (0.0053) (0.0083) Advanced degree1 0.3378*** 0.3479*** (0.0082) (0.0134) Central city1 0.0398*** 0.0321*** (0.0051) (0.0070) Midwest1 0.0530*** 0.0337*** (0.0045) (0.0065) South1 0.0196*** 0.0813*** (0.0042) (0.0064) West1 0.0233 0.0218*** (0.0046) (0.0067) Single household1 0.2148*** — (0.0036) Nonlabor income (000000) 16.6473*** — (0.2922) Worked last year1 2.0763*** — (0.0035) Weeks worked last year (00) — 3.2187*** (0.0151) State unemployment rate (0) 0.0901*** 0.6357*** (0.0076) (0.0103) disable1 0.7624*** 0.2012*** (0.0080) (0.0143) Employment 33 Table 2.1 (continued) Labor force participation Employment Regressor equation equation post (year1992 or later)1 0.0677*** 0.0139*** (0.0035) (0.0051) disablepost1 0.1706*** 0.0298 (0.0120) (0.0225) Rho 0.0371*** (0.0065) Log-likelihood 596,816 Number of observations 1,359,885 NOTE: Standard errors are in parentheses. *** significant at the 99 percent confidence level. Notation of, for example, (00) indicates regressor has been scaled by dividing by 100. level), being disabled after ADA implementation is not one of them; the disabled are no more or less likely to be employed than the nondis- abled, post-ADA relative to pre-ADA. In other words, the ADA has not changed the relative employment probability between disabled and nondisabled workers.18 Table 2.2 translates the parameter coefficients in Table 2.1 into marginal effects. These marginal effects indicate that the employment probability of disabled labor force participants, relative to nondisabled labor force participants, declines at most 0.6 of a percentage point post- Table 2.2 Change in Marginal Effect of Disability on Labor Force Participation and Employment Probabilities Probability Probability Probability (lfp1) (emp1) (emp1, lfp1) Before After Before After Before After ADA ADA ADA ADA ADA ADA Nondisabled 0.7284 0.7397 0.8592 0.8569 0.6718 0.6798 Disabled 0.5693 0.5431 0.8233 0.8148 0.5202 0.4942 Marginal effect 0.1591 0.1966 0.0359 0.0421 0.1516 0.1856 Change in 0.0375 0.0062 0.0340 marginal effect NOTE: Probabilities calculated using parameter coefficients from Table 2.1. 34 Hotchkiss and Rovba ADA (see column 2, last row). However, this effect is not significantly different from zero; in a model where all other coefficients are signifi- cantly different from zero, this is notable. On the other hand, the labor force participation rate declined significantly, by nearly 4 percentage points more for the disabled than for the nondisabled, post-ADA.19 EVIDENCE FROM THE SIPP The analysis detailed in Equations 2.3 and 2.4 is reestimated using the sample obtained from the SIPP for the years 1986 through 1997. Table 2.3 reports the coefficients of interest from estimating the bivari- ate probit model with selection using the SIPP data. The results re- ported in Table 2.3 mirror those in Table 2.1, with one difference: employment among the disabled increased more post- versus pre-ADA than did the employment of the nondisabled. This positive 0.0768 coefficient on disable post translates into a 0.8 of a percentage point higher employment probability for the disabled relative to the Table 2.3 Labor Force Participation and Employment Bivariate Probit with Selection Results, SIPP Combined Years 1986–1997 Labor force participation Employment Regressor equation equation disable1 0.9404*** 0.2435*** (0.0105) (0.0211) post (year1992 or later)1 0.0293*** 0.0348*** (0.0048) (0.0077) disablepost1 0.1360*** 0.0768*** (0.0129) (0.0250) Rho 0.4811*** (0.0204) Log-likelihood 292,341 Number of observations 500,560 NOTE: Additional regressors included age; age squared; state unemployment rate; female, nonwhite, education, regional dummy variables; an indicator for SMSA resi- dence (employment); and non-labor income and marital status (labor force participa- tion). Standard errors are in parentheses. *** significant at the 99 percent confidence level. Employment 35 nondisabled. In addition, the relative decline in labor force participa- tion among the disabled found in the CPS data is also seen using the SIPP data as well. Along with the reestimation of Equations 2.3 and 2.4, a specifica- tion is estimated in which the impact of having a disability post-ADA is allowed to vary by type of impairment:20 (2.5) lfpi 1 1X1i S 1 musculoskeletali I 1 internali M 1 mentali O 1 otheri 1posti S 1 musculoskeletali posti I 1 internali posti M 1 mentali posti O 1 otheri posti 1i (2.6) empi 2 2X2i S 2 musculoskeletali I 2 internali M 2 mentali O 2 otheri 2posti S 2 musculoskeletali posti I 2 internali posti M 2 mentali posti O 2 otheri posti 2i where lfpi is equal to 1 if person i is in the labor force, 0 otherwise, empi is equal to 1 if person i is employed, 0 otherwise, Xi is a set of covariates for each person (individual demographic characteristics), musculoskeletali is equal to 1 if person i has a musculoskel- etal disability,21 internali is equal to 1 if person i has a disability involving the internal systems, mentali is equal to 1 if person i has a mental disability, otheri is equal to 1 if person i has a disability classified as ‘‘other,’’ and posti is equal to 1 if person i is observed in 1992 or later. Again, these equations are estimated via maximum likelihood as a bi- variate probit with selection, where empi is only observed if lfpi 1. In this framework, the type of disability is controlled for by dummy variables indicating whether the individual has a musculoskeletal, in- ternal systems, mental, or other disability; and the time period is con- trolled for by a dummy variable indicating whether the ADA had been implemented yet or not. The coefficients of particular interest (j 1 and 36 Hotchkiss and Rovba j 2, j S,I,M,O), therefore, allow us to calculate the labor force partici- pation and employment changes among disabled workers post- versus pre-ADA relative to the changes for nondisabled workers. Table 2.4 provides selected estimated coefficients and regression details. The estimation results presented in Table 2.4 from the SIPP data set are also consistent with the conclusions drawn using the CPS data: labor force participation declined more for all classifications of disabil- ity, relative to nondisability, post- versus pre-ADA. However, employ- Table 2.4 Labor Force Participation and Employment Bivariate Probit with Selection Results by Type of Disability, SIPP Combined Years, 1986–1997 Labor force participation Employment Regressor equation equation musculoskeletal1 0.8253*** 0.2798*** (0.0150) (0.0281) internal1 0.9597*** 0.1660*** (0.0192) (0.0409) mental 1 1.2722*** 0.1599*** (0.0237) (0.0487) other1 0.8396*** 0.3429*** (0.0280) (0.0508) post (year1992 or later)1 0.0305*** 0.0348*** (0.0048) (0.0077) musculoskeletalpost1 0.1416*** 0.0542 (0.0187) (0.0348) internalpost1 0.1137*** 0.1693 (0.0247) (0.0532) mentalpost1 0.0850*** 0.1187** (0.0282) (0.0573) otherpost1 0.0829** 0.1484** (0.0360) (0.0675) Rho 0.4799*** (0.0205) Log-likelihood 292,164 Number of observations 500,560 NOTE: See notes to Table 2.3 regarding additional regressors. Standard errors are in parentheses. *** significant at the 99 percent confidence level. ** significant at the 95 percent confidence level. Employment 37 ment probabilities (controlling for labor force participation) increased significantly more for the disability classifications of mental and other than for the nondisabled, post- versus pre-ADA. Relative em- ployment probabilities did not change significantly for those with mus- culoskeletal or internal disabilities. While it is difficult to interpret the employment impact for those with disabilities classified as other, the major role that those with mental disorders play in explaining the overall relative employment improvement is not surprising, given the attention paid to and policies developed for those with mental disabilities in recent years.22 In addi- tion, if we expect costs of accommodation to influence employment outcomes of the disabled, these results might suggest that accommo- dating workers with mental disabilities (such as through flexible work scheduling) has been relatively less expensive for employers than ac- commodating workers with musculoskeletal or internal disabilities (for example, through physical modification of the work environment). EMPLOYMENT PROBABILITY AND FIRM SIZE The phased-in nature of the ADA yields an additional dimension across which to examine its impact on employment.23 After enactment in 1990, the ADA covered employers with 25 or more employees starting in 1992, and employers with 15 or more employees starting in 1994. One might expect a differential employment impact of the ADA based on whether a particular firm is covered by the legislation. In addition, because of the potential costs of accommodating workers’ disabilities, there is reason to expect that disabled workers might migrate toward covered employers (based on size), toward employers who are more able to absorb the cost of accommodation (larger firms may have more re- sources to devote to such investments), and toward employers who can spread the fixed costs of accommodation across more workers (again, this would be true of larger firms). While most estimates indicate that per-worker costs of accommodations only range between $100 and $1,000, this expenditure is clearly easier to absorb for larger, more afflu- ent firms (LaPlante 1992; Kujala 1996).24 The federal government recog- nizes this burden to small business by making a targeted tax credit available for up to half of an accommodation expenditure that exceeds $250 but is less than $10,250 (Dykxhoorn and Sinning 1993; Hays 1999). 38 Hotchkiss and Rovba Figure 2.4 plots the distributions of disabled and nondisabled workers across firm sizes. Here, a small firm is one that employs fewer than 25 workers, a medium firm employs at least 25 but fewer than 100, and a large firm employs at least 100 workers.25 The CPS began asking about the size (number of employees) of a worker’s firm in 1988. This question refers to a person’s main job during the previous year and is therefore available for the years 1987–1999. Large firms employ by far the greatest percentage of both disabled and nondisabled workers. While the average (over time) percentage in medium-sized firms is practically identical across disability status (14 percent), a greater proportion of nondisabled workers (62 percent versus 58 per- cent) is employed in large firms, and a greater proportion of disabled workers (28 percent versus 24 percent) is employed in small firms. As far as trends are concerned, nothing obvious is apparent from Figure 2.4. Trend regression indicates that there have been statistically sig- nificant declines in medium-firm employment among both disabled and nondisabled workers. While most of this decline among the nondis- abled shifted toward small firms, the shift among the disabled was toward large firms. The analysis that follows will allow quantification of these movements and a direct comparison across disability status. A multinomial logit analysis was undertaken to determine how the relative employment of disabled and nondisabled workers in different- sized firms has shifted over the entire time period for which firm size is available.26 This approach allows us to specify multiple possible outcomes (e.g., employment in a small, medium, or large firm) as a function of a variety of observed characteristics and unobservable fac- tors, recognizing that as one’s probability of being in one firm size increases, the probability of being in another firm size necessarily de- creases. A person’s employment outcome is divided into three catego- ries (where n refers to the number of employees at the worker’s firm): 1) employed by a small (n 25) firm, 2) employed by a medium (25 n 100) firm, and 3) employed by a large (n 100) firm.27 It is assumed that the individual selects the firm size (ceteris pari- bus) that maximizes the utility gained from that choice. The employer plays a role in that decision by making different job packages available, such as wages and other characteristics. The probability of person i being employed in firm size 1 is defined as (where u refers to utility): Employment 39 Figure 2.4 Distribution of Disabled and Nondisabled Workers across Firm Size, CPS, 1987–1999 (A) Disabled workers 70 Large 60 (Firm size ² 100) 50 40 Small (Firm size < 25) 30 20 Medium (25 ¢ firm size < 100) 10 0 1987 1989 1991 1993 1995 1997 1999 (B) Nondisabled workers 70 Large (Firm size ² 100) 60 50 40 (%) 30 Small (Firm size < 25) 20 10 Medium 0 (25 ¢ firm size < 100) 1987 1989 1991 1993 1995 1997 1999 40 Hotchkiss and Rovba (2.7) P1 P(ni |
1) P(ui1 uij) for j 2,3. Let Pj (2.8) F(X) for j 1,2, P j j P3 where F () is the cumulative distribution function, X are individual characteristics, and are parameter coefficients. This means that Pj F( jX) (2.9) G(X) for j 1,2. P j 3 1 F( jX) Because of the rules of summation, (2.10) P3 1/1 2 G( jX) G( jX) and Pj j1 1 2 . G( jX) j1 If we let (2.11) G( jX) exp( jX) and Yij if person i falls in firm size category j 1 0 otherwise the log likelihood function (ln L) can be written as (2.12) ln L 3 3 YijlnPij, i1 j1 exp(X ij) 1 where Pij 2 and Pi3 2 1 exp(X ik) 1 . exp(X ik) k1 k1 The multinomial logit results in three sets of parameter estimates, each set describing the probability of one of the firm size outcomes. Employment 41 Every person has a probability of being employed by each size firm, and those three probabilities sum to one (since the analysis is restricted to employed individuals). Figure 2.5 summarizes the predicted proba- bilities of disabled workers, relative to the predicted probabilities of nondisabled workers, being employed by each size firm for the years from 1987 to 1999.28 The probability of employment of disabled workers relative to non- disabled workers in both small- and medium-size firms declined over this time period, whereas the relative probability of employment of disabled workers in large firms increased.29 This means that relative to nondisabled workers, disabled workers were increasingly likely to be employed in large firms between 1987 and 1999. This result is consis- tent with Kaye (2002), who finds growing employment rates among the disabled in ‘‘big-business’’ industries (500 or more employees). The increased probability of employment among larger firms may sug- gest that they have been able to accommodate (i.e., afford, spread costs over greater numbers of workers, find appropriate job matches) work- ers’ disabilities more than small- or even medium-sized firms, and that disabled workers have found it fruitful to seek out jobs at the largest firms. In fact, large companies have typically been at the forefront of implementing costly accommodations, either because of public rela- tions initiatives or because of other considerations not faced by smaller Figure 2.5 Ratio of Predicted Employment Probabilities for Disabled versus Nondisabled Workers by Firm Size, CPS, 1987–1999 1.25 Small firms 1.20 1.15 1.10 Medium firms 1.05 1.00 0.95 0.90 Large firms 0.85 0.80 1987 1989 1991 1993 1995 1997 1999 42 Hotchkiss and Rovba businesses (Johnson 1997). These visible efforts make larger compa- nies more attractive for disabled job seekers. In addition, one study has found that large firms are significantly more likely to comply with the ADA and to have specific policies in place guiding the hiring of workers with disabilities (Scheid 1998). It is important to point out, however, that since the ADA has no affirmative action component, the relative shift in employment of disabled workers toward larger firms is not likely the result of active recruitment efforts. Since employers with 25 or more workers were covered by the ADA beginning in 1992, one additional computation can help to quan- tify any adjustment that may have occurred at that time in the relative employment probabilities. Table 2.5 presents a form of differences-in- differences-in-differences (DDD) calculation for the average predicted probabilities of employment across firm size, time, and disability status. These DDD results are not derived from an estimation proce- dure, but are merely the differences in predicted probabilities across coverage, firm size, and time. The predicted probabilities from the Table 2.5 DDD Calculation for Average Predicted Probability of Employment by Firm Size, Disability Status, and across Time, CPS, 1987–1999 Time difference for Firm size / year 1987–91 1992–98 a given firm size A. Disabled workers n 25 0.7434 0.7280 0.0154 n25 0.2566 0.2720 0.0154 Firm size difference at a point in time 0.4868 0.4560 Differences-in-differences 0.0308 B. Nondisabled workers n 25 0.7798 0.7571 0.0227 n25 0.2202 0.2429 0.0227 Firm size difference at a point in time 0.5596 0.5142 Differences-in-differences 0.0454 DDD: 0.0146 NOTE: n refers to the number of employees in the firm. Predicted probabilities for each firm size from the multinomial logit results presented in Figure 2.3 are averaged across the years indicated and disability status to obtain the average predicted proba- bilities. Employment 43 multinomial logit estimation are used for differencing, and the proba- bilities for the medium and large firm sizes are combined to correspond to the coverage of the ADA beginning in 1992. This analysis is not as precise as we might like, since employers with 15 or more workers were covered by the ADA beginning in 1994, and since there are no standard errors available to determine significance of the results. Con- sequently, the results in Table 2.5 should be viewed only as suggestive. The DDD analysis suggests that covered disabled workers have, at most, a 1.5 percentage point greater probability of being employed, relative to noncovered disabled workers, post-ADA, relative to pre- ADA, relative to the employment probability differences among non- disabled workers. CONCLUSIONS The purpose of this chapter was to evaluate the relative employ- ment experiences of disabled and nondisabled workers. A pooled, cross-sectional analysis determined that the joint labor force and em- ployment probability of the disabled decreased significantly after im- plementation of the ADA relative to a nondisabled person’s employment probability. This joint probability is influenced by both supply and demand factors and therefore confounds the employment experience of disabled workers with labor supply influences. In order to get a picture of the expected employment outcome, the unconditional em- ployment probability was calculated. It was found that the uncondi- tional employment probability among the disabled did not change after implementation of the ADA relative to the employment probability among the nondisabled. In other words, although improvements in relative employment outcomes have not been realized, there has not been the deterioration of the employment position of the disabled as claimed by others. This suggests that adjustments in the labor supply of disabled workers are not likely the result of feedback effects or fear of negative outcomes, since the employment outcomes for disabled workers relative to those of nondisabled workers did not deteriorate post-ADA. It was also shown that the decline in labor force participa- tion was likely the result of the reclassification of nondisabled, nonpar- 44 Hotchkiss and Rovba ticipants as disabled, post-welfare reform and potentially in response to the growing generosity of disability benefit policies. Analysis of the SIPP data produced a confirmation of the CPS results and allowed a closer evaluation of employment probabilities by type of disability. In fact, the SIPP results suggest that the relative employment position actually improved, with greater unconditional employment probabilities among the disabled post-ADA, compared to the nondisabled. It was found that those with mental disorders and those with disabilities classified as other experienced the greatest pos- itive employment impact of the ADA. Workers with musculoskeletal and internal system disabilities did not experience any different em- ployment probability growth from those without disabilities. Evidence that the cost of accommodation is not irrelevant in the labor market’s adjustment to the ADA was found in a DDD analysis, which accounted for the size of a worker’s employer, allowing for identification of disabled workers who were covered by the legislation and those who were not. Disabled workers employed by large or me- dium firms (covered employers) have, at most, a 1.5 percentage point greater probability of being employed, relative to disabled workers in small firms, post-ADA, relative to pre-ADA, relative to nondisabled workers. In addition, employment of disabled workers was shown to shift more towards large firms post-ADA than did employment of non- disabled workers. Since the fixed cost of disability accommodations can be spread over a greater number of workers in large firms, this result suggests that larger firms were better poised and able to absorb the costs of accommodations dictated by the ADA and/or better able to match disabled workers’ job skills with recruitment needs. Notes 1. Also see DeLeire (1997, Section 3). 2. See Table C.2 in Appendix C for the percentages used to generate Figure 2.1. 3. See Stern (1996). 4. It has also been suggested that persons with disabilities entering the labor force after the ADA will have more severe disabilities than those employed prior to the ADA, making the potential for ‘‘binding’’ accommodation requirements that much more likely and expensive (Chirikos 1991). 5. This model specification is similar to that familiar to most labor economists: con- trolling for selection into the labor market (or employment) when estimating a Employment 45 wage equation. In that problem, we are interested in the (unconditional) expected wage for anyone in the population. By controlling for selection into the labor market (since we can only estimate the wage equation on those for whom we observe wages), we are able to make unconditional predictions that correspond to the population. If selection is not controlled for, the only prediction of wages that can be made is that conditional on labor force participation. 6. The bivariate probit model with selection gives rise to the following likelihood function: ln L LFP1, EMP1 ln 2 1X1i, 2X2i, LFP1,EMP0 ln 2 1X1i, 2X2i, LFP0 ln 1X1i, where 2 is the bivariate normal cumulative distribution function and is the univariate normal cumulative distribution function. 7. This method of calculating the marginal effect of a change in a dummy variable is referred to as a measure of discrete change and is described in greater detail by Long (1997, pp. 135–138). Specifically, the average marginal impact of having a disability on the joint labor force and employment outcome is calculated as 1 N N Pilfp1, emp1 Xi, disable1Pilfp1, emp1 Xi, disable0 , i1 and the average marginal impact of having a disability on the unconditional prob- ability of employment is calculated as 1 P N N iemp 1 Xi, disable 1 Piemp 1 Xi, disable 0 . Both of i1 these are calculated, of course, using the parameter estimates obtained from the bivariate probit model with selection detailed in endnote 6. 8. This model specification allows a comparison to results with earlier studies, as well (through calculation of the joint probability). 9. See Table C.3 in Appendix C for the numbers used to generate Figure 2.2 (num- bers in column 3 minus numbers in column 1). 10. In addition, Stern (1996) presents empirical evidence that labor supply decisions of disabled people are driven more by labor supply factors than by labor demand factors. Also see Averett, et al. (1999) for further evidence on this point. 11. One can easily show that, for C 0 for lfprd C/(C D), lfprd/D 0 and lfprd/C 0. 12. Acemoglu and Angrist (2001) dismiss this theory by showing that controlling for receipt of disability benefits only marginally impacts their results. They fail to point out, however, that the receipt of benefits will reflect only a fraction of the desire to receive benefits (see Kubik 1999). Consequently, the actual impact of increasing program generosity on the disability status change for nonparticipants could be much larger than that measured by growing recipiency. 13. These trend coefficient estimates for each cell were obtained from simple linear regressions of the percentage of people represented in that cell as a function of a time trend corresponding to the period 1990–2000, in order to focus on post- ADA changes. 46 Hotchkiss and Rovba 14. The strategy described here can be likened to the popular differences-in-differ- ences (DD) methodology, but it is applied to a nonlinear statistical model. 15. Acemoglu and Angrist (2001, Appendix A) show that results are fairly consistent across a variety of sample restrictions based on differences between the 1993 and 1994 samples (crossing the survey modification time period). Consequently, it is not expected that the results reported here are significantly biased by changes in the CPS survey design. 16. The cyclicality of disabled and nondisabled employment is explored by Burk- hauser, Daly, and Houtenville (2000), although, like Acemoglu |
and Angrist (2001) and DeLeire (2000), their analysis confounds employment outcomes with labor supply effects. 17. See endnote 7. 18. The remaining parameter estimates are consistent with labor/leisure choice the- ory. For example, higher nonlabor income and being female lead to lower labor force participation, and the age/participation profile is concave. They also con- form to standard human capital theory with more education and greater labor market experience (measured through number of weeks worked last year) leading to a greater probability of employment. 19. The marginal effect on the joint probability outcome was 3 percentage points (column 3, last row). While not directly comparable, DeLeire (2000) estimates a 7.2 percentage point drop in employment among all disabled men, and Acemoglu and Angrist (2001) estimate a 10–15 percentage point drop in the number of weeks worked by the disabled. Again, these results are analogous to the joint probability calculated here, although not surprisingly of slightly varying magni- tude given the differences in data used (DeLeire) and in estimation procedure and model specification (DeLeire and Acemoglu and Angrist). 20. See Appendix B for the source of classification of disability. 21. The musculoskeletal grouping includes disabilities involving the special senses (e.g., hearing, sight). 22. The President’s Committee on Employment of People with Disabilities had placed an emphasis in the late 1990s on individuals with mental impairments. This committee has more recently been replaced by the Presidential Task Force on Employment of Adults with Disabilities. Information about the activities of this task force can be found on the U.S. Department of Labor web site, http:// www.dol.gov/ sec/programs/ptfead/. 23. Chay (1996) and Carrington, McCue, and Pierce (2000) represent other research exploiting the natural phase-in periods across firm size or geographic differences in dates of implementation in order to measure the labor market impact of social policy legislation. 24. In addition to the direct costs of accommodation, efficiency costs not directly absorbed by the employer, but felt by the labor market as a whole, are identified by Rosen (1991). 25. This definition of small, medium, and large firms follows that of Acemoglu and Angrist (2001); the definition will change in the next chapter. Employment 47 26. Multinomial logits have come under frequent criticism because of the assumption of independence of irrelevant alternatives (IIA) that is implied by the logit speci- fication. Alternative specifications that retain the desired probability structure (i.e., multinomial probit) are riddled with their own problems and not considered here to add value greater than the cost imposed. It has been pointed out that under the framework of what is called a ‘‘universal’’ logit, the estimation procedure can be applied, but the utility interpretation of the structural estimates is lost. In addition, the more regressors included to describe the multiple outcomes, the less bothersome is the assumption of IIA. For these reasons, the logit structure is retained. For further discussion on these points, see Ben-Akiva and Lerman (1985, section 5.2) and Moffitt (1999, pp. 1382–1387). 27. The results of this analysis are relevant for workers only and not generalizable to the entire population. 28. The predicted probabilities are found in Table C.4 in Appendix C. 29. A firm-size analysis was also undertaken by Acemoglu and Angrist (2001). Since they did not restrict their analysis to workers, they found that relative employment declined across all firm sizes (compared with not working), and that there was no change in relative employment of disabled workers in large firms, as compared with the nondisabled. This Page Intentionally Left Blank 3 Compensation: Wages and Benefits The issue of compensation has generated numerous contributions to the demand side of the disability literature. For example, Haveman and Wolfe (1990) evaluate the economic well-being (in which a major factor is earnings, or compensation) of the disabled over an extended period of time (1962–1984). A large part of their measure of well- being, however, is accounted for by transfer income (a nonlabor market source of income).1 In addition, while Salkever and Domino (1997), Johnson and Lambrinos (1985), and Baldwin and Johnson (2000) have examined the issue of wage discrimination against the disabled, evi- dence on how these measures of discrimination have changed over time is sparse (see DeLeire 2001). Depending on the nature of the impairment, one would expect a disabled worker to be less productive than an otherwise identical non- disabled worker; thus, lower wages would be seen for disabled workers. The implementation of a policy that is expected to raise productivity, however, would increase those individuals’ wages. The ADA, through its accommodation requirements, should unambiguously increase the productivity of disabled workers. The impact of this process on work- ers’ earnings, however, is uncertain. If productivity is increased by more than the cost of accommodations, wages of disabled workers should rise. If, on the other hand, the cost of accommodation exceeds the gains in productivity, disabled workers are likely to bear some of the increased costs through lower wages. In addition, since accommo- dation should not impact the productivity of workers not in need of those accommodations (i.e., nondisabled workers), we should not ob- serve a substantial wage change for nondisabled workers post-ADA. The CPS contains data on wages paid and hours employed for all workers. Information on the availability of health insurance and pen- sion plans through one’s employer is also available. This chapter com- pares how relative earnings for workers with disabilities have changed over time and if there was any significant alteration coinciding with the implementation of the ADA. These comparisons are also made across types of disability with the help of the SIPP data set. Earnings of 49 50 Hotchkiss disabled workers are compared with those of workers without disabili- ties to determine whether there has been any improvement in the com- pensation disparity over time and how much of that disparity is left unexplained by differences in productivity (i.e., potential discrimina- tion), particularly around the period that the ADA became law and was fully implemented. The methodology employed will also allow an examination of how much of the earnings disparity is accounted for by different representations of disabled workers across occupations and/ or industries. Nonwage compensation is growing in importance for all employees and may be of particular importance to disabled workers. As such, the probability of being covered by health insurance and a pension plan is evaluated as a function of disability status, also across time. These probabilities are compared, again, to see if any change occurred when the ADA was implemented. WAGE LEVELS Figure 3.1 depicts the average real (1982–1984 100) hourly wages for disabled and non-disabled workers for each year from 1981 Figure 3.1 Average Real Hourly Wages, CPS, 1981–2000 10 9 Nondisabled workers 8 ($) 7 6 Disabled workers 5 1981 1983 1985 1987 1989 1991 1993 1995 1997 1999 (a) (b) (c) (a) ADA Enactment (b) ADA Phase I (c) ADA Phase II Compensation: Wages and Benefits 51 to 2000. As theorized, wages for disabled workers lie below those of nondisabled workers for every year, although these raw figures do not control for differences in human capital or other demographic and job characteristics. Real wages of nondisabled workers exhibit a clear up- ward trend (a significant raw trend average of about 0.03 of a percent- age point per year), and real wages of disabled workers exhibit a downward trend (a significant average of about –0.02 of a percentage point per year, in spite of the recent upward swing). The net result is a growing differential between wages of nondisabled and disabled workers. These relative trends will be examined to determine whether there was a significant difference pre- and post-ADA after controlling for individual and job characteristics. In addition, the wage differential will be decomposed to determine what factors are the greatest contribu- tors to its level and its growth. For example, it could be the case that wages are falling among disabled workers because the nature of disabilities is becoming more severe in the population (Kaye 2002), making disabled workers as a whole less productive. Alternatively, the human capital of disabled workers may be deteriorating for some rea- son, disabled workers are shifting to lower-paying jobs, or employers may be passing along the costs of accommodations through lower wages for disabled workers. Splitting the time series, the negative trend in wages for disabled workers observed in Figure 3.1 is clearly driven by the early years (a significant average decline of 1 percentage point per year from 1981 to 1991), while the years between 1992 and 2000 exhibit no trend at all, statistically. One could interpret this as a positive outcome of the ADA if the policy actually halted, or mitigated, a long-running downward trend in wages of disabled workers. However, this observation tells us nothing about the relative wage trend or components of the differential. DIFFERENCES IN WAGES OVER TIME Pooled, Cross-Sectional Analysis The first analysis of wages in this chapter is a simple, pooled, cross-sectional one.2 A linear relationship is specified in which the log of real wages is a function of demographic and job characteristics, as 52 Hotchkiss well as indicators for disability status, time period, and the interaction between disability status and time. The following specification is esti- mated via OLS for the time period 1984–2000:3 (3.1) lnrwagei Xi 1disablei 2posti 3disablei posti i where lnrwagei is the natural log hourly real (1982–1984 100) wage of worker i, Xi is a set of covariates for each person (demographic and job characteristics), disablei is equal to 1 if person i has a work-limiting disability, and posti is equal to one if person i is observed in 1992 or later. The affected group (the disabled) is controlled for by a dummy variable indicating whether the individual has a work-limiting disability, and the time period is controlled for by a dummy variable indicating whether the ADA had been implemented yet or not. The coefficient of interest (3) measures the change in real wages of disabled workers, relative to nondisabled workers, after implementation of the ADA, rela- tive to before implementation. In other words, 3 tells us how wages changed for disabled workers versus nondisabled workers. Xi includes individual demographic and job characteristics detailed in Table 3.1, which contains the estimation results; are additional parameter coef- ficients to be estimated, and i is the random error term. Since wages are observed for workers only, and since the charac- teristics of workers may be changing over time in unobservable ways, it is important to control for any potential unobserved self-selection into the labor market. Consequently, Equation 3.1 is modified by sim- ply adding the standard inverse-Mills ratio obtained from a first-stage probit estimation of a labor force participation/employment equation. This standard Heckman (1979) two-step procedure for controlling for self-selection is presented in greater detail in the section on wage de- compositions. Briefly, including the selection term in the regression allows 3 to be interpreted as relevant for the entire disabled and non- disabled population, even though the sample for the regression in- cluded workers only. The parameters of the model are identified Compensation: Wages and Benefits 53 Table 3.1 OLS Selectivity-Corrected Regression Results for Log Real Wages, across Disability Status and ADA Implementation, CPS, 1984–2000 Regressor Parameter estimates Intercept 1.1277*** (0.0121) Age 0.0498*** (0.0059) Age squared 0.0005 (0.0023) Female 1 0.2249*** (0.0016) Nonwhite 1 0.0434*** (0.0018) Single household 1 0.0524*** (0.0015) High school grad 1 0.0834*** (0.0020) Some college 1 0.1614*** (0.0022) College grad 1 0.2806*** (0.0025) Advanced degree 1 0.3072*** (0.0013) Hours 0.0024 (0.0055) Union 1 0.1976*** (0.0005) disable 1 0.1719*** (0.0018) post (year1992 or later)1 0.0033*** (0.0011) disablepost 1 0.0286*** (0.0064) ̂ (selection term) 0.0327*** (0.0043) Number of observations 766,060 F statistic 18,486*** Adjusted R2 0.4279 NOTE: Other regressors included in the estimation, but not reported here, include seven industry and five occupation dummy variables, region, and government em- ployer dummy variables. *** significant at the 99 percent confidence level. Asymptotically consistent stan- dard errors are in parentheses. 54 Hotchkiss through inclusion of some regressors in the first-stage probit estimation that are not in the wage regression; these regressors include nonlabor income and an indicator of whether the person worked last year or not. Since the purpose of |
this two-stage estimation approach is merely to obtain unbiased estimates of the coefficients in the wage equation, in- terpretation of those coefficients is not changed by controlling for selection. All of the parameter estimates in Table 3.1 are of the magnitude and direction one might expect from standard human capital and other labor market theories. For example, women and nonwhites earn lower wages, union workers earn higher wages, and increased wages accrue to those with greater levels of education. The positive coefficient on the selection term ( ̂) indicates positive selection into the labor market; the more likely someone is to enter the labor market, the more likely he or she will earn a wage above the population average. The coefficient on the interaction term disable post is 0.0286 (and significantly different from zero), indicating that dis- abled workers experienced about a 3 percent decline in wages, relative to nondisabled workers, post-ADA implementation, relative to pre-im- plementation. In other words, wages of the disabled fell by 3 percent more post-ADA than the wages of the nondisabled. This finding is not consistent with the result of DeLeire (2000), who found no significant change in the wages of disabled workers relative to those of nondis- abled workers, post-ADA.4 However, the result does suggest that the cost of accommodating disabled workers, overall, potentially exceeded their gains in productivity.5 It is important to note that this result was obtained by controlling for job characteristic differences, such as hours of work, occupation, and industry. The potential implication of shifts in occupation and industry distributions on these results is explored in Chapter 4. Evidence from the SIPP The pooled, cross-sectional analysis specified in Equation 3.1 was reestimated using the SIPP data set for the years 1986–1997 (and, again, controlling for selection of workers into the labor market through a two-step estimation strategy). Selected coefficient estimates from the reestimation are presented in Table 3.2. While not statistically Compensation: Wages and Benefits 55 Table 3.2 OLS Selectivity-Corrected DD Regression Results for Log Real Wages, across Disability Status and Type of Disability Status, SIPP 1986–1997 Parameter estimates Disability indicator Type of disability Regressor only indicated disable 1 0.1535*** — (0.0027) post (year 1992 or later) 1 0.0515*** 0.0305*** (0.0017) (0.0017) disable post 1 0.0070 — (0.0072) musculoskeletal 1 — 0.1230*** (0.0084) internal 1 — 0.1537*** (0.0115) mental 1 — 0.3427*** (0.0157) other 1 — 0.1124*** (0.0153) musculoskeletal post 1 — 0.0424 *** (0.0098) internal post 1 — 0.0125 (0.0148) mental post 1 — 0.0220 (0.0183) other post 1 — 0.0130 (0.0193) ̂ (selection term) 0.0046 0.0116* (0.0067) (0.0065) Number of observations 353,651 287,343 F statistic 8,855 6,502 Adjusted R2 0.4289 0.4489 NOTE: Other regressors included in the estimation, but not reported here, include seven industry and five occupation dummy variables, hours of work, age, age squared, and race, education, union, gender, marital status, region, and government employer dummy variables. Asymptotically consistent standard errors are in parentheses. *** significant at the 99 percent confidence level. * significant at the 90 percent confidence level. 56 Hotchkiss significant, the negative coefficient on the disable post regressor is at least consistent (in sign) with the results obtained from the CPS data. Table 3.2 presents an additional specification, which identifies type of disability. In the following equation, the impact of a worker’s dis- ability on the real wage is allowed to vary by type of impairment:6 (3.2) lnrwagei Xi S 1 musculoskeletali I 1 internali M 1 mentali O 1 otheri 2posti S 3 musculoskeletali posti I 3 internali posti M 3 mentali posti O 3 other posti i where lnrwagei is the natural log hourly real (1982–1984 100) wage of worker i, Xi is a set of covariates for each person (individual demographic characteristics), musculoskeletali is equal to 1 if person i has a musculoskel- etal disability,7 internali is equal to 1 if person i has a disability involving the internal systems, mentali is equal to 1 if person i has a mental disability, otheri is equal to 1 if person i has a disability classified as ‘‘other,’’ and posti is equal to 1 if person i is observed in 1992 or later. In this framework, the type of disability is controlled for by dummy variables indicating whether the individual has a musculoskeletal, in- ternal systems, mental, or other limitation, and the time period is con- trolled for by a dummy variable indicating whether the ADA had been implemented yet or not. The coefficients of interest (j 3, j S,I,M,O), therefore, measure the change in log real wages of workers with each type of disability, relative to nondisabled workers, after implementa- tion of the ADA, relative to before implementation. Xi includes indi- vidual demographic and job characteristics, detailed in Table 3.2. Again, selection into the labor market has been controlled for.8 As it turns out, the type of disability that appears to be driving the observed overall decline in real wages of disabled workers relative to nondisabled workers, post-ADA, is musculoskeletal. The real wages Compensation: Wages and Benefits 57 of workers with musculoskeletal disabilities declined 4 percent more than for workers without disabilities post-ADA, relative to pre-ADA (the coefficient on musculoskeletal post is 0.0424). This is of interest because it lends support to the theory that wages of disabled workers are sensitive to the degree of accommodation required of the employer. Whereas accommodation of a worker with a mental disor- der, such as depression, may simply be a flexible work schedule, indi- viduals with musculoskeletal disabilities might require more investment in infrastructure, such as specially constructed office furni- ture.9 In light of evidence that the typical per-worker cost of accommo- dation is fairly modest (on the order of $100–$1,000), according to Kujala (1996), employers may be setting wages on some perceived higher cost. Firm Size Analysis The CPS contains a question about how large (i.e., number of em- ployees) a worker’s main employer was in the previous year. Given that the ADA covers employers only of certain size, this information can be exploited to perform an additional analysis across covered and noncovered disabled workers. Covered disabled workers would be those employed by a firm with 25 or more employees in 1992 or later or employed by a firm with 15 or more employees in 1994 or later. Unfortunately, classifications of firms with fewer than 25 employees were not made until the 1992 survey year, which limits the amount of pre-ADA data available for the analysis. The post-ADA years were restricted to balance this survey-imposed limitation. The following model will be estimated twice: once for a large versus not-large firm classification, and a second time for a medium versus small firm classi- fication. Selection into the labor market will be controlled for in both estimations, using the standard Heckman (1979) two-step procedure detailed later in this chapter. The impact on wages across firm size (ADA coverage) is obtained from the following linear specification: (3.3) lnrwagei Xi 1disablei 2posti 3coveredi 4disablei posti 5disablei coveredi 6posti coveredi 7disablei posti coveredi i 58 Hotchkiss where lnrwagei is the natural log hourly real (1982–1984 100) wage of worker i, Xi is a set of covariates for each person (demographic and job characteristics), disablei is equal to 1 if person i has a work-limiting disability, posti is equal to 1 if person i is observed in 1992–1993 for the large firm analysis and equal to 1 if person i is observed in 1994–1996 for the medium firm analysis,10 and coveredi is equal to 1 if person i is employed by a firm covered by ADA legislation. The dummy variables (disable, post, and covered) control for the time-invariant characteristics of the affected group, disabled workers (1); the time-series changes in wages (2); and the time-invariant char- acteristics of the covered firm size, large or medium (3). The second- level interactions control for changes over time for disabled workers (4), time-invariant characteristics of disabled workers in the covered firm size (5), and changes over time within a covered firm size (6). The third-level interaction (7) captures all variation in wages specific to the disabled workers (relative to nondisabled workers) in the covered firm size (relative to uncovered firms) in the years after the firm was covered by ADA (relative to before ADA). The uncovered firms for the large firm analysis contain both small- and medium-sized organiza- tions (n 25). Uncovered firms for the medium firm analysis contain small entities only (n 10); large firms are not included in the medium firm analysis.11 The results of the medium firm analysis are somewhat contaminated by the fact that the ADA covers firms with 15 or more employees, so the indicator for medium firms contains some employers not technically covered by the ADA (those who employ more than 10 but fewer than 15 workers). The covariates included in the regression are detailed in Table 3.3, which presents the estimation results. The results in Table 3.3 indicate the following. Workers in large and medium (covered) firms earn higher wages than workers in small firms (see the coefficient on covered); disabled workers in large and medium firms earn higher wages, holding everything else constant, than nondisabled workers in those firms (see the coefficient on disable covered); and wages of disabled workers covered by the ADA did not change post-ADA relative to disabled workers not covered (see the Compensation: Wages and Benefits 59 Table 3.3 OLS Selectivity-Corrected Regression Results for Log Real Wages, across Disability Status, Covered Firm Size, and ADA Implementation, CPS Medium firms Large firms (n 25) (10n25) as Regressor as covered group covered group Intercept 4.4252*** 3.9121*** (0.0368) (0.0820) Age 0.0838*** 0.0966*** (0.0169) (0.0266) Age squared 0.0009 0.0011 (0.0061) (0.0131) Female 1 0.3505*** 0.4264*** (0.0237) (0.0357) Nonwhite 1 0.0079* 0.0041 (0.0044) (0.0098) Single household 1 0.0905*** 0.0683*** (0.0013) (0.0023) High school grad 1 0.1374*** 0.2670*** (0.0032) (0.0099) Some college 1 0.2023*** 0.3086*** (0.0055) (0.0112) College grad 1 0.3093*** 0.3965*** (0.0055) (0.0102) Advanced degree 1 0.4246*** 0.5948*** (0.0064) (0.0124) disable 1 0.2780*** 0.4490*** (0.0047) (0.0210) post 1 0.0273*** 0.1071** (0.0057) (0.0081) covered 1 0.0982*** 0.1174*** (0.0047) (0.0086) disable post 1 0.0570* 0.0317 (0.0322) (0.0431) disable covered 1 0.0572** 0.1074** (0.0264) (0.0492) postcovered 1 0.0245*** 0.0146 (0.0066) (0.0123) disablepostcovered1 0.0517 0.0879 (0.0382) (0.0707) 60 Hotchkiss Table 3.3 (continued) Medium firms Large firms (n 25) (10n25) as Regressor as covered group covered group (selection term) 0.2767*** 0.0897 (0.0279) (0.0735) Number of observations 182,318 55,459 F statistic 5,253 1,048 Adjusted R2 0.51 0.40 NOTE: Reference group for large firm analysis is small and medium firms (n25); reference group for medium firm analysis is small firms only (n10). Other regress- ors included in the estimation, but not reported here, include seven industry and five occupation dummy variables, and region, central city, benefit receipt, and government employer dummy variables. For the large firm comparison, post0 for 1990–91 and post1 for 1992–93. For the medium firm comparison, post0 for 1991–93 and post1 for 1994–96. Asymptotically consistent standard errors are in parentheses. *** significant at the 99 percent confidence level. ** significant at the 95 percent confidence level. * significant at the 90 percent confidence level. coefficient on disable post covered, which is not significant). The implication is that the decline in wages of disabled workers relative to those of nondisabled workers found in Tables 3.1 and 3.2 (and in Table 3.3 by the coefficient on disable post) is attributable to something other than ADA coverage. It is tempting to attribute the wage decline among disabled workers relative to nondisabled workers found earlier as indication that firms are passing accommodation costs on to disabled workers through lower pay. However, given that the wage difference between covered and noncovered disabled workers does not change post-ADA, there must be some other explanation than direct accommodation costs for the decline in wages relative to those of nondisabled workers. In other words, |
if the lower wages among disabled workers were the result of accommodation costs directly, then the wages of covered workers should fall relative to those of noncovered workers (whose employers are not required to incur the cost of accommodation). This is not what we see from the firm-size analysis. It appears that all disabled workers (covered or not) are suffering some ramifications of the ADA not di- rectly attributable to the costs of accommodating their disabilities. The Compensation: Wages and Benefits 61 ADA may have created an environment in which firms view all dis- abled workers as a hiring risk (perhaps through fear of litigation upon termination), and are passing that perceived greater risk on through lower wages. WAGE DECOMPOSITION This section decomposes the wage differentials observed in Figure 3.1 to determine which factors have the greatest influence over their levels and growth. Standard log wage equations are estimated sepa- rately for disabled and nondisabled workers. The following specifica- tion, presented for person i, is estimated separately for each year. In these equations, ‘‘nd’’ denotes nondisabled and ‘‘d’’ denotes disabled: (3.4) lnWind Xindnd ind lnWid Xidd id where lnWi is the natural log hourly wage of workers, Xi are explanatory variables, are coefficients to be estimated, and i is the random error term. As was seen in Chapter 2, there may exist significant self-selection into the labor market, particularly among the disabled population. In order to obtain an estimate of representative of the population, this selec- tion is controlled for using the standard Heckman (1979) two-step pro- cedure.12 The first stage of this procedure involves estimating a binary choice model of the following form: (3.5) Ỹi Z i ui , ui N(0,1) where Zi are explanatory variables, are parameters to be estimated, ui is the normally distributed random error, and individual i enters the labor force if Ỹi 0. Since Ỹi is unobserved, a binary variable, Yi, is defined as 62 Hotchkiss (3.6) Yi 1 as Ỹ 0 i 0. The parameters, , are estimated via maximum likelihood probit, and the inverse-Mill’s ratio is constructed for inclusion in the wage equa- tions, which are then estimated via OLS. The modified wage equations are (3.7) lnWind Xind nd nd ̂ind vind, lnWid Xid d d ̂id vid, (Zijj) where all variables are as previously defined, ̂ij , j d, nd, (Zijj) and vi is the newly defined random error. The parameter values that result from OLS estimation of the rela- tionships in Equation 7 can be used to decompose the wage differential between disabled and nondisabled workers as follows:13 (3.8) lnWnd lnWd ̂knd(Xknd Xkd) Xkd(̂knd ̂d) k k ( ̂nd nd ̂d d). The first term on the right-hand side reflects the role of differences in characteristics (endowments) that disabled and nondisabled workers bring to the labor market; it is referred to as the ‘‘endowment effect.’’ The second term represents the differences among groups of workers in how their characteristics are valued in the workplace. This second term is often referred to as the ‘‘coefficient effect’’ or the ‘‘unexplained portion’’ and is cautiously attributed to discriminatory behavior on the part of the employer. The third term reflects the role of selection into the labor market (across disability status). The selectivity-corrected wage differential is calculated by subtracting the third (selectivity ef- fect) term from the observed wage differential. Figure 3.2 presents the results from this empirical analysis. The solid and dashed lines that move together toward the bottom of the figure represent the observed wage differential and the wage differen- Compensation: Wages and Benefits 63 Figure 3.2 Observed and Selectivity-Corrected Wage Differentials and the Coefficient Effect as Percentage of Corrected Wage Differential, CPS, 1981–2000 1 120 0.9 100 0.8 Coefficient effect as 0.7 percent of corrected wage differential 80 Coefficient Log wage 0.6 effect as a differential nondisabled 60 percent of corrected vs. disabled 0.5 wage differential 0.4 40 Wage differential 0.3 corrected for selection 20 0.2 Observed wage differential 0.1 0 1981 1983 1985 1987 1989 1991 1993 1995 1997 1999 (a) ADA Enactment (a) (b) (c) (b) ADA Phase I (c) ADA Phase II tial corrected for selection, respectively. The dotted line represents the coefficient effect as a percentage of the corrected wage differential.14 Observed and Selectivity-Corrected Wage Differentials Since 1981 (the earliest year of data), there is a clear and persistent increase in both the observed and selectivity-corrected wage differen- tials between disabled and nondisabled workers. Both differentials show that over this whole time period, nondisabled workers earned, on average, wages that were 23 percent higher than those of disabled workers. In addition, the corrected wage differential increased from 13 percent to 30 percent, indicating a deterioration of earnings of disabled workers relative to nondisabled workers over this time period. The decline in relative earnings is consistent with a downward trend identi- fied by Haveman and Wolfe (1990) beginning in 1974. However, the growth in the wage differential appears to have been mitigated since 1992; the selectivity-corrected wage differential grew from 13 to 29 percent between 1981 and 1992, and has hovered around a mean of 28 percent since 1992, which was the first year of implementation of the ADA. 64 Hotchkiss In addition, and particularly since 1996, individual selection into the labor market, or differences in selection between disabled and non- disabled workers, does not seem to be biasing the observed wage dif- ferentials between the two groups. The one exception to this might be the period 1992–1995. During this four-year span, the observed wage differential underrepresented the wage differential corrected for selec- tion. The implication of this is that disabled workers were positively selecting into the labor market to a greater extent than nondisabled workers, driving the observed wage of disabled workers as a whole upward (and the wage differential downward). This is consistent with the labor force participation decline observed in Chapter 2, if the dis- abled labor force nonparticipants beginning around 1992 had systemat- ically lower earnings potential than the disabled persons who stayed in the labor market. This would likely be the case as a result of the flow of Aid to Families with Dependent Children (AFDC) recipients to SSI (Lewin Group 1999). This result is not consistent, however, with the conjecture that the disabled workers entering the labor force post-ADA were those with the most limiting disabilities (Chirikos 1991). What- ever might have been making the observed and selectivity-corrected wage differentials diverge in the mid 1990s seems to have disappeared, since the two series have basically followed identical paths since 1996. The implication of this is that since 1996, selection into the labor mar- ket has had essentially the same impact on wages for disabled and nondisabled workers; self-selection explains none of the remaining wage differentials since that time. Potential Wage Discrimination against Disabled Workers The dotted line in the top part of Figure 3.2 reflects the coefficient effect as a percent of the corrected wage differential. Over the entire time period, the coefficient effect averages 77 percent of the corrected wage differential, or clearly a majority of the difference in wages be- tween disabled and nondisabled workers. While there is quite a bit of variation over the years, the coefficient effect dominates the endow- ment effect in each year. The regressors in each year explain the usual 30–40 percent of the variation in wages of disabled workers and about 45 percent of the variation in wages of nondisabled workers (as indi- cated by the adjusted R2 of the regressions). Consequently, interpreting Compensation: Wages and Benefits 65 the entire coefficient effect as an indication of discrimination would not be prudent. However, given the relative magnitude of the coeffi- cient effect, the expected success in explaining wage variation, and the number of observable characteristics included in the regression, it is also unlikely that the coefficient effect can be completely dismissed as the result of unmeasured characteristics of either the disabled or nondisabled. Using data from the SIPP, Baldwin and Johnson (1995, 2000) also find that the coefficient effect is larger than the endowment effect as a percentage of the selectivity-corrected differential in 1984 and in 1990. Using a similar methodology and data from 1972, John- son and Lambrinos (1985) show that only 34–40 percent of the wage differential between disabled and nondisabled workers was left unex- plained by differences in endowments. Examining SIPP data from 1984 and 1993, DeLeire (2001) finds that only between 5 and 8 percent of the earnings gap is attributable to the coefficient effect. Examining the endowment and coefficient effects in greater detail, it is of interest to see which set of regressors makes the largest contri- butions to these components. Table 3.4 presents the median contribu- tion (across years) of the groups of regressors that control for occupation, industry, and education. While the contributions vary across the years, these median values represent the typical scenario (i.e., there is no obvious trend in any of these contributing factors), and it is usually the case that occupation and education were the largest Table 3.4 Contribution of Regressors to Log Wage Differentials, Median across Years, CPS, 1981–2000 Contribution Contribution to the to the endowment coefficient effect effect Occupation 0.0452 0.0424 Industry 0.0085 0.0817 Education 0.0363 0.0419 Median total effects 0.0768 0.1738 NOTE: The contributions of occupation, industry, and education do not add up to the total effect because these numbers represent the median across all years and also do not represent all regressors in the wage regression. 66 Hotchkiss contributors to the endowment effect and that industry was the largest contributor to the coefficient effect. It is also of interest to note that in 18 of the 20 years, the return to education acted to decrease the wage differential between disabled and nondisabled workers (the contribu- tion of the education regressors to the coefficient effect was negative). In other words, disabled workers typically received a greater return to their educational investment than nondisabled workers.15 Regarding endowments, it is clear that nondisabled workers bring greater educa- tional attainment to the labor market and are more likely to locate in the higher-paying occupations and industries (a phenomenon that will be explored more fully in Chapter 4); these observations are evidenced by positive contributions made by the occupation, industry, and educa- tion regressors to the endowment effect. An additional feature provided by the analysis is that the relative importance of the coefficient effect over time can be evaluated. While perhaps not very obvious in Figure 3.2, there is actually a (slightly) significant negative trend in the coefficient effect as a percentage of the corrected wage differential. On average, the contribution of the coefficient effect to the overall wage differential declines an average of 1.7 percentage points per year from 1981 to 2000.16 In addition, the endowment effect as a percentage of the corrected wage differential increased an average of 0.6 of a percentage point per year over the same time period.17 Consequently, another silver lining to the rising wage differential between disabled and nondisabled workers, and to the large portion of that differential not explained by differences in endowments, is that any potential discrimination against disabled workers, as measured by the coefficient effect, is declining. Addition- ally, this result suggests that one way to combat the rising wage differ- ential is to improve disabled workers’ endowments (e.g., greater investments in human capital, or placement in higher-paying occupa- tions or industries). It is also important to note, however, that these improvements appear to be a continuation of a trend rather than any dramatic post-ADA shift. BENEFIT ANALYSIS As the percentage of fringe benefits in total compensation contin- ues to increase, benefits become an increasingly important contributor Compensation: Wages and Benefits 67 to workers’ labor market experience. The CPS allows identification of a worker receiving two fringe benefits from his or her employer: health insurance and a pension plan. The data used for this analysis were obtained from the CPS March supplemental questionnaire and there- fore refer to benefit coverage in the years 1980–1999. The probabili- ties of being included in an employer’s pension plan or of receiving health insurance through an employer were fairly stable |
across the years; however, as Figure 3.3 shows, the proportion of nondisabled workers relative to disabled workers included in a pension plan has grown over the time period. In 1980, nearly 11 percent more of nondisabled workers were in- cluded in a pension plan than disabled workers were. This difference grew to 17 percentage points by 1999. The greater proportion of non- disabled workers receiving either benefit could be closely related to the types of jobs disabled versus nondisabled workers hold. The increase in the difference in proportions could also be related to disabled work- ers moving into jobs less likely to offer these benefits. For example, Chapter 4 will detail the growth in part-time employment among dis- abled workers. Neither phenomenon, however, appears to have been impacted by events surrounding the passage and implementation of the ADA. The goal of the analysis of this section is to determine whether Figure 3.3 Difference in Proportion of Nondisabled and Disabled Workers Receiving Benefits, CPS, 1980–1999 Percentage 19 points 18 17 Health 16 insurance 15 14 13 12 Included in pension plan 11 10 1980 1982 1984 1986 1988 1990 1992 1994 1996 1998 (a) ADA Enactment (a) (b) (c) (b) ADA Phase I (c) ADA Phase II 68 Hotchkiss disabled workers are more or less likely than nondisabled workers to be included in their employers’ pension plan or to have their employers pay for health insurance, while controlling for all other individual and job characteristics. Since the observed model is an indicator of coverage/inclusion or not, the empirical model is specified as a probit: (3.9) B̃ij Q ij vi , i N(0,1) where individual i receives benefit j ( j health insurance, pension plan inclusion) if B̃ij 0. Since B̃ij is unobserved, a binary variable, B̃ij, is defined as (3.10) Bij 1 as B̃ij 0. 0 The parameters, , are estimated via maximum likelihood probit. Qi comprises various individual and job characteristics for worker i, in- cluding a dummy variable indicating whether the worker is disabled or not. The model is estimated on a sample of workers only; thus, the results are generalizable solely to workers. The marginal effect of being disabled on receiving a benefit is calculated as the partial deriva- tive for each worker, then averaged over the entire sample.18 The esti- mation results are depicted in Figure 3.4.19 A reliable measure of annual earnings is available only since 1987; therefore, the marginal effects only cover the period 1987–1999.20 The marginal impact of being disabled on fringe benefit receipt follows the same path for both health insurance and pension plan inclu- sion: an increasingly negative impact of being disabled on the probabil- ity of receiving benefits. Since these marginal effects are calculated from specifications which included a control for earnings, the increase cannot be attributed to disabled workers merely being employed in jobs that are lower paying (thus, less likely to offer fringe benefits). The specification also included controls for hours of work (thus the poten- tial impact of part-time employment), occupation, industry, and indi- vidual human capital characteristics. While there does seem to be a fairly significant intensification in the negative impact of being dis- abled in 1995, it would be hard to attribute that to anything other than Compensation: Wages and Benefits 69 Figure 3.4 Marginal Effect of Disability on the Probability of Fringe Benefit Receipt, CPS, 1987–1999 Impact on 0 probability -0.02 -0.04 -0.06 Health insurance -0.08 -0.10 Pension plan -0.12 1987 1989 1991 1993 1995 1997 1999 (a) ADA Enactment (a) (b) (c) (b) ADA Phase I (c) ADA Phase II the continuation of a trend, since the negative impact has diminished somewhat in recent years. However, the negative trend cannot be ig- nored. There is some evidence that a weakening in 1989 of antidis- crimination laws governing provision of health insurance resulted in lower rates of benefit incidence among ‘‘peripheral’’ workers, such as recent hires or those working part-time (Farber and Levy 2000). If disabled workers fall into the category of ‘‘peripheral,’’ this might ex- plain some of the deterioration in health insurance receipt among dis- abled relative to nondisabled workers. An additional consideration that might explain the deterioration of relative health insurance coverage is that the Employment Opportuni- ties for Disabled Americans Act and the Omnibus Budget Reconcilia- tion Act of 1990 amended Title XVI of the Social Security Act to allow SSI recipients to continue participating in Medicaid (under specific circumstances) even if their earnings exceeded the SSI qualifying level (59 FR 41403, 12 August 1994). This amendment became effective in August 1994. The change would not have typically affected disabled workers already employed but would have encouraged disabled indi- viduals who previously had not sought employment because of a lack of health insurance to do so. While this law says nothing about the 70 Hotchkiss provision of pension plans, fringe benefits are highly correlated with one another, so it is not a surprise that as the proportion of disabled workers without employer-provided health insurance increased, the proportion without a pension plan also increased. CONCLUSIONS The purpose of this chapter was to evaluate the relative compensa- tion experience of disabled and nondisabled workers over time, and to determine whether any change in that experience is evident in relation to the implementation of the ADA. A pooled, cross-sectional analysis using the CPS data indicated that overall, disabled workers experienced a 3 percent decline in real wages, relative to nondisabled workers, post- ADA, relative to pre-ADA. Results from the SIPP are consistent with the CPS results and show that the wage experience of those with mus- culoskeletal disabilities is driving that observed wage decline. The real wages of workers with musculoskeletal disabilities declined 4 percent more than for workers without disabilities post-ADA, relative to pre- ADA; workers with other types of disabilities did not experience any different wage change than did nondisabled workers. These results together indicate that overall, the cost of accommodating workers’ dis- abilities exceeds the gain in productivity of those workers. In addition, if accommodating musculoskeletal disabilities results in more costly structural investments, the SIPP results lend support to the theory that wages of disabled workers are sensitive to the degree of accommoda- tion (in terms of cost) required of the employer. This result is consis- tent with the finding by Gunderson and Hyatt (1996) that firms pass on (through lower wages) the cost of workplace modifications to the hired disabled worker. In light of this, the tax credits in place to assist certain employers in absorbing these costs (Hays 1999) either have not gone far enough or are not being widely used. In contrast with these overall (disabled versus nondisabled) results, it was found that disabled workers employed by firms covered by the ADA did not experience any wage deterioration relative to disabled workers not covered by the ADA. This combination of results suggests that the wage decline experience by disabled workers relative to non- Compensation: Wages and Benefits 71 disabled workers is not the result of explicit accommodation costs being passed on to disabled workers through lower wages (in which case, the wages of covered disabled workers should have deteriorated the most). Rather, all disabled workers seem to be bearing the burden of a perceived additional hiring risk associated with them that may exist post-ADA. Consistent with the overall relative wage decline identified through the pooled, cross-sectional analysis, further study illustrates that the positive wage differential between disabled and nondisabled workers has risen considerably since 1981. However, the trend does seem to have flattened out since the early 1990s. The large portion of that differential not explained by differences in endowments has also been declining over time, indicating that any potential wage discrimination against disabled workers is at least falling. Additionally, the fact that worker endowments (occupation, education, etc.) contribute positively to the measured wage differential suggests that one way to fight the rising wage differential is to enhance disabled workers’ endowments (e.g., greater investments in human capital, or placement in higher- paying occupations or industries). In addition to the rising wage differentials, the negative impact of being disabled on the probability of receiving benefits has also been rising. One potential contributor to this situation is the allowance (as of August 1994) for some disabled workers to continue receiving Medicaid even when their earnings surpass SSI cut-off levels. The combination of the rising wage differential and decreasing probability of disabled workers receiving employer-sponsored health and pension benefits leads to the conclusion that the relative position of disabled workers regarding compensation is deteriorating overall. The ADA provides a clear mandate ‘‘for the elimination of dis- crimination against individuals with disabilities’’ (section 2 of the ADA). The evidence provided in this chapter suggests that while po- tential wage discrimination against the disabled appears to be declin- ing, the improvement is taking place at a very slow rate, and not necessarily as a result of the ADA, as the trend goes back at least to 1981. In addition, even if discrimination is decreasing, the overall compensation experience (including benefit provision) for disabled workers, relative to nondisabled workers, is declining, as well. 72 Hotchkiss Notes 1. See also Burkhauser, Haveman, and Wolfe (1993) for an analysis of the well- being of the disabled. 2. Examples of other applications of this method of analysis can be found in Card (1992), Gruber (1994, 1996), Zveglich and Rodgers (1996), and Hamermesh and Trejo (2000). The reader is reminded of the caveats detailed by Heckman (1996). Also see further discussion in Chapter 2. 3. The first year in the analysis was 1984 due to the poor representation of disabled workers in some occupations in 1983, and since union status was not indicated in 1981 or 1982. 4. While insignificantly different from zero, the coefficient in DeLeire’s pooled, cross-sectional analysis was also negative. The results reported in Table 3.1 are robust to defining post as years past 1990 and to defining post as 1994 and later. 5. It is important to note that since there is no measure of labor market experience available in the CPS survey, and since disabled workers likely have less labor market experience than nondisabled workers of the same age, the coefficient on the disable dummy variable may be capturing some of the impact of labor market experience on the wage. The inability to control for labor market experience should have a smaller impact, however, on the coefficient for the interaction term of disable post, since the consequence of the absence of an experience vari- able should be similar across time. 6. See Appendix B for disability types grouped for these classifications. 7. The musculoskeletal grouping includes disabilities of the special senses (e.g., hearing, seeing). 8. See the wage decomposition section in this chapter for details of the procedure used to control for self-selection. 9. Whereas the wages of those with mental disorders did not deteriorate post-ADA, it is of interest to note that the largest (negative) coefficient among types of dis- ability (indicating overall relative wage performance) is that on mental (0.3427). This is consistent with the findings of Baldwin (1999). 10. The pre and post periods were chosen to achieve balance in the number of years; the results did not change if the number of years were extended. 11. These definitions of ‘‘large’’ and ‘‘small’’ differ from those used in Chapter 2. 12. This specification could also be modified to account for the likely joint determina- tion of wages and hours worked; Moffitt (1984), Lundberg (1985), Altonji and Paxson (1988), and Tummers and Woittiez (1991) all demonstrate the importance of the simultaneous determination of wages and hours. This joint model is not estimated here for simplification, but hours are included as a covariate in the wage equation. 13. Since only 3 percent of the working sample is disabled, nearly all of the coeffi- cient effect is attributed to the disadvantage experienced by the disabled, since the linear combination of the two worlds yields estimates very close to those experienced in the nondisabled world (see Cotton 1988). Other renditions of this Compensation: Wages and Benefits 73 decomposition, such as Oaxaca and Ransom (1994) would result in a similar outcome, since the disabled make up such a small portion of the whole workforce. |
This same strategy is followed by Baldwin and Johnson (2000) in their analysis of labor market discrimination against disabled workers. 14. The data generating this figure are found in Table C.5 in Appendix C. 15. This finding is consistent with the results reported by Hollenbeck and Kimmel (2001) that people with poor health or disability earn a positive return to educa- tion and training, although they find that return to be equal to that of nondisabled individuals. 16. The coefficient of 0.017 on a linear trend estimation had a standard error of 0.0067, making it significantly different from zero at the 95 percent confidence level. 17. The coefficient of 0.006 on a linear trend estimation had a standard error of 0.0027, making it significantly different from zero at the 95 percent confidence level. 18. This is preferable to calculating the marginal benefit for the average person, since we are most likely to be interested in the marginal effect for a worker drawn at random, rather than the marginal effect for the average person in the sample. 19. Table C.6 contains the marginal effects used to generate Figure 3.4. 20. An identical analysis was performed for the entire 1980–1999 time period, ex- cluding the control for earnings. The marginal effect of being disabled was sig- nificantly larger, as would be expected, but exhibited the same trend going back to 1980 as that depicted in Figure 3.4. This Page Intentionally Left Blank 4 Hours of Work, Distribution, and Representation In addition to the wage, there are a number of other characteristics that can be used to quantify the quality of a worker’s job. One feature is whether a job is full-time or part-time. While the availability of part-time employment may be important to disabled workers (and per- haps more so than to nondisabled workers), part-time jobs are often accompanied by lower pay, fewer benefits, and less stability.1 The first part of this chapter compares and evaluates the incidence of part-time employment and type of part-time employment (voluntary versus in- voluntary) across disability status and across time. If disabled workers are considered marginal workers, then they would be more likely to be employed part-time. If, however, disabled part-time workers are more likely to be voluntarily, versus involuntarily, employed part-time, then their part-time status may indicate a greater flexibility that might be needed to accommodate the worker’s situation. The chapter then ex- plores the full-time wage premium earned by disabled and nondisabled workers. Disabled workers may not earn as great a premium for com- mitting to a full-time schedule as nondisabled workers. Given the po- tentially higher fixed cost of accommodating the worker’s disability, the individual may have to commit to a greater number of hours before seeing the premium; this could show up in a lower premium at any given definition of part-time employment.2 A major characteristic of one’s job is its occupation or industry. A popular indicator of the quality of employment of a disadvantaged group is how well that group is represented in desirable occupations relative to some comparison group, and how the disadvantaged group’s distribution across occupations compares with that of the comparison group. The occupation that a worker holds, or the industry in which someone works, can play an important role in that person’s satisfaction and potential advancement in the labor market. Dual labor market theory suggests that some workers are relegated to undesirable (e.g., low-paying, dead-end) jobs from which they have virtually no escape.3 75 76 Hotchkiss The second part of this chapter will explore the distribution of disabled workers across occupations and industries, relative to the distribution of nondisabled workers, as well as examine the representation of dis- abled workers in ‘‘desirable’’ jobs. The emphasis will be on how the relative distribution and representation have changed over time and whether the ADA seems to have played a role in their current determi- nation. HOURS OF WORK Figure 1.2 in Chapter 1 highlighted a growing disparity in average hours worked per week between disabled and nondisabled workers. This section looks more closely at the role part-time employment plays in that observed decline in hours and determines whether it reflects voluntary or involuntary behavior on the part of disabled workers. Part-time employment among the disabled may not be a sign of mar- ginalization or discrimination because of these individuals’ unique physical or mental capabilities and potential income sources. Such employment may be sought by disabled workers (and employers for their disabled workers) as a way to accommodate health limitations. In addition, part-time employment may provide additional earnings that do not jeopardize disability benefits based on income levels. Incidence of Part-time Employment Figure 4.1 depicts the percentage of both disabled and nondisabled workers that are employed part-time for each year, 1981 to 2000. Al- though there is some discrepancy as to the appropriate definition of part-time employment (see Hotchkiss 1991), the CPS definition of ‘‘less than 35 hours per week’’ is retained here. The use of respondent- supplied reasons (later in the chapter) for working less than 35 hours per week makes this the practical choice. As has been suggested in Chapters 1 and 3, part-time employment has grown among disabled workers between 1981 and 2000 and has declined somewhat among nondisabled workers. By itself, this obser- vation is consistent with the contention that disabled workers are being Hours of Work, Distribution, and Representation 77 Figure 4.1 Percentage of Disabled and Nondisabled Workers That Are Employed Part-Time, CPS, 1981–2000 45 Disabled 40 35 30 25 Nondisabled 20 15 10 5 0 1981 1983 1985 1987 1989 1991 1993 1995 1997 1999 (a) ADA Enactment (a) (b) (c) (b) ADA Phase I (c) ADA Phase II pushed to the fringe and becoming more marginalized. However, these raw numbers do not control for other job or individual characteristics. In order to appropriately model the impact of having a work- limiting disability on the incidence of part-time employment among workers, a bivariate probit with selection model, as in Chapter 2, is specified. This model estimates the probability of being employed part-time while controlling for unobservable determinants of being both employed and employed part-time. The bivariate specification allows for the two outcomes (employment and part-time employment) to be impacted by the same unobservable factors (e.g., motivation). The selectivity part of the model is merely a recognition that we do not get to see the part-time employment outcome unless the person is employed to begin with, and that those we observe as employed may have systematically different part-time options or make different hours choices than those not employed. Correcting for selectivity allows us to make inferences for anyone from the population, not just those we observe as employed; this is what makes the probability unconditional. The following model defines the relationship assumed between the employment of person i (empi), the probability of being employed part- 78 Hotchkiss time (pti), and individual characteristics that are believed to affect the employment outcome (X1i) and the incidence of part-time employment (X2i): (4.1) empi 1 1X1i 1 disablei 1i 1 if person i is employed 0 otherwise (4.2) pti 2 2X2i2 disablei 2i 1 if person i is employed part-time 0 otherwise. disablei is equal to 1 if person i is disabled, 0 otherwise; 1i and 2i are distributed as a bivariate normal with means equal to 0, variances equal to 1, and correlation equal to ; and j, j, and j ( j1, 2) are parame- ter coefficients to be estimated. In addition, of course, pti is only observed if empi1.4 X1i and X2i include individual demographic char- acteristics detailed in the notes to Table 4.1. The impact of having a work-limiting disability on part-time employment, then, is determined by calculating the unconditional probability of being employed part- time for each individual, varying the disability index between 0 and 1, then averaging across the sample.5 Separate specifications are estimated for each year, and the marginal impact of having a work-limiting dis- ability is calculated. The estimation results are depicted in Figure 4.2.6 The line in Figure 4.2 reflects an increase in the impact of being disabled on the determinant of the unconditional probability of being employed part-time. A work-limiting disability increased the probabil- ity of a worker being observed as employed part-time by 12 percentage points in 2000. This is double the 6 percentage points impact of a disability on being employed part-time estimated for 1981. What is also apparent from the graph is that this effect has experienced a rather consistent upward trend during the entire time period, with the largest adjustment occuring during the ADA phase-in period. In order to quantify the apparent growth in selectivity-corrected part-time employment among disabled workers, relative to nondisabled workers, the pooled, cross-sectional analysis introduced in Chapter 2 is applied here. The idea behind the analysis is to estimate a cross- sectional, time-series bivariate probit model with dummy variables rep- Hours of Work, Distribution, and Representation 79 Figure 4.2 Impact of Having a Disability on Being Employed Part-Time, CPS, 1981–2000 Percentage-point 18 impact on 16 probability of 14 being disabled 12 10 8 6 4 2 0 1981 1983 1985 1987 1989 1991 1993 1995 1997 1999 (a) ADA Enactment (a) (b) (c) (b) ADA Phase I (c) ADA Phase II resenting whether the observation shows up in the data pre-ADA or post-ADA and whether the observation is a disabled or nondisabled person. These dummy variables are also interacted to determine whether being disabled had any greater impact on employment after the ADA than before the ADA, relative to the experience of a nondis- abled person.7 The pooled, cross-sectional analysis looks just like the bivariate probit with selection estimated in one year, except with the additional time-period dummy variables: (4.3) empi 1 1X1i 1 disablei 1 posti 1 disablei posti 1i (4.4) pti 2 2X2i 2 disablei 2 posti 2 disablei posti 2i. Again, empi 1 if person i is in the labor force, 0 otherwise, and pti is not observed unless empi 1. disablei is equal to 1 if person i is disabled, 0 otherwise; posti is equal to 1 if person i is observed in 1992 or later (as in Chapter 2); X1i and X2i include individual demographic characteristics; 1i and 2i are distributed as a bivariate normal with means equal to 0, variances equal to 1, and correlation equal to ; and j and j ( j 1, 2) are additional coefficients to be estimated. 80 Hotchkiss In this framework, the affected group (the disabled) is controlled for by a dummy variable indicating whether the individual has a work- limiting disability, and the time period is controlled for by a dummy variable indicating whether the ADA had been implemented yet or not. Because of the model’s nonlinearity, a single parameter coefficient does not tell us the additional impact the ADA had on the difference in employment probabilities between the disabled and nondisabled. Table 4.1 details the regression results. Using the parameter estimates, the difference in the impact of hav- ing a work-limiting disability on part-time employment across the two time periods can be calculated by evaluating the probabilities of inter- est for each person, varying the disable and post dummy variables, then taking the difference between these probabilities and averaging those differences across the sample. This calculation translates the Table 4.1 Employment and Part-Time Employment Bivariate Probit with Selection Results, CPS Combined Years 1981–2000 Part-time Employment employment Regressor equation equation disable 1 0.1118*** 0.3474*** (0.0146) (0.0130) post (year 1992 or later) 1 0.0112** 0.0017 (0.0051) (0.0037) disable post 1 0.0298 0.1775*** (0.0224) (0.0190) Rho 0.7983*** (0.0054) Log-likelihood 477,354 Number of observations 906,646 NOTE: Regressors included both in the employment and part-time employment equa- tions (but not reported here) include age, education, region, race, gender, marital status, and a central city residence indicator. Regressors unique to the employment equation include the state unemployment rate and the number of weeks worked last year. Regressors unique to the part-time employment equation include occupation and industry dummies, nonlabor income, and a government employer indicator. Stan- dard errors are in parentheses. *** significant at the 99 |
percent confidence level. ** significant at the 95 percent confidence level. Hours of Work, Distribution, and Representation 81 estimated coefficients from the bivariate probit into a 5 percentage point greater probability of disabled workers being employed part-time than nondisabled workers, post-ADA relative to pre-ADA. In addition, the probability of nondisabled workers being employed part-time changed by less than one-hundredth of a percentage point post- versus pre-ADA. Type of Part-Time Employment Given the conclusion that disabled workers are more likely than the nondisabled to be employed part-time and that the disparity is growing, an important consideration is what is the nature of the part- time jobs? Are disabled workers more likely to be employed other than full-time by choice? In order to answer this question, a univariate probit analysis is performed. The purpose of the probit analysis is to determine, among part-time workers, whether the probability of being voluntarily (versus involuntarily) employed part-time has increased or decreased for disabled workers, relative to nondisabled part-time work- ers, holding constant other factors that may determine the classifica- tion.8 The results of this probit estimation can be found in Figure 4.3.9 The graph depicts the marginal effect of being disabled on the probability that a part-time worker’s status is voluntary. The results are generalizable to part-time workers only. The observation of inter- est from Figure 4.3 is that prior to 1992, being disabled decreased a part-time worker’s probability of being voluntarily (versus involun- tarily) employed part-time; however after 1992, disabled part-time workers became more likely to be voluntarily employed part-time than nondisabled part-time workers. The implication is that much of the growth in part-time employment has been voluntary (for a given set of individual characteristics) and may actually be in response to the better accommodation of a worker’s disability.10 In order to quantify what may be obvious from Figure 4.3, a pooled, cross-sectional approach is taken to determine the extent to which the disabled are more likely than the nondisabled to be voluntar- ily employed part-time post-ADA versus pre-ADA. Since this analysis is concerned only with part-time workers as a group, a linear probabil- ity model is estimated so that the parameter coefficient is directly inter- pretable as a marginal effect; again, the results are generalizable only 82 Hotchkiss Figure 4.3 Impact of Having a Disability on Being Voluntarily Employed Part-Time, CPS, 1981–2000 Percentage- 8 point impact on 6 probability of 4 being disabled 2 0 -2 -4 -6 -8 -10 1981 1983 1985 1987 1989 1991 1993 1995 1997 1999 (a) ADA Enactment (a) (b) (c) (b) ADA Phase I (c) ADA Phase II to the part-time employed population. The linear probability model takes the following form: (4.5) vpti 3 3X3i 3 disablei 3 posti 3 disablei posti 3i where vpti is equal to 1 if person i is voluntarily employed part-time, 0 if involuntarily part-time, Xi is a set of covariates for each person (individual demographic characteristics), disablei is equal to 1 if person i has a work-limiting disability, and posti is equal to 1 if person i is observed in 1992 or later. In this framework, the affected group (the disabled) is controlled for by a dummy variable indicating whether the individual has a work- limiting disability, and the time period is controlled for by a dummy variable indicating whether the ADA had been implemented yet or not. The coefficient of interest (3), therefore, measures the change in em- ployment probability of disabled workers, relative to nondisabled workers, after implementation of the ADA, relative to before imple- mentation (the other parameter coefficients are analagous to their coun- Hours of Work, Distribution, and Representation 83 terparts in Equations 4.3 and 4.4). X3i includes individual demographic characteristics. Table 4.2 details the regressors included in the estima- tion and the regression results. The coefficient on disable post confirms that the probability of being voluntarily (versus involuntarily) employed part-time increased 4 percentage points more for disabled part-time workers than for non- disabled part-time workers, post-ADA. This result, taken with the overall growth in part-time employment, suggests that part-time em- ployment and flexible hours may be a mechanism by which employers are able and willing to accommodate workers’ disabilities. Evidence from the SIPP The pooled, cross-sectional methodologies are appealed to again in order to determine the impact of different types of disabilities on the incidence of part-time employment and on the kind of part-time Table 4.2 Linear Probability, Voluntary Part-Time Employment Results, CPS Combined Years 1981–2000 Regressor Coefficient disable 1 0.0158** (0.0072) post (year 1992 or later) 1 0.0549*** (0.0023) disable post 1 0.0401*** (0.0102) Adjusted R2 0.08 F statistic 481.91 Number of observations 170,870 NOTE: Observations from 1983 were not included because of the unreliable represen- tation across occupational categories. Regressors included both in the employment and part-time employment equations (but not reported here) include age, education, region, race, gender, marital status, and a central city residence indicator. Regressors unique to the employment equation include the state unemployment rate and the num- ber of weeks worked last year. Regressors unique to the part-time employment equa- tion include occupation and industry dummies, nonlabor income, and a government employer indicator. Standard errors are in parentheses. *** significant at the 99 percent confidence level. ** significant at the 95 percent confidence level. 84 Hotchkiss employment across time using the SIPP data set. The bivariate probit model with selection is estimated with two different specifications. The first includes only a single dummy variable indicator for having a work-limiting disability; the second includes multiple dummies indi- cating the type of disability a person might have. The general structure of the estimation strategies looks like this: (4.6) empi 1 1X1i n k 1 distypek i 1 posti k(S,I,M,O) n k 1 distypek i posti 1i k(S,I,M,O) (4.7) pti 2 2X2i n k 2 distypek i 2 posti k(S,I,M,O) n k 2 distypek i posti 2i k(S,I,M,O) where distypei disablei in specification 1 musculoskeletali(S); internali(I); mentali(M); and otheri(O) in specification 2. Again, empi 1 if person i is in the labor force and employed, 0 otherwise, and pti is not observed unless empi 1. X1i and X2i include individual demographic characteristics; posti is equal to 1 if person i is observed in 1992 or later; disablei is equal to 1 if person i has a work-limiting disability; musculoskeletali is equal to 1 if person i has a musculoskeletal disability;11 internali is equal to 1 if person i has a disability involving the internal systems; mentali is equal to 1 if person i has a mental disability; otheri is equal to 1 if person i has a disability classified as ‘‘other’’; and 1i and 2i are distributed as a bivar- iate normal with means equal to 0, variances equal to 1; and correlation equal to ; and , , , , and are all parameters to be estimated. In this framework, the affected group (the disabled) is controlled for by a dummy variable (or set of dummy variables) indicating whether the individual has a work-limiting disability (or type of dis- ability), and the time period is controlled for by a dummy variable indicating whether the ADA had been implemented yet or not. The Hours of Work, Distribution, and Representation 85 difference in the impact of having a work-limiting disability on em- ployment across the two time periods can be calculated by evaluating the probabilities of interest for each person, varying the distype and post dummy variables, then taking the difference between these proba- bilities, and averaging across the sample. An additional estimation is performed on a subsample of part-time workers only to determine whether the type of disability impacts the incidence of voluntary part-time employment. The following equation is estimated via OLS: (4.8) vpti 3 1X3i k 3 distypek i 3 posti k(S,I,M,O) n k 3 distypek i posti 3i. k(S,I,M,O) Table 4.3 contains the results from estimating both specifications of Equation 4.7 and both specifications of Equation 4.8. The two speci- fications for each equation correspond to how distype is defined. Con- sistent with the findings from the CPS, the results in Table 4.3 indicate that the probability that a disabled worker is employed part-time in- creased more than the probability for a nondisabled worker, post-ADA relative to pre-ADA. The coefficient of 0.0925 in column 1 of Table 4.3 translates into a relative 2 percentage point greater probability for part-time employment for the disabled post-ADA. In addition, the strongest impact was experienced by those with musculoskeletal (0.1084) and mental (0.1730) disabilities. Regarding voluntary part- time employment, the results suggest that while the impact of having a disability on the probability of being voluntarily employed part-time increased post-ADA, that rise was not significantly different from zero for disabled workers as a group. However, those with mental disabili- ties seem to have experienced a greater increase in the probability of being voluntarily employed part-time than nondisabled part-time work- ers, post-ADA. This makes sense if mental disorders are the type of disability most effectively accommodated by a flexible or reduced- hours work schedule.12 Full-Time Wage Premium Even beyond whether a part-time job is voluntary or involuntary is the wage penalty experienced by part-time workers. It is well docu- 86 Hotchkiss Table 4.3 Employment and Part-Time Employment Bivariate Probit with Selection and Linear Probability Model for Voluntary Part-Time Employment, SIPP 1986–1997 Probability of part-time employmenta Probability of voluntary part-timeb Disability Type of Disability Type of Regressor indicator only disability indicated indicator only disability indicated disable 1 0.2024*** — 0.0151 — (0.0188) (0.0102) post (year 1992 or later) 1 0.0090 0.0088 0.0380*** 0.0683*** (0.0059) (0.0059) (0.0035) (0.0038) disable post 1 0.0925*** — 0.0095 — (0.0238) (0.0127) Musculoskeletal disability 1 — 0.0821*** — 0.0221 (0.0262) (0.0156) Internal Systems disability 1 — 0.2743*** — 0.0275 (0.0356) (0.0194) Mental disorder disability 1 — 0.4177*** — 0.0398* (0.0464) (0.0238) Other disability 1 — 0.2587*** — 0.0414 (0.0481) (0.0261) Hours of Work, Distribution, and Representation 87 musculoskeletal post 1 — 0.1084*** — 0.0238 (0.0331) (0.0195) internal post 1 — 0.0013 — 0.0068 (0.0476) (0.0258) mental post 1 — 0.1730*** — 0.0907*** (0.0550) (0.0281) other post 1 — 0.0302 — 0.0266 (0.0627) (0.0344) Adjusted R2 — — 0.06 0.07 Log-likelihood 199,110 199,021 Number of observations 360,036 360,036 72,890 59,059 NOTE: Standard errors are in parentheses. *** significant at the 99 percent confidence level. ** significant at the 95 percent confidence level. * significant at the 90 percent confidence level. aThese results are from estimation of a bivariate probit with selection. Other regressors included in the part-time employment equation include age; age squared; nonlabor income; and gender, education, marital status, race, education, region, urban, government, industry, and occupational dummy variables. The selection equation (not reported here) is an employment equation. bThese results are from estimation of a linear probability model via OLS and are generalizable to the part-time population only. Other regressors included in the voluntary part-time employment equation include age; age squared; and gender, education, marital status, race, education, region, government, industry, and occupational dummy variables 88 Hotchkiss mented that part-time workers earn considerably less per hour for not making a full-time commitment to his/her employer. This penalty can range from 30 to 60 percent lower wages depending on gender and race groups (Averett and Hotchkiss 1996), and it is a main reason that part- time jobs are considered undesirable (Blank 1990). The reason typi- cally given as to why part-time workers earn a lower wage is the pres- ence of fixed costs associated with hiring personnel. Employers are able to spread these fixed costs over more hours for full-time workers, allowing them to pay higher wages to such individuals. One concern might be that the fixed costs of hiring disabled workers are even greater than for nondisabled workers so that the wage differential between full- time and part-time disabled workers is larger than the differential be- tween full-time and part-time nondisabled workers. This section presents the full-time/part-time wage differentials ex- perienced by disabled and nondisabled workers, controlling for their |
selection into the labor market. Standard log wage equations are esti- mated separately for disabled and nondisabled workers. In the equa- tions for person i, ‘‘ft’’ denotes full-time, and ‘‘pt’’ denotes part-time: (4.9) ln Wift Xiftft ift ln Wipt Xiptpt ipt where lnWi is the natural log hourly wage of workers, Xi is the explanatory variable, is the set of coefficients to be estimated, and i is the random error term. As seen in Chapter 2, there may exist significant self-selection into the labor market, particularly among the disabled population. In order to obtain an estimate of representative of the population, this selection is controlled for using the standard Heckman (1979) two-step proce- dure. The first stage of this procedure involves estimating a binary choice model of the following form: (4.10) Ỹi Z i ui , ui N(0,1) where Zi are regressors expected to affect the labor supply decision, are parameter coefficients, ui is the normally distributed random Hours of Work, Distribution, and Representation 89 error, and individual i enters the labor force if Ỹi 0. Since Ỹi is unobserved, a binary variable, Yi, is defined as (4.11) Yi 1 as Ỹ 0 i 0. The parameters, , are estimated via maximum likelihood probit, and the inverse Mill’s ratio is constructed for inclusion in the wage equa- tions, which are then estimated via OLS. The modified wage equations are (4.12) ln Wift X ift ft ft ̂ift ift ln Wipt X ipt pt pt ̂ipt ipt where Xi and are defined in Equation 4.9, is the coefficient on the selectivity term, i is the modified random error term, and all variables (Zijj) are as just defined and ̂ij , j ft, pt. (Zijj) The parameter estimates that result from OLS estimation of the pair of equations in (4.12) can be used to decompose the wage differen- tial between disabled and nondisabled workers as follows: (4.13) ln Wft ln Wpt X ft̂ft X pt̂pt ( ̂ft ̂ft ̂pt ̂pt). The third term on the right-hand side in the parentheses reflects the role differences in selection into the labor market (across part-time status) play in observing differential wages. In order to obtain the selectivity-corrected wage differential, this selectivity term (or differ- ence in selection) is subtracted from the observed wage differential between full-time and part-time workers. This estimation procedure and calculation are performed for each year in the data set to see how different full-time and part-time wages are across disability status and whether that differential has changed over time. If the ADA has forced firms to make environmental changes that also enhance or facilitate a disabled worker’s employment, this full-time/part-time wage differen- tial might fall post-ADA. This would be because what used to be an 90 Hotchkiss extra fixed cost to hiring a disabled worker has been shifted to general access requirements mandated by other provisions of the ADA. Figure 4.4 plots these selectivity-corrected full-time/part-time wage differentials for disabled and nondisabled workers across time. Over the entire period, the part-time wage penalty is declining for both disabled and nondisabled workers. After full implementation of the ADA, however, the part-time penalty for disabled workers is less than the part-time wage penalty for nondisabled workers for all but one year. There are two potential explanations for this phenomenon. First, it may be the case that disabled workers are able to negotiate part-time hours in occupations or jobs that would not typically accommodate part-time work arrangements. Second, the situation may reflect a change in social attitude about what is ‘‘acceptable’’ behavior of a com- mitted worker. Either way, a smaller (and shrinking) part-time wage penalty (although still at roughly 40 percent) is good news for disabled workers who may require a shorter workweek to accommodate their impairments.13 DISTRIBUTION OF WORKERS An indication of how mobile workers with disabilities are com- pared to workers without disabilities (and how this mobility has Figure 4.4 Full-Time/Part-Time Wage Differentials for Disabled and Nondisabled Workers, CPS, 1981–2000 75 70 65 60 55 (%) 50 Nondisabled 45 40 Disabled 35 30 1981 1983 1985 1987 1989 1991 1993 1995 1997 1999 Hours of Work, Distribution, and Representation 91 changed over time) is their distribution over different occupations and industries. Figure 4.5 presents the distribution of disabled and nondis- abled workers among occupations and industries in 2000. Approxi- mately the same proportions of disabled and nondisabled workers are found in the technical support area and in the farming, fishing, and forestry occupational category. Disabled workers, however, are more heavily concentrated in service and laborer occupations, with nondis- abled workers more concentrated in managerial and craft occupations. As we will see later (and as was seen in Chapter 3), this concentration is split along earnings levels, with the occupations in which disabled workers are concentrated being the lower-paying ones. There does not seem to be as wide a disparity in the distribution of workers across industries. However, disabled workers are slightly more concentrated than nondisabled workers in the trade and service industries. Again, these are the lower-paying fields, on average. Figure 4.5 Distribution of Disabled and Nondisabled Workers across Occupations and Industries, CPS, 2000 (A) Occupational category Proportion 35 of workers Nondisabled 30 (%) Disabled 25 20 15 10 5 0 Professional Technical Service Farm, Craft Laborers & managerial support fishing & forestry (B) Industry category Proportion 45 of workers 40 Nondisabled (%) 35 Disabled 30 25 20 15 10 5 0 Agriculture Mining & Manu. Trans., Trade Fin., ins. Service Public constr. comm. & & real admin. utilities estate 92 Hotchkiss The Duncan Index The Duncan Index is useful for comparing the distributions of dif- ferent workers over various occupational and/or industry groups.14 It can be applied to analyze the distribution of disabled workers in rela- tion to that of nondisabled workers across occupations and industries. The Duncan Index (I) is calculated as follows (Duncan and Duncan 1955): 1 2 K (4.14) I ndj dj , j1 where K is the total number of occupations or industries and ndj and dj are the proportions of all nondisabled and disabled workers, respec- tively, in occupation or industry j. The index is equal to one-half the sum of the absolute differences between the proportion of nondisabled and disabled persons in each occupation or industry. An index equal to zero means that these groups of workers have identical employment distributions across occupations or industries. An index equal to one corresponds to the extreme situation of complete segregation (no dis- abled and nondisabled workers in the same occupation or industry). Another way to interpret I is as the percentage of disabled (or nondis- abled) workers that would have to change occupations (industries) in order to eliminate the difference in occupational (industry) distribu- tions. Figure 4.6 presents the Duncan Index calculated for each year and plotted along with the Duncan Index for white and nonwhite groups of workers as a frame of reference.15 The first noticeable characteristic of these graphs is the growing disparity between the distributions of dis- abled and nondisabled workers in both occupations and industries. This is in comparison to the declining trend in disparity between non- white and white workers. The contrast is particularly interesting since the average occupational index for both disabled versus nondisabled and nonwhite versus white is 0.13, but with very different end points. In other words, an average of 13 percent of disabled or of nondisabled workers would have to change occupations to equalize their distribu- tions across occupations. Hours of Work, Distribution, and Representation 93 Figure 4.6 Duncan Indices of Dissimilarity across Occupations and Industries, Disabled versus Nondisabled and Nonwhite versus White, CPS, 1981–2000 (A) Occupational dissimilarity 0.19 Nonwhite 0.17 vs. white 0.15 0.13 0.11 Disabled vs. nondisabled 0.09 1981 1983 1985 1987 1989 1991 1993 1995 1997 1999 (a) ADA Enactment (a) (b) (c) (b) ADA Phase I (c) ADA Phase II (B) Industry dissimilarity 0.12 0.10 0.08 Nonwhite vs. white 0.06 0.04 Disabled vs. nondisabled 0.02 1981 1983 1985 1987 1989 1991 1993 1995 1997 1999 (a) ADA Enactment (a) (b) (c) (b) ADA Phase I (c) ADA Phase II A second observation is that it appears as though the ADA may have helped to halt the early growth in occupational disparity, since that series (panel A) seems to have begun a new downward trend since 1992 (the first year of implementation of the ADA). This suggests that disabled workers may be able to take advantage of opportunities not available to them or that they merely may not have utilized pre-ADA. To the extent that matching the distribution of nondisabled workers is an objective, this is a positive outcome for disabled workers. 94 Hotchkiss It is of interest to note that other literature concerned with the distribution of workers may present different goals than equalization of distributions. For example, a dissimilarity in occupational distributions between native and immigrant workers can be considered a positive indicator for an economy, as immigrants fill in occupational gaps left by native workers (see Green 1999). In addition, it may not be clear that the equality of occupational distributions across disability status is desirable. The unique skills and abilities of typical disabled workers may make them fundamentally better suited for occupations not held by the typical nondisabled worker. The growth in disparity among industries does not seem to have followed the pattern of improvement seen among occupations; the distribution of disabled and nondisabled workers has become increasingly disparate, particularly in recent years. Evidence from the SIPP Analysis of the SIPP data reveals a similar pattern of growth in the dissimilarity in distributions across occupations between disabled and nondisabled workers. In addition, the SIPP allows for an evaluation of which type of disabilities results in the least similar distribution. Fig- ure 4.7 provides the Duncan Index calculated to compare the distribu- Figure 4.7 Duncan Indices of Dissimilarity across Occupations and Industries, by Type of Disability, SIPP, 1997 Duncan 0.45 Index of dissimilarity 0.40 0.35 Occupation 0.30 Industry 0.25 0.20 0.15 0.10 0.05 0 Musculoskeletal Internal systems Mental disorder Other Hours of Work, Distribution, and Representation 95 tion of workers with each type of disability with the distribution of nondisabled workers across both occupations and industries. Workers with mental disorders are distributed most differently across both in- dustries and occupations from nondisabled workers: 38 percent of ei- ther workers with mental disabilities or nondisabled workers would have to change occupations to equalize the distributions, compared with only 11 percent of workers with a musculoskeletal disability. Workers with mental disorders are much less likely than nondisabled workers to be employed in professional, technical, and craft occupa- tions, whereas they are much more likely to be employed in service and as laborers. Thirteen percent of workers with mental disorders (or of nondis- abled workers) would have to change industries to equalize the distri- bution, whereas only 6 percent of workers with internal system disabilities would have to switch industries. Workers with mental dis- orders are less likely to be employed in the transportation, communica- tion, and utility industry, and more likely to be employed in the service industry. REPRESENTATION OF WORKERS The equality in the distribution of disabled and nondisabled work- ers is a goal only if the disparity in distribution reflects characteristics of jobs or industries that are desirable. In other words, if nondisabled workers are systematically more concentrated in jobs that are more attractive than jobs in which disabled workers are concentrated, there is a call to make the distributions more equal. A ‘‘share of workers’’ measure can be used to determine whether disabled workers are more or less concentrated in occupations and industries with appealing quali- ties, such as higher wages or growth. The desirability of higher wages is obvious, but growth of an occupation could also be considered at- tractive since it may be indicative of stronger demand for workers, perhaps leading to greater wage growth and occupational advancement. Representation and Growth A high-growth indicator for each occupation (and industry) in the sample is constructed as follows: 96 Hotchkiss 1 if emp t1 k emp t k / emp t k (4.15) hgk K |
(1 / K ) emp t1 t j emp j / emp t j j1 0 otherwise where occupation (or industry) k is defined as high-growth if the per- centage change in employment between year t and t 1 for that occu- pation exceeds the average percentage change in employment in all occupations represented in the sample (K corresponds to the total num- ber of occupations or industries). The probability of being employed in a high-growth occupation (and/or industry) is determined as a func- tion of individual characteristics, including disability status. The sample was split into three time periods, and the employment growth of each occupation and industry represented in the sample was determined by a source external to the data file.16 Table 4.4 contains the growth rates of each occupation and industry represented in the sample. For example, for the 1983–1989 period, service occupations, managerial and professional specialty, and technical, sales, and admin- istrative support are considered ‘‘high growth,’’ since their growth ex- ceeds the average for all occupations. Similarly, for the same period, mining and construction; transportation and public utilities; retail trade; finance, insurance, and real estate; services; and public adminis- tration are all considered high-growth industries. Simple probit models were estimated to determine whether dis- abled workers are more or less likely to be employed in growing occu- pations or industries: (4.16) Ỹi Xij i , i N(0,1) where individual i’s job is in a growing occupation/industry if Ỹi 0. Since Ỹi is unobserved, a binary variable, Yij, is defined as (4.17) Yij 1 as Ŷij 0. 0 The set of parameters, , were estimated via maximum likelihood probit. Xi comprises various individual and job characteristics for Hours of Work, Distribution, and Representation 97 Table 4.4 Employment Growth Rates for Industry and Occupational Classifications Growth rate (%) 1983–89 1987–93 1991–98 Occupation Managerial and professional specialty 28.8 16.2 25.9 Technical, sales, and administrative support 15.6 5.6 6.1 Service 12.3 11.7 9.7 Precision production, craft, and repair 12.1 1.0 8.8 Operators, fabricators, and laborers 12.0 0.8 4.6 Farming, forestry, and fishing 7.5 3.6 0.1 Average Growth Rate 12.2 4.7 9.2 Industry Agriculture 9.7 2.9 3.3 Mining and construction 18.8 3.9 16.1 Manufacturing 8.6 5.8 0.7 Transportation and public utilities 15.8 8.2 13.0 Wholesale and retail trade 14.6 7.5 11.4 Finance, insurance, and real estate 22.7 2.7 10.2 Services 23.6 17.7 18.4 Public administration 17.9 10.2 4.1 Average growth rate 14.0 4.2 9.7 SOURCE: Author’s calculations from Jacobs (1998). worker i, including a dummy variable indicating whether the worker is disabled or not. The model was estimated on a sample of workers only; therefore, the results are generalizable to workers only. The mar- ginal effect of disability on being employed in a high-growth occupa- tion or industry was calculated as the marginal benefit for each worker, then averaged over the entire sample. Table 4.5 presents the estimated marginal effects of a work-limiting disability on having a job in a high- growth occupation or industry. In each of the three years analyzed, the probability of a disabled worker being employed in a high-growth occupation was from 2 to 5 percentage points less than the probability of a nondisabled worker being employed in a high-growth occupation. In addition, the marginal (negative) effect was the highest during the post-ADA years, suggest- ing that the ADA has not improved the opportunity of disabled workers to move into high-growth occupations. On the other hand, disabled 98 Hotchkiss Table 4.5 Marginal Effect of Disability on the Probability of Employment in a ‘‘High Growth’’ Occupation or Industry, CPS prob (high growth prob (high growth Year occupation)/disable industry)/disable 1989 0.0299 0.0123 (0.0092) (0.0108) 1993 0.0194 0.0469 (0.0085) (0.0121) 1998 0.0453 0.0261 (0.0140) (0.0129) All three years 0.0381 0.0268 (0.0068) (0.0070) NOTE: Probit estimations included the following regressors, in addition to a disability dummy variable: age; age squared; regional, education, marital, female, and nonwhite dummy variables; and occupation (for the industry probit) and industry (for the occu- pation probit) dummy variables. Standard errors are in parentheses. workers have been more likely to be employed in high-growth indus- tries. Unfortunately, a worker’s industry does not reflect as much on an individual’s job opportunities as one’s occupation does. For exam- ple, for someone with skills suited to a secretarial job, a decline in manufacturing as an industry is not as devastating to the person’s op- portunities as a decline in the administrative support occupation. Of course, occupational representation within an industry, such as the pro- portion of those in the precision production occupation in manufactur- ing industry, could be an important consideration. Representation and High Wages A simple correlation between wages in an industry or occupation and the percentage of workers in that industry or occupation that are disabled was performed to determine whether disabled workers are concentrated in low-paying occupations. The wage decomposition re- sults in Chapter 3 suggest that disabled workers are concentrated in the lower-paying occupations and industries, since occupation and industry regressors contribute positively and significantly to the observed wage differential between disabled and nondisabled workers. Figure 4.8 plots this correlation coefficient for each year for both occupations and industries. First, over the entire time period, the corre- Hours of Work, Distribution, and Representation 99 Figure 4.8 Correlation Coefficients, Concentration of Disabled Workers and Industry/Occupation Wage, CPS, 1981–2000 0 -0.2 Industry -0.4 -0.6 Occupation -0.8 -1.0 1981 1983 1985 1987 1989 1991 1993 1995 1997 1999 (a) (b) (c) (a) ADA Enactment (b) ADA Phase I (c) ADA Phase II NOTE: Correlation coefficients plotted include projections for industry years 1984 and 1999 and occupation year 1983, as these coefficients appeared to be extreme outliers. lation coefficient between concentration of disabled workers in an oc- cupation and the average hourly wage in that occupation is 0.82; the average across industries is 0.55. Disabled workers are more concentrated in the low-wage occupations and industries. Conse- quently, concern about the disparity in distributions across occupations and industries is warranted. While not particularly dramatic, there ap- pears to be some modest improvement (becoming less negative) in these correlation coefficients since 1992 (the first year of ADA imple- mentation). If the ADA did enhance the mobility of disabled workers across occupations and industries, it appears as though these individu- als are moving slightly toward the more desirable jobs, in terms of wage levels. CONCLUSIONS This chapter explored some dimensions of employment not cap- tured merely by employment probabilities or overall compensation. Initially, the incidence of and type of part-time employment were com- 100 Hotchkiss pared across disability status. Then, the distribution of disabled work- ers relative to nondisabled workers across occupations and industries was analyzed. Finally, the representation of disabled workers in what might be considered ‘‘desirable’’ occupations was evaluated. Having a work-limiting disability increased the probability of a worker being observed as employed part-time by 12 percentage points in 2000; this is double the 6-percentage-point impact of a disability on being employed part-time estimated for 1981. The upward trend in the relative occurrence of part-time employment among disabled workers does seem to have gotten a boost during the phase-in period of the ADA. There also seems to have been an ADA-related shift in the type of part-time employment experienced by disabled workers. After 1992, disabled part-time workers went from being less likely voluntar- ily employed part-time to more likely relative to nondisabled part-time workers. The implication is that much of the growth in part-time em- ployment has been voluntary and may actually reflect the required ac- commodation of a worker’s disability. Analysis with the SIPP data indicates that the growth in part-time employment has occurred pri- marily among those with musculoskeletal and mental disabilities, but that only part-time workers with mental disabilities have experienced any significant relative increase in voluntary part-time employment. This may reflect the fact that part-time or flexible work hours may be the best and least costly way to accommodate a worker with a mental disorder. An additional indication that part-time jobs are becoming an ac- ceptable alternative for employing disabled workers is the greater de- cline between 1981 and 2000 in the full-time/part-time wage differential among disabled workers than among nondisabled workers. In 2000, full-time nondisabled workers earned a wage (ceteris paribus) 45 per- cent higher than part-time nondisabled workers, while the full-time/ part-time wage differential between disabled workers was only 39 per- cent. It may also be the case that required accommodation enables disabled workers to negotiate part-time hours on a job that would not normally allow for flexible hours. Either of these reasons translates into an improved labor market experience for disabled workers in the dimension of hours of work. The movement of nondisabled workers away from part-time em- ployment and the movement of disabled workers towards part-time Hours of Work, Distribution, and Representation 101 employment may be one explanation why we observe a growing dis- parity in the distribution of workers across occupations (and indus- tries). It may be the case that some occupations, such as service occupations, are better suited to accommodate workers with disabili- ties. Workers with mental disorders are the most dissimilar in their distribution across both occupations and industries as compared with workers without disabilities. This might be expected considering that workers with mental disorders are the most likely to be voluntarily moving into part-time employment, which may mean that they are re- stricted in the types of occupations or industries open to this type of accommodation. The overall growth in occupational distributional dis- parity, however, is mitigated somewhat post-1992. This may mean that, post-ADA, disabled workers have been able to profit from oppor- tunities not previously available to them or that they merely may not have taken advantage of pre-ADA. To the extent that occupations and industries in which nondisabled workers are concentrated are desirable, this mitigation of dissimilarity since 1992 is a positive outcome for disabled workers. Further analysis found that in each of the three years analyzed, nondisabled workers were more likely to be employed in high-growth occupations and in the highest-paying occupations and industries. Consequently, concern about the disparity in distributions across occupations and industries is warranted, since nondisabled workers seem to be more concentrated in what might be considered desirable occupations and industries than are disabled workers. On the upside, there does appear to be modest movement of disabled workers into more high-paying occupations and industries since 1992. Notes 1. See Averett and Hotchkiss (1995, 1996, and 1997), Hotchkiss (1991), and Farber and Levy (2000). 2. This phenomenon, identified by Averett and Hotchkiss (1996), has been the expe- rience of women in the labor market. 3. For a discussion of labor market segmentation and dual labor market theory and references to this literature, see Kaufman and Hotchkiss (2000, Chapter 6). 4. The bivariate probit model with selection gives rise to the following likelihood function: ln L EMP1, PT1log 2 1X1i, 2X2i, EMP1, PT0ln 2 1X1i, 2X2i, EMP0ln 1X1i, 102 Hotchkiss where 2 is the bivariate normal cumulative distribution function and is the univariate normal cumulative distribution function. 5. This method of calculating the marginal effect of a change in a dummy variable is referred to as a measure of discrete change and is described in greater detail by Long (1997, pp. 135–138). 6. Table C.7 (column 1) in Appendix C contains the marginal effects used to gener- ate Figure 4.2. 7. This type of pooled, cross-sectional analysis has been applied by many research- ers (for example, Card 1992; Gruber 1994 and 1996; Zveglich and Rodgers 1996; and Hamermesh and Trejo 2000). The technique, however, also has its critics (such as Heckman 1996). The primary criticism of this pooled, cross-sectional approach is that it is impossible to control for unobserved changes in the environ- ment that occurred at the same time as the event of interest. Issues of potential concern in this regard are explored in Chapter 2. 8. Voluntary part-time is defined as (1994–2000) working less than 35 hours per week and did not want to work full-time, and (1981–1993) reason for working less than 35 hours per week coded as 07–15 (see Stratton 1994 for justification). Category reasons 07–15 are holiday, labor dispute, bad weather, own illness, on vacation, too busy with school |
or house, did not want to work full-time, full-time work week is less than 35 hours, or other. 9. Table C.7 (column 2) in Appendix C contains the marginal effects used to gener- ate Figure 4.3. 10. These results are consistent with those of Schur (2002), who finds that part-time and contingent work grows among the disabled during tight labor markets (where demand is strong relative to supply), which would be expected if these arrange- ments are voluntary. 11. The musculoskeletal category includes disabilities of the special senses (e.g., hearing, seeing). 12. See Magill (1997) for a detailed discussion about how flexible and part-time work schedules can often serve as low- or no-cost solutions to the accommodating problem. However, indirect costs, such as having to hire additional workers to cover lost hours of a disabled part-time worker, should not be ignored. 13. The SIPP data showed the same differential decline for both disabled and nondis- abled workers as seen in the CPS data, but essentially inconsequential differences across disability status in any given year. 14. An additional distribution index, the IP Index (see Watts 1992), was also evalu- ated, and the conclusions were the same. While there is a direct mathematical relationship between these two indices, the IP index reflects the percentage of workers in the labor market that would have to switch occupation or industry in order to equalize the distribution of disabled and nondisabled workers across occupations or industries, while maintaining the original occupational structure. Since the conclusions were the same regardless of the index employed, the more familiar Duncan Index is detailed here. 15. The actual indices plotted in Figure 4.6 are contained in Table C.8 in Appendix C. The indices calculated for the distribution across industries are consistent with Hours of Work, Distribution, and Representation 103 what Yelin and Cisternas (1996) calculated using the National Health Interview Survey; their data indicate that the relative distributions of disabled and nondis- abled workers have been fairly steady as far back as 1970. The occupational categories in their data were not comparable to those in the CPS, however. 16. Employment growth was calculated as the percentage change in the number of workers in an occupation from one time period to the next. This Page Intentionally Left Blank 5 Separation, Unemployment, and Job Search Separation from one’s job is an important dimension of the experi- ence of a worker. If separations are dominated by involuntary actions, such as a layoff or being fired, the worker’s experience is obviously diminished. Voluntary separation, however, may or may not be an indicator of a positive situation. On the one hand, voluntary separation (quitting) may indicate that workers are able to respond to better job opportunities through labor market mobility. On the other hand, exces- sive voluntary separations may reflect instability among that group of workers. This may be of particular importance for disabled workers who may need to voluntarily quit jobs for health reasons. The first analysis in this chapter considers a group of labor force participants who have experienced a recent job separation and evaluates the deter- minants, including disability status, of the type of separation.1 Unemployment is another important dimension of the labor market experience. In a given month in 2000, an average of 3.3 million people flowed into unemployment.2 Between the ages of 18 and 27, individu- als average 4.4 unemployment spells and spend an average of 31 weeks unemployed (Veum and Weiss 1993). In addition, Figure 5.1 shows that, in 1999, workers in the CPS data used here spent from roughly one to two weeks on average looking for work.3 Figure 5.1 also shows that while the disabled clearly spend more of their time in a given year looking for work, the movement of weeks spent in this activity essentially mirrors the trend for the nondisabled. The next sections will look more closely at this time spent looking for work. Job separation is only one reason why a worker might be unem- ployed. Workers entering the labor market for the first time and rejoin- ing the labor market after an absence are also considered unemployed until they find a job. Examining the composition of the unemployed over time can tell us something about flows into and out of the labor market. The second analysis of this chapter will explore the probabili- ties of unemployment categories as a function of disability status. 105 106 Hotchkiss Figure 5.1 Weeks Spent Looking for Work, by Disability Status, CPS, 1980–1999 Number 5 of weeks Disabled looking 4 3 2 Nondisabled 1 0 1980 1982 1984 1986 1988 1990 1992 1994 1996 1998 (a) ADA Enactment (a) (b) (c) (b) ADA Phase I (c) ADA Phase II The worker’s situation while unemployed, namely the job search experience, will also be explored in this chapter. For the same reasons argued in Chapter 2, one would expect that disabled workers would have a more difficult time finding a job that suits their skills, and would thus have longer spells of search duration, ceteris paribus. In addition, if disabled workers are subjected to hiring discrimination, search dura- tion would also increase. The third analysis in this chapter will evalu- ate the search spells of disabled and nondisabled workers and determine whether differential search strategies are more successful for one group or the other. SEPARATION If disabled workers have a more difficult time finding employment or employers that will accommodate their disabilities, they may experi- ence greater voluntary turnover as they continue to search for the job that will best match their skills. On the other hand, the fear of losing one’s health benefits (‘‘job-lock’’) may be more severe for disabled workers, leading to fewer voluntary separations relative to nondisabled workers (see Kapur 1998; Buchmueller and Valletta 1996). The impact of the ADA on voluntary separations among the disabled is ambiguous. Voluntary separations may increase as more opportunities become Separation, Unemployment, and Job Search 107 available to disabled workers, but may also decrease as employers make disability accommodations, which have been shown to increase tenure and reduce voluntary turnover among disabled workers (Burk- hauser, Butler, and Kim 1995). If disabled workers suffer from discrimination, or overall have less labor market experience or tenure with their employers, they might suffer more frequent involuntary separations through layoffs. Based purely on anecdotal evidence, Yelin (1991) concludes that ‘‘persons with disabilities, like those from minority races, constitute a contingent labor force, suffering displacement first [as an industry declines]’’ (p. 135). However, if disabled workers are a more selected group in the sense that they are less substitutable with other inputs (perhaps the accommodations employers have made for them enhance their produc- tivity beyond that of nondisabled workers, ceteris paribus), they will be less likely to be laid off as marginal workers. In other words, the discrimination or marginalization might be taking place at the hiring stage, rather than at the separation stage of the relationship. The pas- sage of the ADA might decrease involuntary separations among dis- abled workers if employers are fearful of accusations of discrimination. Among workers who have separated from their jobs, the CPS con- tains information about why a separation occurred. Figure 5.2 presents the percentage of disabled and nondisabled individuals who have expe- rienced a recent job separation and the reason for that separation. The series are split into pre- and post-1994, since the universe for the job separation question changed at that time.4 Overall, disabled workers have a greater incidence of voluntary separations, and nondisabled workers have a greater incidence of involuntary separations. The break in 1994 makes it difficult to draw any conclusions regarding trends. In order to look more closely at any possible trends, and to control for individual characteristics, a multinomial logit estimation was per- formed.5 A multinomial logit specification allows us to specify multi- ple possible outcomes (e.g., separation types) as a function of a variety of observed characteristics and unobservable factors, recognizing that as one’s probability of having separated voluntarily increases, the prob- ability of having separated involuntarily necessarily decreases. Job separations have been divided into three categories: 1) volun- tary separation, 2) involuntary separation, and 3) ‘‘other’’ separation.6 108 Hotchkiss Figure 5.2 Percentage of Job Separations by Type and Disability Status, CPS, 1981–2000 (A) Voluntary separations 85 80 Disabled 75 70 65 Nondisabled 60 55 50 1981 1983 1985 1987 1989 1991 1993 1995 1997 1999 (B) Involuntary separations 40 35 30 25 Nondisabled 20 15 10 Disabled 5 0 1981 1983 1985 1987 1989 1991 1993 1995 1997 1999 Separation, Unemployment, and Job Search 109 The separation is modeled as a multinomial logit, where the probability of observing a job separation (S) of type j for person i is equal to (5.1) Pj P(Si j), j 1,2,3. Pj (5.2) F( jX) for j 1,2, Pj P3 where F() is a cumulative distribution function, X corresponds to char- acteristics expected to influence the type of separations, and j dictates how those characteristics affect separation j. This means P j F(jX) (5.3) G( j 1,2. P jX) for 3 1 F( jX) Because of the rules of summation: G( jX) (5.4) P3 1/ 2 1 G( jX) and Pj 2 . j1 1 G( jX) j1 If we let (5.5) G( jX) exp (jX) and Yij gory j 1 if person i falls in separation cate , 0 otherwise the log likelihood function (ln L) can be written as (5.6) In L 3 3 Yij ln Pij, i1 j1 exp(X i j) 1 where Pij and Pi3 2 . 1 2 exp(X i k) 1 exp(X i k) k1 k1 The multinomial logit gives three sets of parameter estimates, each set describing the probability of one of the separation types. Each per- 110 Hotchkiss son has a probability of every type of separation, and those three proba- bilities sum to one (since the sample contains only those who experienced a separation). Figure 5.3 summarizes the marginal effects of having a work-limiting disability on the probability that the separa- tion was involuntary or voluntary for years 1981–2000.7 Over the period, the probability of a separation being voluntary is, on average, 12 percentage points higher for workers with disabilities, relative to workers without disabilities. This result lends support for the theory that disabled workers may have more difficulty finding the right ‘‘match,’’ and are therefore more likely to quit in search of a better accommodation for their disability. It could also point to the higher frequency of health-related quits among the disabled. In addi- tion, with the exception of the most recent two years, the impact of disability on voluntary turnover seems to be declining since the phase- in of the ADA. This suggests that mandated accommodations relieve the disabled worker of the burden of changing jobs in order to search for a better fit; the worker’s current job (or employer) does the chang- ing to better suit the disabled worker. It could also mean that employ- ers are accommodating potential health cycles that in the past would Figure 5.3 Marginal Effect of Being Disabled on the Probability of Separation Type, CPS, 1981–2000 0.20 0.15 0.10 0.05 Impact on probability of voluntary separation 0 -0.05 -0.10 Impact on probability -0.15 of involuntary separation -0.20 1981 1983 1985 1987 1989 1991 1993 1995 1997 1999 (a) ADA Enactment (a) (b) (c) (b) ADA Phase I (c) ADA Phase II Separation, Unemployment, and Job Search 111 have necessitated a job separation. This result is marginally consistent with the research of Baldwin and Schumacher (1999), who find, using 1990 data from the SIPP, that disabled workers are more likely (but insignificantly so) to voluntarily separate from their employers, relative to nondisabled workers. The probability of a separation being involuntary is, on average over the time period, 11 percentage points lower for workers with dis- abilities. This does not support the notion that disabled workers are considered ‘‘marginal.’’ Since this negative impact of being disabled on involuntary separations is in evidence well before the ADA, it may also help alleviate employers’ fears that the ADA makes it more ‘‘dif- ficult’’ to dismiss disabled workers, on average. These results are not consistent with these |
of Baldwin and Schumacher (1999), who find that disabled workers are slightly more likely to experience an involuntary separation than nondisabled workers. Baldwin and Schumacher (1999) explore overall job turnover, where nonseparation plays a large role in the outcomes of workers analyzed; their results are primarily driven by the fact that disabled workers experience more separations overall. The analysis here compares only types of separation and does not consider the nonseparation outcome. This approach is more relevant when con- sidering the separation experience of workers, rather than the question of turnover. In other words, the question answered here is, ‘‘Among those who have separated, what is the most common reason?’’ Further evidence that disabled workers are not marginalized is the experience during the recession of the early 1990s. Separation during the early nineties for disabled workers was even less likely to be the result of involuntary action, relative to nondisabled workers, compared with the years prior to and since the recession. UNEMPLOYMENT Examining the composition of the unemployed over time can tell us something about flows into and out of the labor market. For exam- ple, if most of the unemployed are new entrants or reentrants, these individuals would constitute an inflow of workers into the labor market. In 2000, job losers (fired or laid-off) made up the largest category of all the unemployed (44 percent), and re-entrants represented the next 112 Hotchkiss largest category (36 percent of the unemployed).8 As far as disabled workers are concerned, a policy such as the ADA is expected to de- crease the cost of entering the labor market (with improved accommo- dation and fewer barriers to employment), thus potentially increasing the incidence of new entrants and reentrants to the labor market, rela- tive to these categories for nondisabled workers. Another multinomial logit was estimated to evaluate the determi- nants of unemployment categories, with the type of unemployment di- vided into four classifications: 1) job loser (fired or laid-off), 2) job leaver (quit), 3) reentrant to the labor force, and 4) new entrant to the labor force. The first two categories were considered in detail in the previous section. The focus of the analysis in this section is on the relative probabilities that unemployment spells for disabled workers are of the new entrant or reentrant variety, and on whether the composi- tion of the unemployed was altered by the ADA. The structure of the multinomial logit estimated for this analysis is the same as described by Equations 5.1 through 5.5, except that there are four categories in- stead of just three. The multinomial logit provides four sets of parameter estimates. Each set describes the probability of one of the unemployment types; every person has a probability of each type of unemployment, and those four probabilities sum to one (since the sample contains only those who are unemployed). The CPS started categorizing types of unemployment in 1989, so that is the first year of analysis. The four panels in Figure 5.4 summarize the predicted probabilities of the job- less experiencing each of the categories of unemployment.9 The actual probabilities have been smoothed using a third-order polynomial.10 The smoothing process amounts to taking a plotted series and drawing a smooth line through the middle of the plotted points. The effect is to highlight any trends that are more difficult to decipher from the raw data. The higher the order of the polynomial (e.g., third- versus first- order), the more changes in direction will be captured (the higher the order, the less restrictive is the smoothing). The probabilities of being a job loser (fired or laid-off) and a job leaver (quit) are consistent with the results reported for separations in the previous section (see Figures 5.2 and 5.3). The disabled are less likely to be job losers than the nondisabled (panel A) and (typically) more likely to be job leavers (panel B). The disabled unemployed are Separation, Unemployment, and Job Search 113 Figure 5.4 Probability of Different Types of Unemployment by Disability Status, CPS, 1989–2000 (A) Unemployed is a job loser 0.75 Nondisabled 0.60 0.45 Disabled 0.30 0.15 0 1989 1991 1993 1995 1997 1999 (B) Unemployed is a job leaver 0.24 0.20 Disabled 0.16 0.12 Nondisabled 0.08 0.04 0 1989 1991 1993 1995 1997 1999 also predicted to be more likely to be new entrants and reentrants into the labor market (panels C and D) than the nondisabled. This indicates that the disabled move into and out of the labor market more than do nondisabled workers. This is not good news for the disabled, as shifts between jobs (even with intervening unemployment) typically result in better subsequent outcomes than movements out of and back into the labor market (Horvath and Shack 1986). 114 Hotchkiss Figure 5.4 (continued) Probability of Different Types of Unemployment by Disability Status, CPS, 1989–2000 (C) Unemployed is a new entrant 0.025 0.020 0.015 Disabled 0.010 0.005 Nondisabled 0 1989 1991 1993 1995 1997 1999 (D) Unemployed is a reentrant 0.7 0.6 0.5 Disabled 0.4 0.3 0.2 Nondisabled 0.1 0 1989 1991 1993 1995 1997 1999 Separation, Unemployment, and Job Search 115 There does not seem to be any noticeable effect of the passage and phase-in of the ADA on the probability of unemployed disabled work- ers being in one category of unemployment or another. There is an upswing in the probability of being a reentrant beginning about 1992, but that change is shared by the nondisabled, which likely means it was a general labor market response (by all workers) of recovery from the early 1990s recession; workers discouraged by the recession began to reenter the labor market as the economy recovered. The fairly steady decline in the probability of being a job loser among disabled workers since 1993 deviates somewhat from that observed for nondisabled workers, perhaps signaling that additional accommodations have made disabled workers even that much less marginalized than before. It could also be signaling employers’ fears of being accused of inappro- priately dismissing disabled workers. Perhaps, because of these fears, employers are even more scrutinizing when hiring a disabled worker, improving the chances of a good fit. JOB SEARCH The theory proposed so far as to why the disabled have a lower probability (among those who separate) of being a job loser, or experi- encing an involuntary separation, is that employers are more careful in their hiring of disabled workers. Employers may feel that hiring a disabled worker is more risky, or they may fear the consequences if they would have to dismiss the worker. The greater ‘‘care’’ in hiring a disabled worker should show up in longer search spells. Of course, the observation of longer search spells is also consistent with a theory of discrimination against disabled workers, but it is necessary to provide support for the preceding theory. Figure 5.5 presents the average dif- ference between the expected search spells of disabled workers and of nondisabled workers.11 While exhibiting some degree of variation from year to year, the average length differential ranges from a high of 24 weeks in 1987 to a low of 0.66 weeks in 1998. The median spell length differential (not controlling for any individual characteristics) for the entire time period is approximately 14 weeks.12 The expected impact of the ADA on search spell length of disabled workers is ambiguous. The legislation may reduce search spells by 116 Hotchkiss Figure 5.5 Average Search Spell Length Differential between Unemployed Disabled and Nondisabled Searchers, CPS, 1981–2000 Number 25 of weeks 20 15 10 5 0 1981 1983 1985 1987 1989 1991 1993 1995 1997 1999 (a) (b) (c) (a) ADA Enactment (b) ADA Phase I (c) ADA Phase II making overt hiring discrimination more difficult. It may also shorten spells merely by raising the awareness of employers to the capabilities of workers with disabilities. On the other hand, it may lengthen search spells if the fear of dismissing disabled workers is so great that employ- ers increase their scrutiny of such individuals before hiring them. It appears from Figure 5.5 that the ADA did not have an impact on the average search spell length differential. Fitting a trend line through the data points in Figure 5.5 results in a zero slope; while there is a wide variation in the average from year to year, and while the difference does not exhibit any trend, it is positive throughout the time period. Search Duration Estimation The difficulty of estimating job search spells using CPS data is notorious (Kiefer, Lundberg, and Neumann 1985). Individuals who are currently searching for a job are asked how long they have been searching, so that everyone in the sample is in the middle of a censored spell. Akerlof and Main’s (1981) approach to using CPS data is to double the observed censored search spells and then treat them as com- pleted. This results in an accurate representation of completed search spells under the assumption of a steady state.13 Under this assumption, Separation, Unemployment, and Job Search 117 the impact of various demographic characteristics on the length of a search spell can be determined. The demographic of particular inter- est, of course, is whether someone has a work-limiting disability. The accelerated failure time model that will be described allows for the estimation of these spell lengths, taking into account how long some- one has already been searching. This is of interest if, for example, the longer someone has been searching the harder it is for him or her to escape the search (by finding a job). If a person has a completed search spell length, t, the contribution to likelihood is f(t), where f(.) is the probability density function of the random search duration, T. In order to describe the variation in T conditional on a set of explanatory variables, X, a specific distribution is specified for T as a function of a set of parameters, . If T0 is a random time duration sampled from the baseline distribution for an individual whose covariates are all zero, then for nonzero covariates, X, the event time will be T(X) exp(X)T0 (see Kalbfleisch and Pren- tice 1980; Kiefer 1988). This model specification allows writing the log duration as a linear function of the covariates, lnt X . Assuming T is distributed as a Weibull, the following likelihood func- tion results: 1 (5.7) L(ti,Xi) g((lnti X i)/), i where g(.) is the probability density function of the transformed search duration; in this case, g(.) takes on the form of an extreme value distri- bution. Regressors for the duration analysis include age; age squared; nonlabor income; female, single, nonwhite, education, and regional dummies; dummy variables for availability for employment, whether searcher wanted a full-time job, and whether searcher worked last year; and dummy variables for search methods, disability status, and search methods interacted with disability status. The specification of a duration model, as opposed to merely esti- mating the relationship by OLS, for example, allows for the likelihood that the chance of a search spell ending in time t is related to how large t is (i.e., the probability that someone finds a jobs and stops searching in t depends on how long the individual has already been searching). 118 Hotchkiss This relationship between the chances of finding a job and how long a worker has been searching is referred to as duration dependence. Figure 5.6 plots the predicted expected search duration for the total sample, by disability status, for each year.14 Over this entire time pe- riod, on average, disabled individuals could expect to be looking for a job 3.2 weeks longer than nondisabled workers with identical demo- graphic characteristics and search strategies. The only trends that ap- pear in this graph correspond to the general conditions of the labor market; predicted expected duration for both disabled and nondisabled searchers moves together. There is an obvious rise in search length beginning in the early nineties (corresponding to the recession of the period), and duration begins to fall again in the mid 1990s. Controlling for demographic and search strategy reduces the aver- age marginal effect of being disabled on expected duration over this time period from approximately 14 weeks to approximately 3 weeks. The implication is that the majority of the observed search duration differential is explained by demographic |
and search strategy differ- ences. This suggests that discrimination in hiring may not be of great concern, but it does not rule out that employers are more ‘‘careful’’ in screening disabled workers. In other words, it is possible that the characteristics of disabled and nondisabled workers are being valued equally, but that employers go to greater length to discern the fit of a Figure 5.6 Predicted Expected Search Duration by Disability Status, CPS, 1981–2000 Predicted 60 duration (weeks) 50 40 Disabled 30 Nondisabled 20 10 0 1981 1983 1985 1987 1989 1991 1993 1995 1997 1999 Separation, Unemployment, and Job Search 119 disabled worker with a particular job. This behavior would be consis- tent with a risk-averse employer who has more difficulty determining the productivity of disabled workers than of nondisabled workers from observable traits. This could be due to lack of experience on the part of the employer or because there is greater variance in the productivity among disabled workers for any given set of observable characteristics. Effectiveness of Search Methods One important quality that an individual brings to the job search is the type of strategies used. It is of interest to determine whether dis- abled job seekers consistently use different search strategies and whether those methods are consistently more or less effective for dis- abled searchers than for the nondisabled. Several researchers have found that certain search methods are more effective in finding em- ployment than others (Bortnick and Ports 1992; Thomas 1991), so if disabled individuals are systematically relying on less effective meth- ods, or systematically have less effective methods available, this leads to an obvious remedy. Figure 5.7 details the average percentage of disabled and nondisabled job seekers using each of six search strategies (‘‘did nothing’’ is excluded as a strategy from the illustration). Figure 5.7 Percentage of Disabled and Nondisabled Searchers Using Each Search Strategy, Averaged over the Period 1981–2000, CPS 80 70 Disabled 60 Nonisabled 50 40 30 20 10 0 Public Private Checked Other Checked with Checked agency agency with friends employer ads 120 Hotchkiss Disabled searchers are marginally more likely to check with friends, public agencies, and advertisements. None of the differences across strategies, however, is significantly different from zero. The implication, then, is that disabled and nondisabled job seekers rely, in the same percentages, on the same search strategies. In addition, there is no trend over time in the proportion of people using each method across disabled or nondisabled searchers. Furthermore, out of the 100 possible coefficients (across years and across search strategies) included to control for potential differential impacts of search strategies on length of search for disabled workers, only 17 were significantly different from zero and not in any consistent way. In other words, each strategy never helped or hindered disabled searchers, relative to nondisabled searchers, in any systematic way. The implication is that personal demographics were the primary deter- minants of search outcome, and that merely changing strategies will not improve those outcomes for disabled workers. CONCLUSIONS The ‘‘not working’’ side of the labor market can be important in shaping the overall experience of a worker. This chapter compares the separation, unemployment, and job search experiences of disabled and nondisabled workers over time. The lower probability for disabled workers that a separation is involuntary is clearly good news for dis- abled workers. It implies that disabled individuals are not ‘‘marginal’’ workers, as some have theorized. The higher probability for this group that a separation is voluntary indicates, at a minimum, that disabled workers do enjoy some labor market mobility with which they can seek out the most accommodating employment setting. It may also show that disabled workers have a more difficult time finding a good employ- ment match, which is not entirely unexpected, or that health conditions necessitate more frequent voluntary movements in and out of jobs. There is no indication from the analysis performed here that the ADA has had much impact on the probability that a disabled worker’s sepa- ration is either voluntary or involuntary. Disabled workers are more likely to be reentrants and new entrants into unemployment than nondisabled workers. This is unfortunate be- Separation, Unemployment, and Job Search 121 cause leaving and reentering the labor market typically results in less advantageous outcomes than movements between jobs.15 There are not a lot of policy options, sadly, that might alter this pattern, since much of the movement into and out of the labor market may be dictated by the nature of the disabled worker’s mental or physical condition. On average over the time period, an unemployed disabled worker searches three weeks longer than a similar nondisabled worker before locating a job. This result, in combination with the finding that dis- abled workers are less likely to separate from his/her job for involun- tary reasons, suggests that employers are being more ‘‘careful’’ in their hiring of disabled workers. There is a fine line between discrimination and being discriminating. However, it was also found that differences in individual characteristics between disabled and nondisabled workers explain most of the difference in their search spell lengths. Therefore, it is possible that the characteristics of disabled and nondisabled work- ers are being valued equally (the typical measure for discrimination), but that employers go to greater lengths to discern the fit of a disabled worker’s endowments with a particular job. This behavior on the part of the employer would result both in longer search spells for the dis- abled and in a lower probability that a separation is involuntary. These results, taken together, suggest that policies that assist em- ployers and disabled workers in finding each other would go a long way to improving search outcomes. Active job placement and objective screening of skills might be useful and serve the needs of the ‘‘discern- ing’’ employer. Notes 1. While it may seem natural to first focus on the incidence of separation, the em- ployment analysis contained in Chapter 2 essentially contains the inverse of an analysis of incidence. The CPS does not ask separation questions of those who are currently working, so that an evaluation of separation incidence would amount to an analysis of unemployment incidence (the inverse of what was evaluated in Chapter 2). The results from Chapter 2 indicate that the disabled are more likely at any given time to have separated from their job, and that the difference in probability across disability status is unchanged over time. 2. Unpublished data from the U.S. Bureau of Labor Statistics; obtained November 2001. 3. The sample for whom these statistics were plotted consisted of those who spent at least some (no matter how little) time working in the previous year. This gives 122 Hotchkiss us a better picture of the looking-for-work activity of those with at least some marginal attachment to the labor market. 4. The data used to generate Figure 5.2 and details of the questionnaire change are found in Table C.9 in Appendix C. 5. Multinomial logits have come under frequent criticism because of the assumption of independence of irrelevant alternatives (IIA) that is implied by the logit speci- fication. Alternative specifications that retain the desired probability structure (i.e., multinomial probit) are riddled with their own problems and not considered here to add value greater than the cost that would be imposed. It has been pointed out that under the framework of what is called a ‘‘universal’’ logit, the estimation procedure can be applied, but the utility interpretation of the structural estimates is lost. In addition, the more regressors included to describe the multiple out- comes, the less bothersome is the assumption of IIA. For these reasons, the logit structure is retained. For further discussion on these points, see Ben-Akiva and Lerman (1985, section 5.2) and Moffitt (1999, pp. 1382–1387). 6. Voluntary separations included the following reasons: personal, family, school; personal/family (includes pregnancy); return to school; health; retirement/old age; and unsatisfactory work arrangements (hours/pay/etc.). Involuntary separation included the following reasons: seasonal job completed, temporary seasonal or intermittent job completed, slack work/business, and temporary nonseasonal job completed. The analysis in this chapter is based only on those who experienced a separation either in the past five years (1981–1993) or in the previous year (1994–1999); the results, therefore, are not generalizable to the entire labor force. 7. The predicted probabilities are found in Table C.10 in Appendix C. Whereas the impact of the questionnaire change was obvious in the raw data (see Figure 5.2), the predicted probabilities are comparable across years in the cross section, with the primary impact being larger sample sizes prior to 1994. 8. U.S. Department of Labor, Employment and Earnings (January 2001, p. 203). To be counted as unemployed, the respondent must have undertaken some action within the past four weeks to find a job. 9. The predicted probabilities from the multinomial logit analysis used to generate these figures are found in Table C.11 in Appendix C. The figures plot a ‘‘smoothed’’ version of the series of numbers reported in Table C.11. 10. This simply involves calculating a least squares third-order polynomial fit through the data points. 11. Following the suggestion of Akerlof and Main (1981) to compensate for the defi- ciencies of the job search data collected by the CPS, expected search duration is calculated as twice the observed duration at a given point in time. This represen- tation of expected duration relies on the assumption of a steady state, which may be difficult to support for a statistic across time (i.e., business cycles; Sider 1985); however, this may be less critical when making cross-sectional comparisons, as is done here. It is also assumed that this assumption has the same implication across disability status. 12. The numbers used to prepare Figure 5.5 can be found in Table C.12 (column 1) in Appendix C. Separation, Unemployment, and Job Search 123 13. See note 11. 14. Predicted expected duration was calculated using the coefficient estimates re- sulting from the accelerated failure time model. Where search duration is as- sumed to be distributed as a Weibull, expected search duration is calculated as Etiti 0;Xi,, exp(X i )(1 ), where is the gamma distribution function. The characteristics (other than disability) for which the predicted ex- pected durations were calculated (X) are the means corresponding to the entire sample. See Long (1997). The numbers used to prepare Figure 5.6 can be found in Table C.12 (columns 2 and 3) in Appendix C. 15. There is even some evidence that disabled workers experience more discrimina- tion between employers (from switching jobs) than they experience with any given employer (on their current job). See O’Hara (2000). The implication is that any job separation may worsen a disabled person’s labor market outcome. This Page Intentionally Left Blank 6 State versus Federal Legislation Whenever major federal legislation to regulate the functioning of a market is enacted, a key question raised is whether that law is redun- dant or whether it has the potential of actually altering the functioning of the market (i.e., is ‘‘binding’’). By the time the ADA was passed, all states had some form of legislation addressing discrimination against the disabled (see Table 6.1).1 Thus, the environment in which the ADA was approved was arguably already a post-ADA one. One might suggest that the ADA was superfluous; the states were already addressing the problem of discrimination against the disabled and there was no need for federal legislation. This situation may be an explana- tion for finding no or very little labor market impact attributable to the ADA in previous chapters. In other words, it may be the case that the state legislation ‘‘crowded out’’ any potential impact of the ADA. On the other hand, legislation at the state level may have served as a state- ment of ethical beliefs already integrated into the economy. To determine whether state-level protective legislation ‘‘crowded out’’ or had a differential impact on the experience of disabled workers than the federal ADA, employment, wage, and hours analyses mirror- ing those contained in Chapters 2, 3, and 4 are repeated here, but only for a subsample of states that enacted disability legislation between 1981 (the beginning of available data) and 1991 (the last year before implementation of the federal legislation). The employment impact is determined by estimation of a pooled, cross-sectional bivariate probit |
with selection model analogous to that estimated in Chapter 2. The state-level impact of disability legislation on wages is determined by a pooled, cross-sectional estimation of log wages, controlling for selec- tion into the labor market, mirroring the wage analysis in Chapter 3. The bivariate probit with selection will again be used to parallel the part-time employment analysis of Chapter 4. Only the CPS data set will be used for analyses in this chapter. The condition for being included in the subsample for analysis is whether the worker resided in a state that adopted protection for the disabled during this period.2 To coincide with the provisions of the 125 126 Hotchkiss Table 6.1 Summary of State-Level Disability Legislation First year disability Public/ First year disability Public/ State legislation in place private coverage State legislation in place private coverage Alabama 1975 public Montana 1974 public/private Alaska 1987 public/privatea Nebraska 1971 public Arizona 1985 public/private 1973 public/private Arkansas 1973 public Nevada 1971 public/private 1993 public/private New Hampshire 1975 public/private California 1980 public/privatea New Jersey 1978 public/private Colorado 1979 public/private New Mexico 1973 public/private Connecticut 1973 public/private New York 1974 public/privatea Delaware Before 1988 public North Carolina 1985 public/private 1988 public/private North Dakota 1983 public/private Florida 1977 public/private Ohio 1976 public/privatea Georgia 1978 public Oklahoma 1981 public/private 1981 public/private Oregon 1973 public/private Hawaii 1981 public/private Pennsylvania 1974 public/private State versus Federal Legislation 127 Idaho 1969 public Rhode Island 1973 public/private 1988 public/private South Carolina 1972 public Illinois 1980 public/private 1996 public/private Indiana 1975 public/private South Dakota 1973 public Iowa Before 1971 public 1984 public/privatea 1972 public/privatea Tennessee 1976 public/private Kansas 1974 public/private Texas 1989 public/private Kentucky 1976 public/private Utah 1979 public/private Louisiana 1975 public Vermont 1981 public/private 1980 public/private Virginia 1972 public Maine 1973 public/privatea Washington 1973 public/privatea Maryland 1974 public/private Washington, DC Before 1972 public Massachusetts 1983 public/private 1994 public/private Michigan 1976 public/private West Virginia 1981 public/private Minnesota 1973 public/private Wisconsin 1965 public/private Mississippi 1974 public Wyoming 1985 public/privatea Missouri 1978 public/private NOTE: Some further details of each of these state’s laws can be found in Appendix D. a Exact original coverage not available; classification based on current coverage definitions. 128 Hotchkiss ADA, the date at which legislation covering both public and private employers became effective was used to distinguish pre- and post-time periods. As can be seen from Table 6.1, 10 states passed disability legislation between (but not including) 1981 and 1991. These states were Alaska (1987), Arizona (1985), Delaware (1988), Idaho (1988), Massachusetts (1988), North Carolina (1985), North Dakota (1983), South Dakota (1984), Texas (1989), and Wyoming (1985). A preliminary look at the potential impact on employment proba- bilities and labor force participation is shown in Figures 6.1 and 6.2, which plot these statistics for the disabled and the nondisabled. These Figure 6.1 Labor Force Participation Rates for the Disabled and the Nondisabled, CPS, 1981–1991 90 80 70 Nondisabled 60 50 (%) 40 30 20 Disabled 10 0 -9 -8 -7 -6 -5 -4 -3 -2 -1 0 1 2 3 4 5 6 7 8 Event period Figure 6.2 Proportion of Disabled and Nondisabled Labor Force Participants That Are Employed, CPS, 1981–1991 100 Nondisabled 95 90 85 80 Disabled (%) 75 70 65 60 55 50 -9 -8 -7 -6 -5 -4 -3 -2 -1 0 1 2 3 4 5 6 7 8 Event period State versus Federal Legislation 129 illustrations show the averages across all 10 states, event-study style, with t 0 corresponding to the year disability legislation was in place in the state; t 0 corresponds to the pre-legislation period and t 0 corresponds to the post-legislation period. There is no obvious change in either the labor force participation rate or conditional employment rate for either the disabled or nondisabled, except for perhaps a higher employment rate for both groups, in the post-legislation period. IMPACT ON EMPLOYMENT To determine the employment impact of state-level disability legis- lation, a pooled, cross-sectional bivariate probit model with selection was estimated with dummy variables representing whether the observa- tion shows up in the data pre-legislation or post-legislation and whether the observation is a disabled or nondisabled person. These dummy variables were also interacted to determine whether being disabled had any greater effect on employment after the legislation than before, rela- tive to the experience of a nondisabled person.3 The bivariate specifi- cation allows for the two outcomes (labor force participation and employment) to be impacted by the same unobservable factors (e.g., motivation). The selectivity part of the model is merely a recognition that we do not get to see the employment outcome unless the person is in the labor market to begin with, and that those we observe in the labor market may have systematically different employment outcomes than those not in the labor market. Correcting for selectivity allows us to make inferences for anyone from the population, not just those we observe in the labor market; this is what makes the probability uncon- ditional. The empirical model is specified as follows: (6.1) lfpis 1 1X1i 1disablei 1 posts 1 disablei posts 1is empis 2 2X2i 2disablei 2 posts 2 disablei posts 2is empis1 if person i in state s is employed, 0 otherwise; lfpis 1 if person i in state s is in the labor force, 0 otherwise, and empis is not 130 Hotchkiss observed unless lfpis 1. disablei is equal to 1 if person i is disabled, 0 otherwise; X1i and X2i include individual demographic characteristics; posts is equal to 1 if person is observed in state s post legislation for that state; 1is and 2is are distributed as a bivariate normal with means equal to 0, variances equal to 1, and correlation equal to ; and j, j, j, j, and j ( j1,2) are parameters to be estimated. In this framework, the affected group (the disabled) is controlled for by a dummy variable indicating whether the individual has a work- limiting disability, and the time period is controlled for by a dummy variable indicating whether disability legislation in the state had been implemented yet or not. Given the nonlinearity of the bivariate probit estimation procedure, a single parameter coefficient does not tell us the additional effect the legislation had on the difference in employment probabilities between the disabled and nondisabled; however, the sig- nificance of the coefficient on the interacted disablei posts will yield significance levels of that impact. Table 6.2 details the results from the estimation. The first thing to notice from Table 6.2 is that the parameter esti- mates on the vast majority of regressors are of the same sign and the same magnitude as those in Table 2.1 in Chapter 2, corresponding to the national sample. The only exceptions to this are the west, central city, college, and advanced degree dummy variables; and the state un- employment rate (the signs across the tables are the same, but the mag- nitudes differ slightly) and the Midwest dummy variable (less significant in the state analysis). The implication of the similarity across the national and state-level analyses is that the observations in this subset of states are not at all far from the norm and that the results on the regressors of interest (those related to disability status) should be considered generalizable beyond these states. The second result to note from Table 6.2 is the lack of significance of the coefficient on the disable post regressor in the employment equation. This means that the employment probability of a disabled person, relative to a nondisabled person, did not change post-legisla- tion. Again, in a set of results where most other regressors are signifi- cant at the 99 percent confidence level, this is notable. The lack of impact of the ADA at the national level could have been the result of state legislation crowding out any potential effect of the federal law, in which case we should see an influence of enactment State versus Federal Legislation 131 Table 6.2 Labor Force Participation and Employment Bivariate Probit with Selection Results, CPS, 1981–1991 Labor force Regressor participation equation Employment equation Intercept 2.9613*** 0.8355*** (0.0492) (0.2396) Age (00) 13.3187*** 1.2545*** (0.2278) (0.3533) Age Squared (0000) 16.4768*** 2.3317*** (0.2828) (0.4673) Female 1 0.5123*** 0.2041 (0.010) (0.0143) Nonwhite 1 0.0340** 0.2871*** (0.0148) (0.0194) High school grad 1 0.2689*** 0.0614*** (0.0127) (0.0180) Some college 1 0.1187*** 0.1680*** (0.0135) (0.0198) College grad 1 0.3347*** 0.3606*** (0.1784) (0.0262) Advanced degree 1 0.1836*** 0.1843*** (0.0310) (0.0463) Central city 1 0.0781*** 0.0040 (0.0150) (0.0216) Midwest 1 0.0406** 0.0010 (0.0175) (0.0336) South 1 0.0108 0.0771*** (0.0142) (0.0222) West 1 0.1120*** 0.0788*** (0.0166) (0.0298) Single household 1 0.2345*** — (0.0117) Nonlabor income (000000) 21.2445*** — (0.8830) Worked last year 1 1.9908*** — (0.0110) Weeks worked last year (00) — 3.0181*** (0.0457) State unemployment rate (0) 0.0389 0.8264*** (0.0334) (0.0483) 132 Hotchkiss Table 6.2 (continued) Labor force Regressor participation equation Employment equation Real gross state product (000000) — 0.0593 (0.1539) Log population — 0.0042 (0.0159) disable 1 0.7197*** 0.2095*** (0.0301) (0.0514) post legislation 1 0.0442*** 0.0273 (0.0127) (0.0185) disable post 1 0.0523 0.0057 (0.0377) (0.0663) Rho 0.0403*** (0.0065) Log-likelihood 65,190 Number of observations 140,707 NOTE: States included in the analysis are Alaska, Arizona, Delaware, Idaho, Massa- chusetts, North Carolina, North Dakota, South Dakota, Texas, and Wyoming. Standard errors are in parentheses. *** significant at the 99 percent confidence level. ** significant at the 95 percent confidence level. Notation of, for example (00), indicates regressor has been scaled by dividing by 100. of disability legislation at the state level. Alternatively, it may be the case, as has been pointed out with other social legislation, that the law itself merely was the culmination of changes already incorporated into the labor market experience of the affected group. In this instance, we should see no effect of enactment of such legislation at the state level either. This latter scenario is what we observe. While, overall, persons with disabilities have a lower probability of unconditional employment, there is no relative change in that employment probability post-legisla- tion versus pre-legislation. The third result of particular interest is related to the determination of labor force participation. Recall that in the national analysis (see Table 2.1) there was a dramatic decline in labor force participation rates among the disabled post-ADA. If, indeed, the ADA legislation caused individuals to flee the labor market, similar legislation at the state level should result in the same behavior. The results in Table 6.2, however, indicate that state-level disability legislation had no such State versus Federal Legislation 133 impact; the coefficient on disable post in the labor force participa- tion equation is not significantly different from zero. Again, this is in an estimation where nearly all the other regressors are significant at the 99 percent confidence level. These findings support the theory posited in Chapter 2 that the drop in the labor force participation rate that occurred in 1994 at the national level (see Figure 2.2) cannot be attrib- utable to the ADA and is likely the result of some other confounding factor (i.e., modifications in welfare and Social Security Administration policies). Lastly, while the state unemployment rate has a large negative im- pact on employment probabilities, the new regressors of real gross state product and log population are insignificant determinants of employ- ment; the positive sign of real gross state product does, however, make intuitive sense. IMPACT ON WAGES It was found in Chapter 3 that the ADA seems to have had a nega- tive impact on wages of disabled workers overall, although it did not appear to be directly related to the cost of accommodations required of firms covered by the legislation. This section looks at the state level to see whether a similar impact on wages occurred when protective legislation was passed. Log real wages are specified as a function of demographic and job characteristics, as well as indicators for disability status, time period, and the interaction between disability status and time. The following specification is estimated via OLS for the time period 1981–1991: (6.2) lnrwageis Xi 1 disablei 2 posts 3disablei |
posts is where lnrwageis is the natural log hourly real (1982–19841) wage of worker i in state s, Xi is a set of covariates for each person (demographic and job characteristics), disablei is equal to 1 if person i has a work-limiting disability, and posts is equal to 1 if person is observed in state s post-legislation for that state. 134 Hotchkiss The affected group (the disabled) is controlled for by a dummy variable indicating whether the individual has a work-limiting disability, and the post-legislation time period in each state is controlled for by a dummy variable indicating whether disability legislation was in place yet or not. The coefficient of interest (3) measures the change in real wages, relative to nondisabled workers, after passage of disability legislation, relative to before legislation was in place. Xi includes indi- vidual demographic and job characteristics. Wages are observed for workers only, and because the characteris- tics of workers may be changing over time in unobservable ways, it is important to control for any potential unobserved self-selection into the labor market. Consequently, Equation 6.2 is modified by simply adding the standard inverse-Mills ratio obtained from the first-stage probit estimation of a labor force participation/employment equation. This standard Heckman (1979) two-step procedure for controlling for self-selection is presented in greater detail in Chapter 3. The parame- ters of the model are identified through some regressors in the first- stage probit estimation that are not in the wage regression; these re- gressors include nonlabor income and an indicator of whether the per- son worked last year or not. Since the purpose of this two-stage approach is merely to obtain unbiased estimates of the coefficients in the wage equation, interpretation of those coefficients is not changed by controlling for selection. Table 6.3 contains the estimation results from the log wage equation estimation. As with the employment analysis, the results in Table 6.3 mirror those at the national level, as reported in Table 3.1 in Chapter 3; most coefficients on the control variables are of the same sign, and they are roughly of the same magnitude. Two exceptions are the coefficient on the advanced degree dummy variable, which is about one third the size of that estimated at the national level, and the coefficient on the selec- tion term. In Chapter 3, there was evidence of positive self-selection, meaning that those entering the labor market could expect to earn higher wages than the population as a whole. In the state-level analy- sis, the coefficient on the selection term is negative, indicating that those entering the labor market typically will earn less than the popula- tion as a whole. Since the purpose of controlling for selection is to obtain consistent estimates of the other coefficients in the wage equa- tion, this difference in sign between the national and state-level analy- State versus Federal Legislation 135 Table 6.3 Log Real Wage OLS Estimation with Selection, CPS, 1981–1991 Labor force Regressor participation equation Intercept 2.5415*** (0.0509) Age (00) 0.0415*** (0.0051) Age Squared (0000) 0.0004 (0.0140) Female 1 0.2266*** (0.0048) Nonwhite 1 0.0416*** (0.0042) High school grad 1 0.1230*** (0.0046) Some college 1 0.2072*** (0.0055) College grad 1 0.3863*** (0.0067) Advanced degree 1 0.1071*** (0.0032) Midwest 1 0.3072*** (0.0010) South 1 0.1441*** (0.0000) West 1 0.1125*** (0.0001) Hours worked per week 0.0017 (0.0142) Union 1 0.1496*** (0.0008) Single household 1 0.0659*** (0.0033) State unemployment rate (0) 0.0109*** (0.0003) Real gross state product (000000) 0.0081 (0.0052) Log population 0.0953*** (0.0047) disable 1 0.0802*** (0.0033) 136 Hotchkiss Table 6.3 (continued) Labor force participation Regressor equation post legislation 1 0.0307*** (0.0039) disable post 1 0.0452** (0.0176) (selection term) 0.0811*** (0.0057) R2 0.46 F statistic 2,354 Number of observations 95,604 NOTE: States included in the analysis are Alaska, Arizona, Delaware, Idaho, Massa- chusetts, North Carolina, North Dakota, South Dakota, Texas, and Wyoming. The wage regression also included seven industry and five occupational dummy variables, and a government dummy variable not reported here. The first-stage probit estimation included age; age squared; gender, race, education, and disability dummies; and the state unemployment rate. Nonlabor income and an indicator of working last year were included as identifying regressors. All estimated coefficients in the first-stage estimation were significantly different from zero at the 99 percent confidence level. Standard errors are in parentheses. *** significant at the 99 percent confidence level. ** significant at the 95 percent confidence level. ses is not a concern here but may be worth exploring elsewhere from a behavioral perspective. The coefficient on the interaction term (disable post) is 0.0452, indicating that disabled workers experienced a 4.5 percent decline in wages, relative to nondisabled workers, post-disability legis- lation, relative to pre-disability legislation. This is roughly of the same magnitude as the 3 percent decline in wages experienced post-ADA implementation (see Table 3.1). The implication is that we see the same relative decline in wages of disabled versus nondisabled persons at the state and national levels. This may mean that the measured impact of the federal ADA on relative wages is muted, given that some adjustment to disability legislation had already taken place as a result of state laws. In addition, this lower wage of disabled workers relative to that of nondisabled workers may not be the consequence of adjust- ment cost, but, rather, reflect the overall negative impact on the dis- State versus Federal Legislation 137 abled, not just those covered by the legislation; this was the result discovered in Chapter 3. IMPACT ON HOURS The increase in part-time employment post-ADA found in Chapter 4 is worth exploring at the state level, as well. It is of interest since flexibility in hours may serve as an important mechanism through which employers can accommodate many types of disabilities. If this is the case, then requirements to accommodate workers’ disabilities at the state level should result in similar adjustments as seen post-ADA. Figure 6.3 plots the average proportion across states of disabled and nondisabled workers that are employed part-time. The reference verti- cal line corresponds to the time when legislation was in place in each state. There appears to be an increase in the proportion of disabled workers that are employed part-time, as well as a modest divergence in the two series. The pooled, cross-sectional analysis of Chapter 4 is repeated here in order to determine whether there is any significant growth in part- time employment among disabled workers, post-legislation, relative to Figure 6.3 Proportion of Disabled and Nondisabled Workers That Are Employed Part-Time, CPS, 1981–1991 45 40 35 Disabled 30 (%) 25 20 15 Nondisabled 10 5 0 -9 -8 -7 -6 -5 -4 -3 -2 -1 0 1 2 3 4 5 6 7 8 Event period 138 Hotchkiss nondisabled workers. The model estimated is the bivariate probit with selection: (6.3) empis 1 1X1i 1 disablei 1 posts 1 disablei posts 1is ptis 2 2X2i 2 disablei 2 posts 2 disablei posts 2is. empis 1 if person i in state s is employed, 0 otherwise, and ptis 1 if person i in state s is employed part-time and is not observed unless empis 1. disablei is equal to 1 if person i is disabled, 0 otherwise; posts is equal to 1 if the person is observed after passage of the state legislation; X1i and X2i include individual demographic characteristics; 1is and 2is are distributed as a bivariate normal with means equal to 0, variances equal to 1, and correlation equal to . Again, the coefficient in the part-time equation on the disable post regressor is what tells us whether there is any change in the proba- bility of part-time employment among disabled workers, post-legisla- tion, relative to nondisabled workers. Table 6.4 details the regression results. Using the parameter estimates, the difference in the impact of having a work-limiting disability on part-time employment across the two time periods can be calculated by evaluating the probabilities of interest for each person, varying the disable and post dummy vari- ables, then taking the difference between these probabilities and aver- aging the differences across the sample. This calculation translates the estimated coefficients into a 2-percentage-point greater probability of disabled workers being employed part-time than nondisabled workers, post-legislation relative to pre-legislation. This result is only signifi- cantly different from zero at the 85 percent confidence level, but it does provide some support for the notion that disability legislation, whether by the states or national, influences the hours of work of dis- abled workers.4 Also, as with the preceding wage analysis, these find- ings suggest that the impact of the ADA was dampened somewhat by the adjustments in hours that had already taken place as a result of the state-level legislation. CONCLUSIONS The goal of this chapter was to determine what impact state-level disability legislation has had on the employment, wage, and hours out- State versus Federal Legislation 139 Table 6.4 Employment and Part-Time Employment Bivariate Probit with Selection Results, CPS, 1981–1991 Employment Part-time Regressor equation employment equation disable 1 0.1311*** 0.3406*** (0.0498) (0.0462) post legislation 1 0.0280* 0.0208* (0.0165) (0.0118) disable post 1 0.0129 0.0828^ (0.0654) (0.0582) Rho 0.7707*** (0.0169) Log-likelihood 54,402 Number of observations 101,584 NOTE: States included in the analysis are Alaska, Arizona, Delaware, Idaho, Massa- chusetts, North Carolina, North Dakota, South Dakota, Texas, and Wyoming. Re- gressors included both in the employment and part-time employment equations (but not reported here) include age, education, region, race, gender, marital status, and central city residence indicator. Regressors unique to the employment equation in- clude the state unemployment rate and the number of weeks worked last year. Re- gressors unique to the part-time employment equation include occupation and industry dummies, nonlabor income, and a government employer indicator. Standard errors are in parentheses. *** significant at the 99 percent confidence level. * significant at the 90 percent confidence level. ^ significant at the 85 percent confidence level. comes of disabled workers. The question is whether the ADA is redun- dant with laws passed at the state level. The results indicate that the state-level legislation operates on the labor market in the same way as does the federal ADA. Namely, relative employment probabilities of persons with disabilities are not affected by state-level disability legis- lation. It was also found that labor force participation rates were unaf- fected by the state-level legislation, lending support for the theory that the decline in labor force participation rates observed post-ADA at the national level was not ADA-induced. In addition, the disabled also experienced a relative wage decline and a tentative rise in relative part- time employment at the state level following legislation. The main implication of these results is that the lack of impact of the ADA on employment, while perhaps disappointing to proponents, is consistent with the contention that this type of legislation arrives after society has already adopted its main principles, both at the na- 140 Hotchkiss tional and the state level. On the other hand, observing similar wage and hours effects in states and nationally indicates that the wage and hours impacts of the ADA would likely have been greater in magnitude had the disabled not already partially experienced the impact of protec- tive legislation at the state level. The analyses in this chapter clearly indicate that state-level disability legislation did not fully crowd out the impact of the ADA (not at all regarding employment, and poten- tially only partially regarding wages and hours). Can we conclude, then, that the ADA was redundant? The answer is ‘‘no.’’ There was no employment effect to crowd out (no employment effect at the na- tional level), and there was still a measurable impact on wages and hours at the national level. In addition, the federal legislation served as a mechanism to instill uniformity of expectations of employers (even though some state laws have a broader definition of coverage), and it brought the issue of discrimination against disabled workers to the na- tional forefront. Notes 1. Also see Advisory Commission on Intergovernmental Relations (1989) for addi- tional information. 2. Methodologies that take advantage of differing legislative statuses among states (or, |
more generally, across observations) have often been referred to as ‘‘natural experiments’’ and have been applied by a number of researchers. For example, see Chay (1996) and Carrington, McCue, and Pierce (2000). 3. The strategy described here can be likened to a differences-in-differences (DD) methodology but is applied to a nonlinear statistical model. While this type of pooled, cross-sectional analysis has been used by many researchers (for example, Card 1992; Gruber 1994 and 1996; Zveglich and Rodgers 1996; and Hamermesh and Trejo 2000), the technique also has its critics (such as Heckman 1996). The primary criticism of this approach is that it is impossible to control for unobserved changes in the environment that occurred at the same time as the event of interest. The concern is mitigated in the analysis in this chapter, however, by the fact that the post-legislation period varies across states. 4. Also, similar to the approach in Chapter 4, an additional analysis was performed to determine whether, as at the national level, there was a marked increase in voluntary part-time employment, but the results were inconclusive. The coeffi- cient on the interaction disable post term was not significantly different from zero, and the adjusted R2 was only 0.08. 7 Conclusions and Policy Implications This book has examined and documented the relative labor market experience of workers with disabilities with an eye to evaluating the impact of the ADA. A worker’s labor market experience goes beyond simply whether a person has a job and what he or she is being paid. While these dimensions are fundamental, the quality or characteristics of the worker’s job, the process of obtaining it, and the nature of job separation are also important factors. One intention of the ADA is to break down barriers in the labor market; thus the focus of all analyses in this book is on the experience of the disabled in that environment, not on factors that influence decisions to enter the labor market. Ac- counting for those choices, however, is important in obtaining results generalizable to the disabled population, so measures are taken, where appropriate, to control for the decision to seek employment. In addi- tion to the multiple dimensions of the potential impact of the ADA on disabled Americans in the labor market, there are at least as many more ways in which the ADA affects the lives of all disabled Americans; such issues are not the subject of this work, but they may in fact amount to a much greater overall effect than that experienced by disabled workers alone. Overall, the analyses presented here lead to the conclusion that the labor market experience of disabled workers is quantitatively lower in all dimensions than that of nondisabled workers. In addition, while this relative situation has improved over time in some ways, there is no strong evidence that it has been substantively impacted by the ADA. There are two primary reasons why the ADA may not have had the hoped-for dramatic effect. It could be the case that no one is paying attention to the legislation. In other words, employers may not be complying (either through lack of awareness or refusal) with the man- dates of the ADA, workers may not be aware of their rights under the law, or workers may not be pursuing these rights. Alternatively, it may be the case that the bulk of the experience of disabled workers in the labor market is being defined by factors other than those corrected for by the ADA. 141 142 Hotchkiss It is not likely that the former is the case. For example, cognizance of the ADA is widespread. A 1999 Harris poll indicated that 67 percent of those surveyed were aware of the ADA, and it is likely that even a higher percentage of people with disabilities (and employers) know of the legislation (Roper Center for Public Opinion Research 1999). In addition, the rate of ADA litigation suggests that disabled workers are actively pursuing their rights. After climbing to a height of almost 20,000 in 1995, the number of claims tapered off to about 16,000 in 2001.1 Lastly, there is evidence that at least large employers and mu- nicipalities are complying with the provisions of the ADA (see Scheid 1998; Condrey and Brudney 1998). Additional evidence of compliance is implied by the Equal Employment Opportunity Commission’s ‘‘de- termination of no reasonable cause to believe that discrimination oc- curred based upon evidence obtained in investigation’’ in 54.1 percent (fiscal year 2001) of the ADA charges made.2 This statistic has stayed at 54 percent or higher since 1996. It is probable, therefore, that the lack of notable impact of the ADA on the labor market experience of the disabled implies that, like many other pieces of legislation with a strong social and moral content, it was adopted in an environment that had already embraced its principles and mandates, for the most part. For example, by 1990, every state had adopted some form of legislation granting protection to disabled workers. Results in Chapter 6 indicate that these state-level policies had influences on employment, wages, and hours similar to those found when the federal legislation was implemented. The implication is that some of the anticipated effect of the ADA had already been experi- enced at the state level over a longer period of time, beginning typically in the 1970s. This is not to say that the ADA was an unnecessary piece of legislation from the perspective of the labor market. Even if the ADA merely reflects the environment in which it was passed, it serves to strongly proclaim our social values and to provide a uniform legal mechanism with which to arrest the activities of those who have not yet embraced those values. As such, however, we are left with the nagging question of, ‘‘What do we do now to improve the labor market experience of workers with disabilities?’’ The results of the analyses presented in this book can provide some guidance in answering this question. Conclusions and Policy Implications 143 The dimensions of a worker’s labor market experience evaluated include employment, compensation, hours of work, distribution across and representation in occupations and industries, job separation, unem- ployment, and job search. The CPS is the primary source of data for each analysis. Various repeated cross-sectional and pooled cross- sectional analyses were performed with data spanning the years 1981– 2000. Some of the analyses were supplemented with information in the SIPP. The SIPP is primarily used to identify whether any experience or impact differs across type of disability. The years of analyses with the SIPP are limited to 1986–1997 but generally confirm the conclusions from the longer data series available from the CPS. The results of most notable interest are summarized in the following discussion and are accompanied by policy recommendations. This chapter ends with an overall assessment of the implications of the findings for the ADA and beyond. EMPLOYMENT INCENTIVES Chapter 2 presents evidence that while the joint labor force partici- pation and employment outcome declined among the disabled (driven by a decreasing labor force participation rate), the unconditional em- ployment probability of the disabled did not change, relative to that of the nondisabled. In other words, the employment prospects for the disabled, while not improved by the ADA, were also not harmed. Analysis of the SIPP data set revealed that workers with mental disabil- ities (and disabilities classified as ‘‘other’’) actually experienced an in- crease in employment relative to the nondisabled. This may be the result of easier accommodation of mental impairments or the recent emphasis on providing employment opportunities for the mentally dis- abled by the Presidential Task Force on Employment of Adults with Disabilities (formerly, the President’s Committee on Employment of People with Disabilities).3 In addition, there has been a relative gain in employment in large firms among the disabled, as compared with the nondisabled; of course, large employers are those most able to absorb the cost of accommodation. These results lead to some obvious policy suggestions: providing incentives for the disabled to enter the labor force and facilitating the accommodation process. 144 Hotchkiss Incentives for the Disabled The most recent initiative to encourage labor force participation among the disabled is the Ticket to Work and Work Incentives Im- provement Act of 1999; it applies to recipients of Supplemental Secur- ity Income (SSI) or Social Security Disability Insurance (SSDI) government cash payment programs for people with disabilities. The main provisions that encourage labor force participation under these programs involve reducing the risk and cost associated with ‘‘trying’’ work. One provision is a disregard for impairment-related work ex- penses (e.g., special equipment modified to accommodate a worker’s disability, medical devices, and special transportation needs). These expenses are deducted from a worker’s income before it is evaluated for payment eligibility purposes. In order to encourage and facilitate labor force participation, this provision could be expanded to provide for direct reimbursement of these fixed (out-of-pocket) expenses. The criteria for determining reimbursement could be the same for current deductibility. Another current work incentive provision allows for the exclusion of earned income for SSI recipients. Under this policy, the first $65 a month and half of the remainder of earnings are disregarded in calcu- lating the SSI payment amount. This provision could be made more generous and match that of the Trial Work Period (TWP) available for SSDI recipients. The TWP allows SSDI recipients to work for nine months without any reduction in benefit payments; after that period, payments are discontinued if the person is able to maintain his or her work activity. The continuation of Medicare and Medicaid benefits beyond SSI or SSDI eligibility is an important feature of the current incentives. Many jobs for which disabled workers can qualify might not offer ben- efits, especially if the person must work part-time in order to accom- modate his or her impairment. In addition, the extended period of eligibility (SSDI) and reinstatement of payments without a new appli- cation (SSI) are important safety nets for the disabled worker not sure if he or she should give employment a try. These provisions basically allow recipients to reinstate payments without once again going through the lengthy application process if they discover they are not yet ready to permanently enter or reenter the labor force. SSDI can be Conclusions and Policy Implications 145 reinstated up to 36 months after ineligibility, but former SSI recipients only have 12 months to apply for reinstatement. While the SSI time allowance is considerably shorter than the SSDI time allowance, eligi- bility requirements for the programs likely necessitate this differentia- tion. In addition to these programmatic incentives, strategies encourag- ing labor force participation among all disabled individuals (not just those receiving disability benefits) are warranted, based on the results in Chapter 2. One suggestion, the Disabled Worker Tax Credit (Burk- hauser, Glenn, and Wittenburg 1997), would provide incentives similar to the current Earned Income Tax Credit for the working poor, but be targeted at the disabled worker. Under this program, disabled workers would essentially receive a subsidy to their employment wage. It is not clear whether this program, however, would be effective in improv- ing the labor market experience along compensation or job quality di- mensions. The subsidy may encourage disabled workers to take lower- paying jobs while not holding employers responsible for valuing the skills (with accommodation) of this group equally with those of non- disabled workers. Incentives for Employers There has been a shift of employment among disabled workers toward larger firms. The implication is that cost might be an important factor in the willingness to hire a person with disabilities, and if that cost were reduced, disabled labor force participants would make even greater gains in employment. The federal government currently pro- vides tax incentives to smaller firms to help pay for the expense of accommodating workers with disabilities. Section 44 (Title 26) of the Internal Revenue Service (IRS) Code allows for a tax credit to cover 50 percent (up to $5,000) of an ‘‘eligible access expenditure’’ in one year incurred by a business with total revenues of $1 million or less, or 30 or fewer full-time employees (Hays 1999). Qualifying expenditures under this section include adaptations of existing structures and pur- chase of special equipment and services (such as sign language inter- |
preters).4 While this provision allows firms to be reimbursed for out- of-pocket expenses for accommodating disabled workers, the actual physical process of accommodating (i.e., evaluation of need and modi- 146 Hotchkiss fication of the environment) distracts the organization from its primary focus of business. One thing the government could do to ease this situation would be to equip the disabled worker with knowledge and information regarding any specific accommodation he or she might require in the type of job being sought. It is not the intention of the ADA to put the burden of acquiring this background on the worker. However, the more information workers can provide and the easier they can make it for the employer, the better chance the individuals will not be seen merely for the burden they might cause, but for the attributes they provide to the firm. The Work Opportunity Tax Credit (Title 26, Section 51 of the IRS Code) provides a tax credit for hiring individuals from specific target groups, with SSI recipients being one of those groups. The employer can claim 40 percent (up to $6,000) of the hired worker’s first-year wages. The maximum credit applies to individuals employed at least 400 hours during the year, and lesser credit applies to those employed between 125 and 400 hours per year. While it is difficult to find the number of employers who have taken advantage of the tax credit op- portunities associated with hiring the disabled, it is likely that these programs might suffer the same sort of administrative burdens that have resulted in the ineffectiveness of other tax credit and employment subsidy programs (for example, see Tannenwald 1982 and Katz 1998). The Job Accommodations Network (JAN), sponsored by the Office of Disability Employment Policy of the U.S. Department of Labor, is a government resource that provides both employers and workers with valuable information. Network members share experiences in success- ful accommodation strategies; employers who utilize the service are required to join the network (Magill 1997).5 One benefit provided by JAN is Searchable Online Accommodation Resource (SOAR), which allows someone on the Internet to go through a series of steps (select a disability, functional limitation, an affected job function, and an ac- commodation solution) and to obtain a list of vendors (from across the nation) providing the accommodation solution identified that could help a worker with a specified job function. There is also the opportu- nity on the SOAR website to enter specifics about an employer’s or worker’s unique situation and to obtain personal feedback. In addition, JAN provides information services to individuals with disabilities re- garding starting a small business or becoming self-employed. Conclusions and Policy Implications 147 Armed with the data obtained through JAN, the disabled job seeker leaves the employer little excuse for not considering only the qualifica- tions of the disabled applicant (i.e., productivity with accommodations in place). Clearly, if one could document the usefulness and success of these information dissemination efforts, a case might be made for devoting even more resources toward such efforts and perhaps provid- ing regional consultants that could evaluate a worker’s or employer’s situation in person. EDUCATION, TRAINING, AND JOB CHARACTERISTICS One analysis in Chapter 3 indicates that the disabled overall have suffered a cost in terms of lower relative wages post-ADA. With the exception of large firms, wages of disabled workers declined by about 3 percent post-ADA, relative to those of nondisabled workers. People with musculoskeletal disabilities suffered the bulk of the wage loss. Policy suggestions made in the previous section to facilitate worker accommodation should also go toward improving the apparent com- pensation tax on disabled workers for whatever workplace adjustments are required. Further analysis in Chapter 3 indicates that these wage losses may not be directly related to accommodation costs, however, but are suffered by disabled workers whether or not they are covered by the ADA. By facilitating the accommodation process (through in- formation and resources provided by JAN or some other organization), a person with disabilities is in a better position to negotiate a wage comparable to that of nondisabled individuals. Decomposing the wage differential between disabled and nondis- abled workers indicates that only about 30–40 percent of the gap is explained by observed characteristics of the workers themselves. While the remainder cannot all be interpreted as discrimination against the disabled, there is a significant portion of the differential that re- mains unexplained. Within the explained part, the greatest contribu- tions to the wage discrepancy are made by differences in industry, occupation, and educational attainment. In addition, it was found that disabled workers actually typically received a higher return on their education than did nondisabled workers, ceteris paribus. The implica- tion is that investment in disabled workers’ education and training for 148 Hotchkiss high-paying jobs would go a long way to improving their compensation experience in the labor market and is consistent with the results found in Chapter 4. The analyses in Chapter 4 indicate that the distribution of disabled and nondisabled workers across occupations has actually become more dissimilar over time (with some recent improvements), with disabled individuals being significantly more concentrated in the lower-paying occupations. Workers with mental disorders are the most dissimilar in their distribution across occupations, compared with non- disabled workers. The SSI and SSDI programs have a number of provisions that as- sist with training, rehabilitation, and educational attainment. The pri- mary one is that benefit payments will continue while an individual is participating in a rehabilitation program, even if the recipient recovers from his or her disability. Recipients of SSI may also participate in what is called a PASS (Plan for Achieving Self-Support) program, under which a SSI recipient may put aside assets and money toward a plan that helps the recipient become self-sufficient, including rehabili- tation or starting a business. These assets will be ignored in continuing determination of eligibility. In addition, the 1999 Ticket to Work legis- lation provides (as of December 2000) SSI and SSDI recipients with a ‘‘ticket’’ that can be used to obtain vocational rehabilitation, job or other support services from an employment network of the recipient’s choice. This provision makes obtaining vocational rehabilitation more flexible, and thus more accessible. In spite of such provisions, Chatterjee and Mitra (1998) indicate that less than 5 percent of federal spending for SSI and SSDI goes to training and rehabilitation. They suggest that this type of expenditure pattern on the disabled is the result of ‘‘a bias in disability programs in favor of short term equity considerations as opposed to the long run efficiency objectives’’ (p. 360). These authors also show that there is a positive link between enhancing a disabled person’s human capital and his or her chances of participating in the labor market. The impli- cation is that devoting more resources toward education and training would not only improve disabled workers’ labor market experiences, but also help the bottom line of the SSI and SSDI programs by leading to more disabled people becoming self-sufficient. In addition, the focus of SSI and SSDI on vocational rehabilitation may not direct resources where they will provide the greatest boost Conclusions and Policy Implications 149 in compensation and occupational attainment outcomes for disabled workers. The growing earnings gap between those with and without college educations is well documented (for example, see Murphy, Juhn, and Pierce 1993). Training disabled workers for jobs requiring a col- lege degree is an idea that has not received a great deal of attention. According to the results in Chapter 3, workers with musculoskeletal disorders appear to have suffered the most in terms of compensation. One reason for this may be that the cost of accommodating a worker’s musculoskeletal disability in a blue-collar or physically-challenging position is likely much more expensive than if that worker became skilled in a less physically but more mentally demanding, and poten- tially higher-paying, job. Further evidence of the general lack of sup- port for higher education is found in the income exclusion for earnings of disabled students. While attending school, students only under the age of 22 are allowed to earn income that is excluded from calculating benefit eligibility and levels. This income exclusion could be extended to individuals over the age of 22 when they are working toward a termi- nal degree that would improve their occupational outcome.6 One area in which further general education for older SSI recipi- ents is supported is in the development of a PASS; tuition, fees, books, and supplies for school are among those expenses that can be set aside as part of the SSI recipient’s plan for self-support. While laudable, this provision is not likely to be very practical since it requires the SSI recipient, who is subject to strict earnings limitations, to set aside sav- ings and assets that are likely difficult to acquire. An additional provi- sion that allows the recipient to work (without penalty) while attending school may place attainment of higher education within the realm of financial possibility. The federal government does allow educational grants, fellowships, and scholarships used for tuition and fees to be excluded from earnings limitations. Portions of those sources used for room and board, however, are not currently excluded. A report by the Social Security Administration (2000) suggests that all portions of grants, scholarships, and fellowships be excluded from the earnings test.7 Given the importance of general education in improving the em- ployment experience of disabled workers (as demonstrated in the anal- yses of this book), the federal government should explore the possibilities of providing more active support. One could also argue 150 Hotchkiss that if the basic goal is to improve the labor market experience of workers with disabilities, subsidized training and education should be made available to all disabled individuals, not only those affiliated with a government cash payment disability program. Improving the labor market experience of a single disabled worker could also provide exter- nalities to the experience of other disabled workers. As employers and fellow workers become more comfortable working alongside the disabled and become more aware of such individuals’ capabilities, even more doors would open to disabled workers who follow. One policy change that seems to have had an unambiguous effect on the characteristics of jobs held by disabled workers is the extension of Medicaid and Medicare for SSI and SSDI recipients who have be- come ineligible for disability payments. Most part-time jobs do not offer health insurance, but many disabled workers may prefer part-time employment as a means of accommodation for their disability. Due to the extension of Medicaid and Medicare, disabled workers can now consider part-time employment without the risk of losing medical ben- efits. The results in Chapter 4 support this outcome; disabled workers are increasingly more likely to be employed part-time (versus full- time), but they are also increasingly more likely to be voluntarily (ver- sus involuntarily) employed on a part-time basis. On the one hand, the extension of Medicaid and Medicare has opened up work opportunities that may improve a disabled worker’s life. On the other hand, there is some evidence that part-time jobs are more likely to be marginal, temporary, unstable, and lower-paying (Blank 1990). The government might be able to provide assistance to (particularly, small) employers who want to explore flextime in order to accommodate workers’ dis- abilities in occupations that may not be typical candidates for such scheduling, but that pay more and provide for advancement opportuni- ties within the firm. One step that will likely contribute positively to this effort is the President’s ‘‘New Freedom Initiative.’’8 This concept calls for the fulfillment of the promise made by the government to people with disabilities through the passage of the ADA; it includes education, home ownership, access, and employment provisions. Ex- panding telecommuting opportunities is one example: ‘‘The Adminis- tration will provide Federal matching funds to states to guarantee low- interest loans for individuals with disabilities to purchase computers and other equipment necessary to telework from home. In addition, Conclusions and Policy Implications 151 legislation will be proposed to make a company’s contribution of com- puter and Internet access for home use by employees with disabilities a tax-free benefit.’’9 Given the results in Chapter 4, that flexible work arrangements (i.e., part-time jobs) may be an important aspect of greater employment opportunities for people with disabilities, this |
pro- posal holds promise. SCREENING AND MATCHING The evidence of job separation and job search experiences of dis- abled workers presented in Chapter 5 is ambiguous. On the one hand, disabled workers search three weeks longer, on average, than similar nondisabled individuals before finding a job. On the other hand, job separations are less likely to be for involuntary reasons among disabled than among nondisabled workers, implying that disabled workers are not likely the ‘‘marginal’’ employees that some have speculated they are. While longer search spells are consistent with discriminatory hir- ing practices on the part of employers, the finding that most of the observed longer search spell is explained by individual characteristics suggests that endowments of disabled and nondisabled workers are being valued equally, but that employers go to greater lengths to dis- cern the fit of a disabled worker’s traits with a particular job. This care in hiring on the part of the employer would also lead to the lower probability that a separation is involuntary. In addition, the firm may have made some expenditures in accommodating the worker’s disabil- ity and thus will be reluctant to lose that investment by laying off or firing the worker. The lower probability that a separation is involuntary means that disabled workers experience a higher likelihood that a separation is voluntary. While this may be interpreted as disabled workers having a fair amount of mobility in the labor market, it may also mean that they have more difficulty than nondisabled individuals in finding a good job match. What is called for is a policy that assists employers in discern- ing the qualifications and fit of a disabled worker more quickly and that helps disabled workers in determining the appropriateness of a particular job. Measures for improving the efficacy and speed of job matches would include a clearing house at which employers could post 152 Hotchkiss job openings and workers could advertise skills (with appropriate ac- commodations); third-party certification of worker skills; and assis- tance with information (such as JAN) and with cost (such as tax credits) for accommodating a particular disability for the job to be filled. The National Easter Seal Society provides many services that would facilitate matching of workers with employers. Skills evaluation and screening, employment skills training, and job placement services are among the programs offered through Easter Seals. JAN could also be expanded to provide job placement services, which it currently does not do.10 The U.S. Office of Disability Employment Policy, however, has some initiatives that do assist in employment on a limited basis.11 The Employer Assistance Referral Network (EARN) is designed to help employers in locating and recruiting qualified individuals with disabilities. The Workforce Recruitment Program is involved with se- curing summer employment and internships for students with disabili- ties, and Project EMPLOY is designed to expand and enhance job opportunities for people with cognitive disabilities by, primarily, pro- viding funding to other organizations to provide employment services. One thing that might be difficult for an employer to assess is the productivity of a disabled worker with accommodating equipment or services in place. If the government, or some private entity, could certify a particular skill (such as typing or editing) when a disabled individual has access to facilitating equipment, the employer would not be forced to bear the risk of hiring the worker and installing the neces- sary equipment without knowing what the outcome will be. There could be testing centers set up regionally, or mobile testing centers, that would contain the most common equipment needed for the worker to do the job in question. THE ADA AND BEYOND The labor market provisions of the ADA comprise a small part of the overall goals of the legislation. Furthermore, given the relatively low proportion of the disabled population that is actually in the labor force, and smaller yet that is employed, the potential impact of these provisions is not nearly as widespread as the effect of other elements Conclusions and Policy Implications 153 of the legislation that cover aspects of a disabled person’s life outside the labor market. As such, measuring the influence of the ADA on the overall quality of life of the disabled goes far beyond the potential impact on the labor market experience. Indeed, the key contributions of the ADA may be beyond quantification in economic terms; it is difficult to put a price on the dignity and respect that proponents might argue are among the most important dividends of the ADA. Nevertheless, learning that the ADA did not result in dramatic, or even notable, improvement across multiple dimensions of the labor market experience of the disabled must be quite disappointing for the proponents of the legislation. In light of these findings, we are left with the question of why no such impact was forthcoming. One possi- ble reason for legislation not having an effect on the intended benefi- ciaries is that there was nothing to improve: the disadvantaged are not really as disadvantaged as they might appear (because of factors the researcher may not be able to observe, for example). If this is the case, then the ADA is directed at a nonexistent target. A second possibility for finding no influence of the ADA on labor market outcomes among the disabled might be that the labor market provisions of the legislation are focused on the wrong things. Title I of the ADA is couched in terms of eliminating discriminatory behavior on the part of employers. It could be the case that discrimination is not the culprit determining inferior labor market outcomes for the disabled; in other words, the ADA is aiming at the wrong target. A third potential explanation for finding no impact is that the ADA is focused on the right target, but just missed. In other words, it may be the case that the legislation is ineffective, that employers are finding ways to get around the provi- sions and that workers are not able to exercise their rights under the law. With the amount of evidence presented in this book, as well as that provided elsewhere, it is not likely that the ADA is aiming at a nonexis- tent target. One advantage of examining labor market outcomes from multiple dimensions, as was done here, is to be able to rule out numer- ous explanations for inferior labor market outcomes. The disabled clearly have further to go before enjoying labor market outcomes com- parable to those experienced by the nondisabled. The possibility that the ADA has missed the target and that employers are able to somehow get around complying with the legislation is also not likely. The inabil- 154 Hotchkiss ity of employers to ignore the ADA is evidenced by the fact that dis- ability claims made up 20 percent of all claims made to the EEOC during fiscal year 2001. This percentage was not too far behind the ratio of claims filed based on race (36 percent), sex (31 percent), and age (22 percent) during the same year and suggests that workers are aware of their rights and are holding employers accountable. The chance, then, that the ADA is aiming at the wrong target is still a possibility. While individual cases of discrimination (as evidenced by the number of EEOC claims) indicate that discrimination against dis- abled workers is likely occurring in the labor market, it still may not be the overwhelming determinant of inferior labor market outcomes. As suggested earlier in this chapter, other policies, such as promoting education and training, may go further toward improving labor market outcomes than a policy outlawing discrimination (which may only touch a small portion of the disabled). Regardless of why the ADA does not seem to have affected the labor market experience of the disabled, this absence of impact begs the question of whether the ADA is necessary. Clearly, it is possible to argue the merits of the ADA on the ways in which it has likely improved the quality of life among the disabled beyond its labor market or quantifiable influence. However, even with regard to its labor mar- ket provisions, the ADA does serve as a statement of our social values, and it provides a legal mechanism with which to stem the activities of those who have not yet accepted those values. In addition, there is no question that it does serve to set the stage and to provide a labor market environment in which effective reforms, more narrowly focused on the needs of the disabled for improving outcomes, can be introduced. Notes 1. See table of statistics titled, ‘‘Americans with Disabilities Act of 1990 (ADA) Charges FY1992–FY2001,’’ found at http://www.eeoc.gov/stats/ada-charges .html. 2. See table of statistics titled, ‘‘Americans with Disabilities Act of 1900 (ADA) Charges FY1992–FY2001,’’ found at http://www.eeoc.gov/stats/ada-charges .html. 3. Other possible explanations include the potential for the ADA to have a greater impact on overcoming negative social attitudes against people with mental dis- abilities (versus other types of disabilities) or improvements in medications occur- Conclusions and Policy Implications 155 ring during the same time period, which facilitated the labor market performance of people with mental disabilities. 4. More substantial architectural and transportation adaptation expenses can be de- ducted from tax liability by all businesses under IRS Code Section 190. 5. The web site for JAN is http://www.jan.wvu.edu/. Additional government re- sources for people with disabilities can be found at http://www.disabilitydirect .gov. The National Easter Seal Society (http://www.easter-seals.org/) also of- fers free information referral and suggestions for technological devices to help workers do their jobs. 6. This recommendation is also made by the Social Security Administration’s March 2000 report to the Congress on income and resource exclusions. That report also recommends that the amount of earnings excluded be increased and then indexed to the CPI. 7. The report also suggests that grants, fellowships, and scholarships be excluded from resource limitations for nine months, based on the reality that many forms of financial aid are received at the beginning and paid out over the balance of the school year. 8. See the U.S. Health and Human Services Web site, ‘‘New Freedom Initiative: Fulfilling America’s Promise to Americans with Disabilities,’’ found at http://www .hhs.gov/newfreedom/. 9. See the U.S. Health and Human Services Web site, ‘‘New Freedom Initiative: Fulfilling America’s Promise to Americans with Disabilities,’’ found at http://www .hhs.gov/newfreedom/. Also see Chen (2001). 10. See note 5. 11. These job search and placement efforts (and others) can be located from the http:// www.disabilitydirect.gov Web site. This Page Intentionally Left Blank Appendix A CPS Sample Construction This appendix provides information regarding the use of the Current Pop- ulation Survey data set for the analyses in this book. The lessons learned might be useful to others creating successive cross-sections across many years using the CPS. The notes and recommendations reflect the experience of the author only. 1. The complete set of outgoing rotation groups from the CPS was ob- tained from Unicon Research Corporation (http://www.unicon.com). The out- going rotation group in the CPS consists of individuals in their 4th and 8th month of eight monthly interviews. A CPS respondent is interviewed for four consecutive months, not interviewed for four months, then interviewed again for four consecutive months. This source is highly recommended for not only outgoing rotation groups, but for all of the CPS data sets one might want. The data arrive on CDs with easy-to-use extraction software. The documentation is excellent; the coding across years is consistent; technical support is accessi- ble and helpful; and the documentation also makes note of known data anoma- lies or errors. Unicon makes these data available for a fee. 2. The March supplemental files for each year were obtained from the Inter-University Consortium for Political and Social Research (ICPSR), http:// www.icpsr.umich.edu/. We identified tremendous (un-correctable) prob- lems with the 1994 March CPS obtained from ICPSR and ultimately obtained the data needed for 1994 from Unicon. 3. A variable of crucial importance to the analyses in this book is the indicator of disability status. That indicator is not available in the CPS public use file between 1981 and 1987; we contracted with the Census Bureau to extract the necessary variable and individual identifiers essential for matching with the rest of the CPS file for those years. 4. Creation of the CPS data sets for each year |
required matching individ- uals in each of the outgoing rotation groups from March, April, May, and June with the supplemental questionnaire in March. The match rate was approxi- mately 90 percent for each month, except March, where the match rate, of course, was 100 percent. 5. The coding of the variable in the March supplement indicating whether an individual worked last year changed over the entire time period. Although this coding change is well documented, it could confound analyses if the dif- ference is not noticed. Specifically, for 1981–1987, a ‘‘1’’ indicates that the 157 158 Hotchkiss person did not work during the previous year, and, for 1988–1999, a ‘‘1’’ indicates that the person did work during the previous year. 6. Prior to 1994, the question of usual hours worked per week was asked of those who were earner eligible (outgoing rotation groups) and employed during the previous week. Starting in 1994, this variable was coded as zero for workers with variable hours, and the question regarding how many hours were worked at all jobs last week was changed to read, ‘‘Last week, how many hours did you actually work at your (main) job?’’ Unfortunately, the Census code book (which accompanies data from ICPSR) does not reflect the change in this question since 1994 (it still indicates that the question refers to hours worked at all jobs, when in fact, it now only reflects hours at the main job). Appendix B SIPP Sample Construction In the terminology of the Survey of Income and Program Participation, a Panel refers to a group of interviewees and the year in which that group was first interviewed. A Wave refers to an interview within a Panel. Each Panel has anywhere from 3 (1989 Panel) to 12 (1996 Panel) interviews. Further details of the SIPP can be found on the Internet at http://www.bls.census .gov/sipp/. Core data from each Wave within a Panel used for sample con- struction were merged with the topical module for Wave 2 from the same Panel. Wave 2 topical modules were used for identification of a work disabil- ity for consistency over as many consecutive years as possible. When avail- able, core data from Wave 2 in one Panel were combined with core data from Wave 5 in the previous Panel and with core data from Wave 8 in the Panel before that in order to construct a larger sample year. Table B.1 presents the layout of the SIPP sampling structure. The Waves merged across Panels (col- umns in Table B.1) are combined for illustration using a bold box outline. Since the goal was to create multiple cross sections comparable to the CPS, only Waves 2, 5, and 8 in each Panel were exploited. Combining data across Panels was not possible for sample years 1986, 1989, 1990, 1995, 1996, and 1997 due to the lack of availability of overlap- ping Panels for which disability information is available. The labor market information, due to the rotation of sets of questions in the SIPP, corresponds to June of the year referenced. The exception to this pattern is the 1997 sample labor market information, which came from Wave 5 of the 1996 panel, which corresponds to August of 1997. Of course, these waves were merged with the disability topical module for that panel. The disability check in the topical module was the variable used to desig- nate a work-limiting disability. There are two checks in topical modules for the 1986–1993 Panels, but only one check in the 1996 Panel, resulting in the slightly smaller incidence of individuals with work-limiting disabilities in the 1996 and 1997 samples. The match rate across Waves within a Panel ranged from 81 to 89 percent success. Labor status refers to activity during the previ- ous month (as opposed to the previous week, as in the CPS), since job infor- mation corresponds to activity over the month. The primary usefulness of the SIPP derives from an ability to identify the nature of a disabled worker’s disability. The categories identified are too numerous for all of them to be included in the analysis, so they are grouped into broad headings based on the classifications used by the Social Security Administration. Table B.2 shows how specific disabilities are classified. 159 160 Hotchkiss Table B.1 SIPP Data Structure Waves Panel Year Month 1984 1985 1986 1987 1988 1989 1990 1991 1992 1993 1996 1983 Oct. 1 1984 Feb. 2 June 3 Oct. 4 1985 Feb. 5 1 June 6 2 Oct. 7 3 1986 Feb. 8 4 1 June 9 5 2 <- 1986 sample Oct. 6 3 1987 Feb. 7 4 1 June 8 5 2 <- 1987 sample Oct. 6 3 1988 Feb. 7 4 1 June 5 2 <- 1988 sample Oct. 6 3 1989 Feb. 7 4 1 June 1989 sample -> 5 2 <-Wave 2 (1989) top. mod. not avail. Oct. 6 3 1990 Feb. 1 June 2 <- 1990 sample Oct. 3 SIPP Sample Construction 161 1991 Feb. 4 1 June 5 2 <- 1991 sample Oct. 6 3 1992 Feb. 7 4 1 June 8 5 2 <- 1992 sample Oct. 6 3 1993 Feb. 7 4 1 June 1993 sample -> 8 5 2 Oct. 6 3 1994 Feb. 7 4 June 1994 sample -> 8 5 Oct. 9 6 1995 Feb. 10 7 June 1995 sample -> 8 Oct. 9 1996 Apr.. 1 Aug. 1996 sample -> 2 Dec. 3 1997 Apr. 4 Aug. 1997 sample -> 5 Dec. 6 NOTE: Wave 2 topical module (number in bold) is where disability information is located. Waves bordered in bold are merged to create the sample year indicated. Each wave used for sample construction was merged with the Wave 2 topical module, then combined across panels as indicated. The 1996 panel continues for 12 waves through 1999, but only six were available at the time of analysis. 162 Hotchkiss Table B.2 Classification of Disabilities in the SIPP Data Set 1. Musculoskeletal Arthritis or rheumatism Back or spine problems Broken bone/fracture Head or spinal cord injury Hernia or spinal injury Missing legs, feet, arms, hands, or fingers Paralysis of any kind Stiffness or deformity of the foot, leg, arm, or hand Blindness or vision problems Deafness or serious trouble hearing Speech disorder 2. Internal systems AIDS or AIDS-related condition Cancer Diabetes Heart trouble, hardening of the arteries High blood pressure Kidney stones or chronic kidney trouble Lung or respiratory problems Stomach trouble Thyroid trouble or goiter 3. Mental disorder Alcohol or drug problem or disordera Learning disability Mental or emotional problem or disorder Mental retardation Senility/dementia/Alzheimer’s disease Cerebral palsy Epilepsy Stroke Tumor, cyst, or growth 4. Other NOTE: Complete classification of disabilities by the Social Security Administration can be found at http://www.ssa.gov/OP_Home/cfr20/404/404-ap09.htm. aDrug addiction is excluded from protection by the ADA. Appendix C Supplemental Tables This Page Intentionally Left Blank Supplemental Tables 165 Table C.1 Trends in the Percentages of Total Sample and of Workers Indicating a Work-Limiting Disability, CPS Combined Outgoing Rotation Groups, 1981–2000 Year % of sample % of workers 1981 9.79 2.68 1982 10.19 2.69 1983 9.73 2.53 1984 10.20 2.74 1985 10.34 2.66 1986 9.89 2.68 1987 9.62 2.69 1988 9.15 2.63 1989 9.26 2.67 1990 9.34 2.74 1991 9.34 2.60 1992 9.44 2.70 1993 9.82 2.87 1994 10.95 2.68 1995 11.14 2.53 1996 10.88 2.73 1997 10.75 2.81 1998 10.05 2.51 1999 9.84 2.37 2000 9.99 2.70 166 Hotchkiss Table C.2 Percentages of Disabled and Nondisabled Individuals Employed, CPS, 1981–2000 Subsample employed (%) Year Disabled Nondisabled 1981 17.76 62.62 1982 17.27 61.39 1983 16.34 60.45 1984 17.21 62.93 1985 16.76 63.57 1986 17.70 63.79 1987 18.32 64.49 1988 19.11 63.98 1989 19.43 65.74 1990 19.35 65.98 1991 18.41 64.74 1992 18.88 64.39 1993 19.05 64.42 1994 16.50 66.16 1995 15.44 66.32 1996 16.41 66.71 1997 17.30 67.40 1998 17.09 67.88 1999 16.60 68.05 2000 17.15 68.70 Supplemental Tables 167 Table C.3 Predicted Joint Probability of Labor Force Participation and Employment and Predicted Unconditional Employment Probability, by Disability Status, CPS, 1981–2000 Average predicted probability Nondisabled Disabled Being in the labor Being in the labor force and employed Employment force and employed Employment (1) (2) (3) (4) Year Prob(lfp1, emp1) Prob(emp1) Prob(lfp1, emp1) Prob(emp1) 1981 0.64271 0.84244 0.47840 0.79271 1982 0.62609 0.81519 0.47742 0.77384 1983 0.61727 0.79255 0.47474 0.76856 1984 0.64824 0.85387 0.50693 0.82802 1985 0.65675 0.85665 0.50837 0.82475 1986 0.66467 0.85364 0.51167 0.81465 1987 0.67498 0.86818 0.51993 0.83475 1988 0.68827 0.87833 0.53576 0.82908 1989 0.69070 0.88346 0.53884 0.85364 1990 0.69150 0.87427 0.52609 0.82427 1991 0.67530 0.84653 0.52123 0.81285 1992 0.67426 0.82397 0.51998 0.76743 1993 0.67738 0.83780 0.53733 0.80476 1994 0.68448 0.84973 0.49882 0.81405 1995 0.68820 0.87372 0.49520 0.83877 1996 0.69305 0.87742 0.50769 0.84971 1997 0.70309 0.87734 0.51408 0.84607 1998 0.71169 0.89380 0.51334 0.86027 1999 0.71529 0.89326 0.50755 0.83657 2000 0.72085 0.91141 0.52832 0.86493 NOTE: Estimates obtained from a bivariate probit model with selection. Regressors for both labor force and employment determination included the state unemployment rate; age; age squared; female, nonwhite, education, and regional dummies; and a disability dummy. The labor force participation equation also included nonlabor income, marital status, and a worked-last-year indicator. The employment equation included the number of weeks worked last year. The probabilities for each column are the average across the entire sample obtained by calculating the probability for each person (varying the disability dummy variable between 0 and 1), then averaging across the sample. 168 Hotchkiss Table C.4 Relative Predicted Probabilities of Working in Each Firm Size, CPS 1987–1999 Ratio of predicted probabilities of a disabled worker relative to the predicted probability for a nondisabled coworker being employed by a firm by size Year Small firm Medium firm Large firm 1987 1.1842 1.0756 0.9189 1988 1.1836 1.1063 0.9134 1989 1.1524 1.0403 0.9409 1990 1.1372 1.0174 0.9507 1991 1.1682 0.9417 0.9493 1992 1.2127 0.8759 0.9501 1993 1.0873 1.0410 0.9512 1994 1.0567 0.9999 0.9787 1995 1.1772 0.9384 0.9399 1996 1.1811 0.8598 0.9575 1997 1.1341 0.9900 0.9511 1998 1.0110 0.9319 1.0106 1999 1.0963 0.9840 0.9675 Change over time period 0.0879 0.0917 0.0487 NOTE: Small firms have fewer than 25 employees; medium firms have 25–99 em- ployees; and large firms have 100 or more employees. Regressors (in addition to a disability dummy variable) in the multinomial logit regression included age; age squared; and regional, education, female, nonwhite, and central city dummy variables. Supplemental Tables 169 Table C.5 Observed and Selectivity-Corrected Wage Differentials, CPS, 1981–2000 Wage differential Observed corrected for wage selectivity into Endowment Coefficient Selection Year differentiala the labor marketb effectc effectd effecte 1981 0.1587 0.1315 0.0386 0.0929 0.0272 1982 0.1294 0.1318 0.0307 0.1011 0.0024 1983 0.1717 0.1991 0.0056 0.1935 0.0275 1984 0.1885 0.1902 0.0312 0.1590 0.0017 1985 0.1706 0.2037 0.0476 0.1561 0.0332 1986 0.1948 0.2144 0.0634 0.1510 0.0197 1987 0.2008 0.2342 0.0591 0.1751 0.0334 1988 0.2089 0.1954 0.0436 0.1518 0.0135 1989 0.2512 0.2009 0.0766 0.1243 0.0503 1990 0.2469 0.2605 0.0807 0.1798 0.0136 1991 0.2649 0.2494 0.0769 0.1725 0.0154 1992 0.2644 0.2901 0.0890 0.2011 0.0258 1993 0.2723 0.3114 0.0852 0.2262 0.0391 1994 0.2733 0.3337 0.0911 0.2427 0.0605 1995 0.2400 0.2768 0.0792 0.1976 0.0368 1996 0.2638 0.2642 0.0929 0.1713 0.0004 1997 0.2117 0.2090 0.0791 0.1299 0.0027 1998 0.2843 0.2776 0.0884 0.1892 0.0066 1999 0.2941 0.3028 0.0881 0.2147 0.0087 2000 0.2809 0.2566 0.0674 0.1892 0.0243 NOTE: The first-stage probit estimation included the following regressors: age; age squared; nonwhite, female, disabled, single household, education, and worked-last- year dummy variables; and nonlabor income. Regressions for 1981 and 1982 do not include a union dummy. Second-stage wage estimations included the following regressors: hour of work; age; age squared; and union, female, single household, nonwhite, education, region, industry, occupation, and government dummy variables. Regressions for 1983 do not include dummies for the service; farming, fishing, and forestry; or the craft occupations due to the absence of representation of disabled workers in these occupations in the sample. ̂nd (coefficients from the nondisabled estimation) was used to represent the ‘‘nondiscriminatory’’ world since the disabled make up such a small proportion of the whole. a ln Wnd ln Wd b ln Wnd ln Wd [(ĉnd nd) (ĉd d)] c ̂nd(Xnd Xd) d Xd(̂nd ̂d) e [(ĉnd nd) (ĉd d)]. 170 Hotchkiss Table C.6 Marginal Effect of Being Disabled on the Probability of Employer-Provided Health Insurance and of Being Included in the Employer’s |
Pension Plan, CPS Measure of earnings not Measure of earnings included in included in probit estimation probit estimation Year (HealthIns) (Pension) (HealthIns) (Pension) Disabled Disabled Disabled Disabled 1980 0.0848 0.0890 — — (0.0094) (0.0098) 1981 0.0859 0.0924 — — (0.0096) (0.0100) 1982 0.0888 0.0751 — — (0.0101) (0.0104) 1983 0.0822 0.0835 — — (0.0099) (0.0102) 1984 0.0740 0.0677 — — (0.0098) (0.0100) 1985 0.0861 0.0849 — — (0.0098) (0.0102) 1986 0.0956 0.0824 — — (0.0099) (0.0103) 1987 0.0850 0.0901 0.0243 0.0356 (0.0100) (0.0105) (0.0096) (0.0101) 1988 0.0990 0.0911 0.0428 0.0402 (0.0099) (0.0104) (0.0095) (0.0100) 1989 0.0891 0.0820 0.0315 0.0285 (0.0095) (0.0097) (0.0091) (0.0093) 1990 0.1050 0.0900 0.0415 0.0347 (0.0099) (0.0101) (0.0095) (0.0097) 1991 0.1150 0.1059 0.0626 0.0595 (0.0099) (0.0101) (0.0095) (0.0097) 1992 0.1188 0.0967 0.0638 0.0462 (0.0101) (0.0101) (0.0098) (0.0097) 1993 0.0741 0.0856 0.0329 0.0424 (0.0100) (0.0102) (0.0097) (0.0098) 1994 0.0831 0.0872 0.0380 0.0450 (0.0107) (0.0108) (0.0104) (0.0105) 1995 0.1070 0.1210 0.0869 0.1045 (0.0105) (0.0108) (0.0105) (0.0108) 1996 0.1159 0.1281 0.0970 0.1094 (0.0104) (0.0108) (0.0104) (0.0107) Supplemental Tables 171 Table C.6 (continued) Measure of earnings not Measure of earnings included in included in probit estimation probit estimation Year (HealthIns) (Pension) (HealthIns) (Pension) Disabled Disabled Disabled Disabled 1997 0.1101 0.1110 0.0913 0.0944 (0.0109) (0.0113) (0.0109) (0.0112) 1998 0.1018 0.1022 0.0822 0.0828 (0.0111) (0.0115) (0.0111) (0.0114) 1999 0.0728 0.1036 0.0526 0.0832 (0.0108) (0.0111) (0.0107) (0.0110) NOTE: A reliable earnings variable was not available in the years 1981–1987. Re- gressors in the probit estimation included nonwhite, female, education, single house- hold, government, industry, occupation, and disabled dummy variables; age; age squared; earnings from the job; and usual hours worked. Standard errors for the partial derivatives are in parentheses. is the standard normal cumulative distribution function. 172 Hotchkiss Table C.7 Impact of Being Disabled on the Probability of Part-Time and Voluntary Part-Time Employment, CPS, 1981–2000 Predicted marginal effect of a disability on probability Being employed part-timea Being voluntarily employed part-timeb Year (1) (2) 1981 0.0557 0.0030 1982 0.0581 0.0010 1983 0.0836 0.0643 1984 0.0665 0.0098 1985 0.0664 0.0744 1986 0.0850 0.0145 1987 0.0594 0.0085 1988 0.0820 0.0399 1989 0.0924 0.0067 1990 0.0824 0.0214 1991 0.0844 0.0367 1992 0.0886 0.0053 1993 0.1134 0.0173 1994 0.1425 0.0365 1995 0.1227 0.0187 1996 0.1380 0.0266 1997 0.1492 0.0676 1998 0.1407 0.0385 1999 0.1569 0.0594 2000 0.1250 0.0182 NOTE: The marginal effects are calculated at the sample means, except disability status, which is varied between 0 and 1 to generate the marginal effect. See Long (1997). a Predicted marginal effects in column 1 result from estimation of a bivariate model of employment and part-time employment, accounting for selection at the employment stage. Regressors in both the employment and part-time employment equations in- cluded age, education, region, race, gender, marital status, and a central city residence indicator. Regressors unique to the employment equation included the state unem- ployment rate and the number of weeks worked last year. Regressors unique to the part-time employment equation included occupation and industry dummies, nonlabor income, and a government employer indicator. b Predicted marginal effects in column 2 result from estimation of a univariate probit model of the probability of being voluntarily employed part-time. The sample is restricted to all part-time workers, so results are not generalizable beyond this sample. Voluntary part-time is defined as did not want to work full time (1994–1999), and the reason for working under 35 hours per week (1981–1993) was coded as 07–15 (see Chapter 4, Note 8, and Stratton 1994). Regressors included age, education, region, race, gender, marital status, nonlabor income, and occupation dummies, industry dummies, a government employer dummy, and an indicator of whether the person worked last year or not. Supplemental Tables 173 Table C.8 The Duncan Index as a Measure of Dissimilarity in Distribution of Workers across Occupations and Industries, CPS, 1981–2000 Disabled vs. nondisabled Nonwhite vs. white Year Occupation Industry Occupation Industry 1981 0.1251 0.0443 0.1514 0.1063 1982 0.1065 0.0438 0.1648 0.1081 1983 0.1077 0.0602 0.1588 0.0923 1984 0.1089 0.0514 0.1528 0.1029 1985 0.1141 0.0394 0.1590 0.1018 1986 0.1455 0.0630 0.1570 0.0915 1987 0.1340 0.0602 0.1430 0.0770 1988 0.1188 0.0670 0.1492 0.0902 1989 0.1431 0.0472 0.1375 0.0885 1990 0.1351 0.0518 0.1357 0.0871 1991 0.1447 0.0878 0.1323 0.0822 1992 0.1506 0.0475 0.1407 0.0711 1993 0.1442 0.0425 0.1247 0.0838 1994 0.1474 0.0684 0.1173 0.0745 1995 0.1336 0.0425 0.1239 0.0754 1996 0.1340 0.0854 0.1264 0.0724 1997 0.1273 0.0682 0.1210 0.0726 1998 0.1316 0.0782 0.1055 0.0693 1999 0.1467 0.0562 0.1107 0.0805 2000 0.1236 0.0771 0.1082 0.0851 NOTE: The Duncan Index reflects the % of workers in the labor market that would have to switch occupation or industry in order to equalize the distribution of workers in both groups across occupations or industries. The index is calculated as 1 D s the number of occupations (industries), and a and b 2 K aj bj, where K i j1 refer to the proportion of the two different groups of interest in occupation/industry j (e.g., a is the proportion of nondisabled workers in occupation/industry j, and b is the proportion of disabled workers in occupation/industry j). The numbers in bold repre- sent projections replacing the actual calculated index for that year, which was clearly an outlier. 174 Hotchkiss Table C.9 Disabled and Nondisabled Job Separators by Reason for Job Separation (%), CPS, 1981–2000 Nondisabled Disabled Voluntary Involuntary Other Voluntary Involuntary Other Year (%) (%) (%) (%) (%) (%) 1981 66.42 19.09 14.50 82.30 8.35 9.36 1982 66.39 19.50 14.11 81.13 11.21 7.66 1983 66.21 20.11 13.68 81.04 10.07 8.89 1984 66.05 19.92 14.03 80.42 10.49 9.09 1985 66.28 18.55 15.16 78.13 11.44 10.43 1986 67.32 18.68 13.99 80.58 9.68 9.74 1987 68.57 17.71 13.72 80.49 10.21 9.30 1988 68.96 17.43 13.61 80.99 9.87 9.14 1989 69.89 24.44 5.67 82.01 12.90 5.09 1990 69.83 24.11 6.06 80.68 14.02 5.30 1991 63.05 30.65 6.30 79.37 14.49 6.14 1992 61.55 32.75 5.70 76.46 18.29 5.25 1993 62.09 31.62 6.30 78.31 16.98 4.71 1994 56.54 36.97 6.49 60.98 33.07 5.94 1995 56.20 36.46 7.34 57.99 31.07 10.95 1996 56.36 35.96 7.68 52.92 36.77 10.31 1997 58.55 33.13 8.32 57.19 33.09 9.71 1998 58.89 33.36 7.75 58.27 29.92 11.81 1999 58.73 32.64 8.63 68.72 26.43 4.85 2000 60.95 30.81 8.24 63.64 27.27 9.09 NOTE: Voluntary separations included the following reasons: personal, family, school; personal/family (includes pregnancy); return to school; health; retirement/old age; and unsatisfactory work arrangements (hours/pay/etc.). Involuntary separations included the following reasons: seasonal job completed, temporary seasonal or inter- mittent job completed, slack work/business, and temporary nonseasonal job com- pleted. Sample sizes for the years 1994–1998 were considerably smaller than in earlier years due to a change in respondents for job separation questions. Prior to 1994, questions were asked of those who worked in the past five years; after 1994, only those who worked in the past 12 months were asked job separation questions. Supplemental Tables 175 Table C.10 Probability of an Employment Separation Being Voluntary and Involuntary by Disability Status, CPS, 1981–2000 Probability Voluntary separation Involuntary separation Year Disabled Nondisabled Disabled Nondisabled 1981 0.8153 0.6767 0.0786 0.1868 1982 0.7989 0.6816 0.1113 0.1879 1983 0.8052 0.6794 0.0950 0.1921 1984 0.8032 0.6803 0.0952 0.1887 1985 0.7751 0.6854 0.1111 0.1740 1986 0.8056 0.6960 0.0903 0.1727 1987 0.8060 0.7067 0.0903 0.1646 1988 0.8089 0.7073 0.0901 0.1648 1989 0.8496 0.7216 0.1011 0.2219 1990 0.8479 0.7271 0.1067 0.2135 1991 0.8144 0.6655 0.1240 0.2708 1992 0.8067 0.6382 0.1395 0.3057 1993 0.8090 0.6456 0.1428 0.2911 1994 0.7115 0.5848 0.2287 0.3514 1995 0.6811 0.5768 0.2134 0.3498 1996 0.6506 0.5843 0.2532 0.3373 1997 0.7068 0.6145 0.2019 0.2997 1998 0.6533 0.6091 0.2238 0.3133 1999 0.7940 0.6121 0.1621 0.2990 2000 0.7346 0.6338 0.1748 0.2794 NOTE: See notes to table C.9 for definitions of voluntary and involuntary. The char- acteristics (other than disability) for which the probabilities were calculated were the means corresponding to the entire sample. See Long (1997). Regressions for 1981, 1982, and 1983 contain more limited industry and occupation classifications. Re- gressors included in the multinomial logit analysis included age; age squared; number of weeks worked last year; and industry, occupation, education, female, nonwhite, single, central city, region, and disability dummy variables. 176 Hotchkiss Table C.11 Probability of an Unemployment Spell Being the Result of Losing a Job, Leaving a Job, Reentering the Labor Force, or Newly Entering the Labor Force, by Disability Status, CPS, 1989–2000 Probability Job loser Job leaver Reentrant New entrant Non- Non- Non- Non- Year Disabled disabled Disabled disabled Disabled disabled Disabled disabled 1989 0.4346 0.4890 0.1459 0.1601 0.3974 0.3315 0.0221 0.0194 1990 0.3980 0.5174 0.1753 0.1536 0.4085 0.3081 0.0182 0.0208 1991 0.5041 0.6294 0.1873 0.1283 0.2988 0.2297 0.0099 0.0126 1992 0.5121 0.6721 0.1299 0.1032 0.3474 0.2150 0.0106 0.0096 1993 0.4925 0.6120 0.1671 0.1235 0.3280 0.2535 0.0123 0.0110 1994 0.3996 0.5155 0.1425 0.0975 0.4546 0.3849 0.0033 0.0020 1995 0.4094 0.5358 0.0994 0.1080 0.4780 0.3497 0.0132 0.0065 1996 0.4947 0.5246 0.0681 0.1082 0.4342 0.3647 0.0029 0.0025 1997 0.3269 0.4712 0.0625 0.1180 0.5826 0.4017 0.0280 0.0091 1998 0.4399 0.5030 0.1380 0.1165 0.4192 0.3773 0.0029 0.0032 1999 0.2005 0.4736 0.1852 0.1410 0.6127 0.3844 0.0015 0.0010 2000 0.3662 0.4757 0.1587 0.1393 0.4695 0.3811 0.0055 0.0039 NOTE: The characteristics (other than disability) for which the probabilities were cal- culated are the means corresponding to the entire sample. See Long (1997). Regress- ors in the multinomial logit analysis included age; age squared; number of weeks worked last year; number of weeks looking last year; and female, single, nonwhite, education, central city, region, and disability dummy variables. Supplemental Tables 177 Table C.12 Mean Difference in Expected Duration and Predicted Expected Duration across Disability Status, CPS, 1981–2000 Predicted expected duration Mean difference in expected duration (weeks) across disability status (weeks) Disabled Nondisabled Year (1) (2) (3) 1981 8.72 24.18 24.20 1982 11.84 27.92 26.79 1983 12.96 37.14 34.43 1984 12.40 31.44 30.52 1985 16.74 33.40 25.55 1986 20.12 26.20 24.57 1987 23.54 32.75 24.81 1988 19.10 25.88 22.07 1989 13.04 26.69 20.81 1990 12.94 22.37 20.56 1991 16.82 27.60 23.82 1992 5.42 32.17 30.84 1993 15.62 36.46 30.25 1994 11.24 37.68 39.56 1995 18.70 41.87 34.27 1996 17.74 47.71 34.19 1997 14.24 32.44 31.81 1998 0.66 22.39 30.03 1999 19.68 32.39 27.90 2000 3.78 30.60 27.64 NOTE: Mean expected duration (used to calculate the difference shown in column 1) is calculated as two times the observed censored search duration at a given point in time, as advocated by Akerlof and Main (1981); this results in a valid representation of completed search spells under the assumption of a steady state. Predicted expected duration (columns 2 and 3) was calculated using coefficient estimates resulting from the estimation of an accelerated failure time model where search duration is assumed to be distributed as a Weibull: E[tilti0;Xi,,] exp(Xi)(1). See the text to Chapter 5 for definition of terms. The characteristics (other than disability) for which the predicted expected durations were calculated (X) are the means corresponding to the entire sample. See Long (1997). Regressors for the duration analysis included age; age squared; non-labor income; female, single, nonwhite, education, and regional dummies; dummy variables for availability to work, whether searcher wanted a full- time job, and whether searcher worked last year; and dummy variables for search methods (private agency, public agency, checked with friends, checked with em- ployer, and checked ads), disability status, and search methods interacted with dis- ability status. This Page Intentionally Left Blank Appendix D State Disability Legislation This Page Intentionally Left Blank State Disability Legislation 181 Table D.1 State Disability Legislation Current covered employer, definitions of disability, and State Legislation exceptions Alabama Title 21 Handicapped No definitions available Persons, Acts 1975, Chapter 7 Rights of Blind and Otherwise Physically Disabled Persons Source: Michie’s Alabama Code 1975, Volume 14A, 1997 Replacement Volume. Alaska Title 18 Health, Safety, and Employer: person including Housing, Chapter 80 State state, political subdivision of Commission for Human state, one or more employees Rights, Article 4 Disability: physical or mental Discriminatory Practices impairment that substantially Prohibited limits one or more major life Language referring to activities; a history of, or a disability added in 1987 misclassification as having Source: Alaska Statutes 1962, such; an impairment treated Volume 5 (1998). as a limitation, regarded by others as such; condition requiring use of prosthesis, special equipment or service animal Exclusions: fraternity, charitable, educational, or religious associations or corporations, if not organized for private profit, domestic |
employment 182 Hotchkiss Table D.1 (continued) Current covered employer, definitions of disability, and State Legislation exceptions Arizona Title 41 State Government, Employer: has 15 or more Chapter 9 Civil Rights, employees, working for 20 or Article 4 Discrimination in more calendar weeks Employment Disability: a physical Language referring to impairment, a record of disability added in 1985 physical impairment, being Source: Arizona Revised regarded as having a physical Statutes Annotated, Volume impairment 12B (1999). Exclusions: U.S. government, departments, agencies; corporations, Indian tribes; private associations; employers of aliens; religious entities Arkansas Title 16 Practice, Procedure, Employer: employs nine or and Courts, Subtitle 7 more employees, 20 or more Particular Proceedings and calendar weeks Remedies, Chapter 123 Civil Disability: a physical or Rights, Subchapter 1 The mental impairment that Arkansas Civil Rights Act of substantially limits a major 1993 life function Source: Arkansas Code of Exclusions: employment by a 1987 Annotated, 1999 religious corporation, Supplement Volume 16. association, society, or other Title 20 Public Health and religious entity, family Welfare, Chapter 14 Disabled employment People, Subchapter 3 Rights General, Section 301 Policy (public employers only) Source: Arkansas Code of 1987 Annotated, 2000 Replacement Volume 20 A. State Disability Legislation 183 Table D.1 (continued) Current covered employer, definitions of disability, and State Legislation exceptions California Title 2 Government of the Employer: regularly employs State of California, Division 3 five or more persons or Part 2.8 Department of Fair representative agents, the Employment and Housing state, political or civil Article added in 1980 subdivision thereof, and cities; for purposes of mental Source: West’s Annotated disability, employs 15 or California more persons Codes—Government Code, Sections 12300–14599 Disability: includes mental (1992). and psychological disorder; health impairment affecting the body systems, or limits an individual’s ability to participate in major life activities; other health impairment requiring special education or related services; being regarded as having or having had such health impairment; being regarded as having or having had such health impairment that may become a disability Exclusions: religious organizations and not-for- profit private corporations, family employment 184 Hotchkiss Table D.1 (continued) Current covered employer, definitions of disability, and State Legislation exceptions Colorado Administrative and Employer: state of Colorado Organization Act of 1968 and any political subdivision, Title 24 Government—State, commission, institution, or Article 34 Department of school district thereof, every Regulatory Services, Part 3 other person employing Colorado Civil Rights persons within the state Division—Commission— Disability: physical Procedures and Part 4 impairment which Employment Practices substantially limits one or Physical impairment more of a person’s major life provision was in place in activities, includes record of 1979; amended after July 1, and being regarded as having 1992, to include mental such an impairment; mental impairment for different impairment means mental or articles psychological disorder Source: Colorado Revised Exclusions: religious Statutes 1997, Volume 7. organizations except those supported by public funds, domestic employment Connecticut Title 46a Human Rights, Employer: includes state and Chapter 814c Human Rights political divisions and any and Opportunities person/employer with three or In 1973 discrimination based more persons in employ on physical disability Disability: any individual including blindness was made who has any chronic physical unfair employment practice handicap, infirmity, or Source: Connecticut General impairment Statutes Annotated, Volume Exclusions: family 21B (1995). employment, domestic service State Disability Legislation 185 Table D.1 (continued) Current covered employer, definitions of disability, and State Legislation exceptions Delaware Title 19 Labor, Chapter 7 Employer: state or any Employment Practices, political subdivision, or Subchapter 3 Handicapped board, department, Persons Employment commission or school district Protections thereof, and any person Handicapped section added employing 20 or more on July 11, 1988 persons, 20 or more calendar weeks Source: Delaware Code Annotated, Revised 1974, Disability: having physical or Volume 11, 1995 mental impairment which Replacement Volume. substantially limits one or more major life activities, has Title 16 Health and Safety, a record of such or is regarded Chapter 95, Delaware White as having such an impairment Cane Law, Section 9501 Public Safety; White Cane Exclusions: agriculture, Day (public employers only) domestic employment, family employment Source: Delaware Code Annotated, Revised 1974, Volume 9, 1995, Replacement Volume. Florida Title XLIV Civil Rights, Employer: person employing Chapter 760 Discrimination 15 or more employees, 20 or in the Treatment of Persons; more calendar weeks, any Minority Representation, Part agent for such a person 1 Florida Civil Rights Act No other definitions available Provided for discrimination based on handicap in 1977 Source: West’s Florida Statutes Annotated, Volume 21A (1997). 186 Hotchkiss Table D.1 (continued) Current covered employer, definitions of disability, and State Legislation exceptions Georgia Title 34, Chapter 6A Equal Employer: person or Employment for Persons with governmental unit or officer, Disabilities or agent of an employer, Act passed in 1981 having 15 or more individuals employed, 20 or more Source: Official Code of calendar weeks Georgia Annotated, Volume 21, 1998 Edition. Disability: any condition or characteristic that renders a Title 45, Chapter 19 person an individual with Labor Practices, Article 2 disabilities Fair Employment Practices Exclusions: no exclusions Act passed in 1978 available (public employers only) Source: Official Code of Georgia Annotated, Volume 33, 1990 Edition. Hawaii Title 21 Labor and Industrial Employer: any person, Relations, Chapter 378 including state or political Employment Practices, Part 1 subdivisions, any agent of Discriminatory Practices such a person, having one or Initially passed in 1981 with more employees reference to physical Disability: the state of having handicap a physical or mental Source: Hawaii Revised impairment which Statutes, Volume 7, 1993 substantially limits one or Replacement. more major life activities, having a record of such an impairment, or being regarded as having such an impairment Exclusions: U.S. government, religious organizations State Disability Legislation 187 Table D.1 (continued) Current covered employer, definitions of disability, and State Legislation exceptions Idaho Title 67 State Government Employer: person who hires 5 and State Affairs, Chapter 59, or more employees, 20 or Commission on Human more calendar weeks Rights Disability: physical or mental Language added in 1988 condition which constitutes a referring to handicap substantial limitation to that Source: Idaho Code, Volume person, person with disability 11 (1995). is one with such a disability, has record of such, or is Title 56 Public Assistance regarded as having such a and Welfare, Chapter 7 Rights disability of Blind and Physically Handicapped Persons, Exclusions: domestic Section 56–707 employment, religious organizations Initially passed in 1969 (public employers only) Source: Idaho Code, Volume 10 (1999). Illinois Chapter 775 Human Rights, Employer: employs 15 or Act 5 Illinois Human Rights more employees, 20 or more Act calendar weeks, employing Effective July 1, 1980, with one or more employees when handicapped provisions in a handicap discriminatory place complaint is made, without regard to number of Source: West’s Illinois Smith employees for governmental and Hurd Illinois Compiled unit or agency, or any party to Statutes Annotated, Chapter a public contract 765 to 799(1993). Disability: determinable physical or mental characteristic of a person which is unrelated to a person’s ability to perform a particular job or position Exclusions: religious entities, domestic servants, elected public officials (as employers) 188 Hotchkiss Table D.1 (continued) Current covered employer, definitions of disability, and State Legislation exceptions Indiana Title 22 Labor and Industrial Employer: state or any Safety, Article 9 Civil Rights, political or civil subdivision Chapter 5 Employment thereof and any person Discrimination against engaged in industry affecting Disabled Persons commerce having 15 or more Handicap language added in employees, 20 calendar 1975 weeks Source: Burns Indiana Disability: physical or mental Statutes Annotated, Title 22, impairment that substantially Articles 4–15, 1997 limits at least one of the major Replacement Volume. life activities, a record of an impairment or being regarded as having an impairment Exclusions: U.S. government or corporation owned by the government of the U.S.A. or an Indian tribe, and a private membership club other than labor organization, religious corporation State Disability Legislation 189 Table D.1 (continued) Current covered employer, definitions of disability, and State Legislation exceptions Iowa Title VI Human Services, Employer: state, political Subtitle 1 Social Justice and subdivision board, Human Rights, Chapter 216 commission, department, Civil Rights Commission, institution, or school district Section 216.6 Unfair thereof, and every other Employment Practices person employing employees Iowans with Disabilities Act within the state 1995 Disability: physical or mental Ch. 216 was transferred from condition of a person which Ch. 601A, Civil Rights constitutes a substantial Commission, Code 1991 handicap; extends definition Legislation initially passed in of disabled to include HIV / 1972 AIDS person Source: Iowa Code Exclusions: employers with Annotated, Volume 10A, fewer than 4 employees, 1999 Cumulative Annual family employment, personal Pocket Part. service to person of the employer and religious Title VI Human Services, entities Subtitle 1 Social Justice and Human Rights, Chapter 216 C Rights of Blind, Partially Blind and Physically Disabled Persons, Section 216C.1, 216C.2 Transferred from Ch. 601D Rights of Blind and Physically Disabled, Code of 1991 In place by 1971 (public employers only) Source: Iowa Code Annotated, Volume 10A, 1994. 190 Hotchkiss Table D.1 (continued) Current covered employer, definitions of disability, and State Legislation exceptions Kansas Chapter 44 Labor and Employer: any person in the Industries, Article 10 Kansas state employing four or more Acts against Discrimination persons, includes any person Included physical handicap in acting directly or indirectly 1974 for an employer, labor organizations, nonsectarian Source: Kansas Statutes corporations, organizations Annotated, Volume 3A engaged in social work and (1993). the state and political and municipal subdivisions; excludes nonprofit fraternal or social associations or corporations Disability: a physical or mental impairment that substantially limits one or more of the major life activities of an individual, a record of such or being regarded as having such an impairment Exclusions: family employment and domestic service State Disability Legislation 191 Table D.1 (continued) Current covered employer, definitions of disability, and State Legislation exceptions Kentucky Title 27 Labor and Human Employer: person engaged in Rights, Chapter 344 Civil an industry affecting Rights commerce who has 15 or Disability provision effective more employees, at least 20 in 1992 weeks per year for purposes of disability discrimination Source: Michie’s Kentucky and any agent of that person; Revised Statutes, Volume otherwise 8 weeks 12A, 1997 Replacement. Disability: physical or mental Title 17 Economic Security impairment that substantially and Public Welfare, Chapter limits one or more of the 207 Aid to the Needy major life activities of an Blind—Equal Opportunities, individual, a record of such or Section150 Prohibited being regarded as having such Employment an impairment Practices—Exceptions Exclusions: U.S. government, Disability section added in U.S. government corporation, 1976 Indian tribe, bona fide private (public employers only) membership club Source: Michie’s Kentucky Revised Statutes, Volume 8B, 1998 Replacement. Louisiana Title 23 Labor and Workers’ Employer: employs 15 or Compensation, Chapter 3-A more employees, 20 or more Prohibited Discrimination in calendar weeks; refers to Employment, Part III person, association, legal or Disability commercial entity, state and Legislation initially passed in its agencies receiving services 1980 from an employee and giving compensation in return Source: West’s Louisiana Statutes Revised Annotated, Disability: any person with Volume 15D (1998). physical or mental impairment limiting one or more of the major life activities, or has record of such, or is regarded as having such an impairment Exclusions: family or domestic employment 192 Hotchkiss Table D.1 (continued) Current covered employer, definitions of disability, and State Legislation exceptions Maine Title 5, Administrative Employer: includes any Procedures and Services, Part person in the state employing 12 Human Rights, Chapter any number of employees, 337 Human Rights Act, whatever the place of Subchapter 3, Fair employment, and any person Employment outside this state whose Physical handicap language employees’ place of in place in 1973 employment is within the state; labor organization Source: Maine Revised Statutes Annotated, Volume Disability: has physical or 2A, Title 5, 1998 mental disability, has a record Supplementary Pamphlet. of or is regarded as having a physical or mental disability Exclusions: none for purposes of disability Maryland Article 49B Human Relations Employer: a person engaged Commission, Discrimination in an industry or business in Employment with 15 or more employees, Disability language added in 20 or more calendar weeks, 1974 includes state Source: Michie’s Annotated Disability: any physical Code of Maryland 1957, disability, infirmity, Volume 4, 1999 Supplement. malformation or disfigurement, and any mental impairment or deficiency Exclusions: bona fide private membership |
club; elected public officials, their chosen personnel staff, appointee, or immediate advisor (as employees) State Disability Legislation 193 Table D.1 (continued) Current covered employer, definitions of disability, and State Legislation exceptions Massachusetts Chapter 151B Unlawful Employer: employs six or Discrimination because of more persons, the race, color, religious creed, commonwealth and all national origin, ancestry or political subdivisions, boards, sex departments and In 1983 added language and commissions thereof section to include Disability: physical or mental discrimination against impairment which handicapped substantially limits one or Source: Massachusetts more major life activities of a General Laws Annotated, person, a record of such or Volume 22A Chapter being regarded as having such 151–151E (1996). impairment Exclusions: social clubs, private nonprofit organizations, religious organizations, family and domestic employment Michigan Chapter 37 Civil Rights, Employer: any person who Persons with Disabilities has one or more employees, Civil Rights Act, Article 2 includes contractor/ Employment subcontractor to state/ Act passed in 1976 government entity Source: Michigan Compiled Disability: a determinable Laws, 1999 Cumulative physical or mental Annual Pocket Part. characteristic of an individual substantially limiting one or more of the major life activities of that individual and is unrelated to the individual’s abilities to perform the duties of a particular job or position, qualifications for employment or promotion; a history of such or being regarded as having a determinable physical or mental characteristic Exclusions: domestic employment 194 Hotchkiss Table D.1 (continued) Current covered employer, definitions of disability, and State Legislation exceptions Minnesota Human Rights Chapter 363 Employer: a person who has Division 03 Department of one or more employees Human Rights Disability: a physical, sensory Disability language added in or mental impairment which 1973 materially limits one or more Source: Minnesota Statutes major life activities, has Annotated, Volume 22B record of or is regarded as (1991). having such an impairment Exclusions: family employment, domestic employment, religious and certain other associations Mississippi Title 43 Public Welfare, Employers: state service, Chapter 6 Rights and political subdivisions, public Liabilities of Blind and Other schools, employment Handicapped Persons, Article supported whole or in part by 1 General Provisions, Section public funds 15 Employment No other definitions available Discrimination Act passed in 1974 (public employers only) Source: West’s Mississippi Code Annotated, Volume 14 (1999). State Disability Legislation 195 Table D.1 (continued) Current covered employer, definitions of disability, and State Legislation exceptions Missouri Title 12 Public Health and Employer: includes state, Welfare, Chapter 213, Human political division, any person Rights employing six or more Language to include handicap persons within the state and added in 1978. any person acting directly in the interest of an employer Source: Vernon’s Annotated Missouri Statutes, Volume Disability: physical or mental 12B 1999 Cumulative Annual impairment which Pocket Part. substantially limits one or more of a person’s major life Title 12 Public Health and activities, being regarded as Welfare, Chapter 209 Aid to having such an impairment or the Blind—Rights of Persons a record of such impairment With Visual, Hearing or which with or without Physical Disabilities, Section reasonable accommodation 180 does not interfere with Section added in 1977 performing the job (public employers only) Exclusions: religious or Source: Vernon’s Annotated sectarian corporations and Missouri Statutes, Volume associations 12A 1996. Montana Title 49 Human Rights Employer: an employer of Enacted in 1974 with one or more persons or an handicap provisions in place agent of the employer Source: Montana Code Disability: physical or mental Annotated 1991, Volume 8. impairment, a record of or a condition regarded as such an impairment Exclusions: associations for nonprofit or those providing exclusive membership services 196 Hotchkiss Table D.1 (continued) Current covered employer, definitions of disability, and State Legislation exceptions Nebraska Chapter 48, Labor, Article 11 Employer: a person engaged Nebraska Fair Employment in an industry who has 15 or Practice Act more employees, 20 or more Disability provisions added in calendar weeks, any agent of 1973. such a person, any party whose business is financed in Source: Revised Statutes of part or whole under the Nebraska Annotated, Volume Nebraska Investment Finance 12 (1995). Act regardless of number of Chapter 20 Civil Rights, employees; includes state, Article 1 Individual Rights, agencies and political (B) Persons with Disabilities, subdivisions Section 131 Employment by Disability: physical or mental State and Political impairment that substantially Subdivisions; Policy limits one or more of the Act passed in 1971 major life activities of such an (public employers only) individual, a record of such or Source: Revised Statutes of being regarded as having such Nebraska Annotated, Volume an impairment 14A (1999) Replacement Exclusions: U.S.A., U.S. Volume. government corporations, Indian tribe corporations, bona fide private membership clubs exempt from taxation, religious organizations, family employment, domestic employment Nevada Title 53 Labor and Industrial Employer: any person who Relations, Chapter 613- has 15 or more employees for Employment Practices, Equal 20 weeks in current or Opportunities for previous year Employment Disability: physical or mental Handicapped language and impairment that substantially provisions added in 1971 limits one or more of the Source: Nevada Revised major life activities of the Statutes Annotated, Volume person, a record of such an 16 (1996). impairment or being regarded as having such an impairment Exclusions: U.S.A., U.S. government corporations, Indian tribes, tax exempt private membership clubs, religious organizations State Disability Legislation 197 Table D.1 (continued) Current covered employer, definitions of disability, and State Legislation exceptions New Hampshire Title 31, Trade and Employer: employs six or Commerce, Chapter 354A more persons, all state, State Commission for Human political subdivisions, boards, Rights, Equal Employment departments and Opportunity commissions thereof Law against discrimination Disability: physical or mental regarding physical or mental impairment which handicap approved June 23, substantially limits one or 1975 more of such person’s major Source: New Hampshire life activities, a record of Revised Statutes Annotated having such an impairment or 1995, Title 31. being regarded as having such an impairment Exclusions: social clubs, fraternal, charitable, educational or religious associations, and nonprofit corporations New Jersey Title 10 Civil Rights, Chapter Employer: all corporations 5 Law against Discrimination, and organizations including Section 29.1 the state, any political or civil Last amendments effective subdivision thereof, and all March 2, 1978 public officers, agencies, boards, or bodies Source: New Jersey Statutes Annotated, Title 9–11A Disability: suffering from (1993). physical disability, infirmity, malformation or disfigurement etc., includes HIV/AIDS sufferers Exclusions: domestic servant and family employment 198 Hotchkiss Table D.1 (continued) Current covered employer, definitions of disability, and State Legislation exceptions New Mexico Chapter 28 Human Rights, Employer: any person Article 1 Human Rights employing four or more Handicap language added in persons and any person acting 1973. Act effective until July for an employer 1, 2000 Disability: physical or mental Source: New Mexico Statutes impairment that substantially 1978 Annotated, Volume 5, limits one or more of an 1996 Replacement Pamphlet. individual’s major life activities, has record of or is regarded as having such Exclusions: no exclusions available New York Article 15 Human Rights Law Employer: minimum four Disability language added in employees 1974 Disability: physical, mental Source: McKinney’s or medical impairment, a Consolidated Laws of New record of such impairment, or York Annotated, Book 18, a condition regarded by Executive Law (1993). others as such an impairment Exclusions: family or domestic employment North Carolina Chapter 168A Handicapped Employer: any person Persons Protection Act employing 15 or more full- Act passed in 1985 with time employees within the provisions in place state Source: General Statutes of Disability: any person who North Carolina Annotated, has a physical or mental Volume 21, Chapters impairment which 160–168A (1944–1999). substantially limits one or more major life activities, has a record of such an impairment, or is regarded as having such an impairment Exclusions: domestic or farm workers at that person’s home or farm State Disability Legislation 199 Table D.1 (continued) Current covered employer, definitions of disability, and State Legislation exceptions North Dakota Title 14 Domestic Relations Employer: person within the and Persons, Chapter 14–02.4 state who employs one or Human Rights more employees for more Initially passed in 1983 than one quarter of the year within the state and a person Source: North Dakota wherever situated who Century Code Annotated, employs one or more Volume 3A, 1997 employees whose services are Replacement. to be partially or wholly performed in the state Disability: physical or mental impairment that substantially limits one or more major life activities, a record of impairment, or being regarded as having impairment Exclusions: elected public officials, person chosen by the officer/an appointee, or advisor (as employees) Ohio Title 41 Labor and Industry, Employer: includes state, any Chapter 4112 Civil Rights political subdivision of the Commission state, any person employing Language in place in 1976 four or more persons within the state, and any person Source: Page’s Ohio Revised acting directly or indirectly in Code Annotated, Title 41 the interest of an employer Labor and Industry, 1998 Replacement Volume. Disability: physical or mental impairment that substantially limits one or more major life activities, has record or is regarded as having such an impairment Exclusions: domestic service 200 Hotchkiss Table D.1 (continued) Current covered employer, definitions of disability, and State Legislation exceptions Oklahoma Title 25 Definitions and Employer: person who has 15 General Provisions, Chapter or more employees, 20 or 21 Discrimination, Article 3 more calendar weeks, Discrimination in includes contractor/ Employment subcontractor for the state or In 1981 language added a government entity or definition and prohibited agency of the state and handicap discrimination includes agent of such a person Source: Oklahoma Statutes Annotated (1987). Disability: physical or mental impairment which substantially limits one or more of such person’s major life activities, has a record of or is regarded as having such an impairment Exclusions: Indian tribes, nonprofit bona fide membership club, family, domestic and religious employment Oregon Title 51 (Part 2) Labor and Employer: any person that Industrial Relations, Chapter employs six or more persons 659 Enforcement of Civil and includes the state, Rights; Unlawful counties, cities, districts, Employment Practices, Civil authorities, public Rights of Physically and corporations and entities and Mentally Handicapped their instrumentalities Language added in 1973 Disability: physical or mental Source: Oregon Revised impairment which Statutes Annotated (1989). substantially limits one or more major life activities, has record or is regarded as having such an impairment Exclusions: Oregon National Guard State Disability Legislation 201 Table D.1 (continued) Current covered employer, definitions of disability, and State Legislation exceptions Pennsylvania Title 43 Labor, Chapter 17 Employer: includes Human Relations commonwealth and any 1974 amendment included political subdivision, board, disability department, commission, school district thereof and any Source: Purdon’s person employing four or Pennsylvania Statutes more persons, includes Annotated, Title 43–45 religious, fraternal, charitable (1991). and sectarian corporations and associations Disability: No definition of disability Exclusions: corporations or associations supported in whole or part by governmental appropriations Rhode Island Title 28 Labor and Labor Employer: includes the state Relations, Chapter 5 Fair and all political subdivisions Employment Practices thereof and any person in the In 1973 initially added state employing four or more language of physical individuals and any person handicap acting in the interest of an employer directly or Source: General Laws of indirectly Rhode Island 1956, Reenactment Code of 1995, Disability: physical or mental Volume 5. impairment which substantially limits one or more major life activities, has a record of or is regarded as having an impairment Exclusions: family and domestic employment, religious organization 202 Hotchkiss Table D.1 (continued) Current covered employer, definitions of disability, and State Legislation exceptions South Carolina Title 1 Administration of the Employer: any person who Government, Chapter 13 has 15 or more employees, 20 State Human Affairs or more calendar weeks, any Commission agent of such a person July 6, 1996, amendments Disability: physical or mental included prohibition of impairment that substantially discrimination based on limits one or more major life disability, declaring it an activities, has a record of or is unlawful employment regarded as having an practice impairment Source: Code of Laws of Exclusions: Indian tribes and South Carolina 1976, Volume bona fide private membership 1, 1998 Cumulative clubs, elected public officials, Supplement. or any person chosen by such Title 43 Social Services, officer Chapter 33 Rights of Physically Disabled Persons, Article 1 In General, Section 60 Policy regarding employment of blind and other physically disabled persons Article in place in 1972 |
(public employers only) Source: Code of Laws of South Carolina 1976, Volume 15. State Disability Legislation 203 Table D.1 (continued) Current covered employer, definitions of disability, and State Legislation exceptions South Dakota Title 20 Personal Rights and Employee: any person who Obligations, performs services for any Chapter 13 Human Rights employer for compensation, Previous act regarded no minimum number of employment discrimination employees based on blindness or partial Disability: physical or mental blindness in 1984. General impairment which term ‘‘disability’’ added in substantially limits one or 1986 more of the person’s major Source: South Dakota life functions, having record Codified Laws, Volume 7A, of such or being regarded as 1995 Revision. having such an impairment Title 3 Public Officers and Exclusions: qualifications Employees, Chapter 3–6A based on religious purpose Career Service Personnel Management System, Section 15 Discrimination Prohibited—Violation Misdemeanor Act established in 1973 (public employers only) Source: South Dakota Codified Laws, Volume 2B, 1994 Revision. Tennessee Title 8 Public Officers and No definitions available Employees, Chapter 50 Miscellaneous Provisions, Part 1 General Provisions Legislation initially passed in 1976 Source: Tennessee Code Annotated Volume 3, 1993 Replacement. 204 Hotchkiss Table D.1 (continued) Current covered employer, definitions of disability, and State Legislation exceptions Texas Title 2 Protection of Employer: a person who is Laborers, Subtitle A engaged in industry affecting Employment Discrimination, commerce and who has 15 or Chapter 21 Employment more employees, 20 or more Discrimination, Subchapter B calendar weeks; an agent of, Unlawful Employment or an elected public official; Practices includes a county, Language added in 1989 municipality, state agency, or state instrumentality, Source: Vernon’s Texas Code including public institution of Annotated, Labor Code, education, regardless of the Volume 1 (1996). number of employees Disability: physical or mental impairment which substantially limits at least one major life activity of an individual, a record of such impairment, or being regarded as having such Exclusions: elected public officials (as employees) Utah Title 34A Utah Labor Code, Employer: the state or any Chapter 5 Utah political subdivision or board, Antidiscrimination Act commission, department Language added in 1979 institution, school district, trust, or agent thereof, and Source: Utah Code Annotated every other person employing 1953, Volume 4B, 1997 15 or more employees, 20 Replacement. calendar weeks Disability: physical or mental impairment which substantially limits one or more of a person’s major life activities Exclusions: religious entities State Disability Legislation 205 Table D.1 (continued) Current covered employer, definitions of disability, and State Legislation exceptions Vermont Title 21 Labor, Chapter 5 Employer: any individual, Employment Practices, organization, or governmental Subchapter 6 Fair body including partnership, Employment Practices association, trustee, estate, Language added in 1981 corporation, joint stock company, insurance Source: Vermont Statutes company, or legal Annotated 1987. representative, whether domestic or foreign, or the receiver, trustee in bankruptcy, trustee or successor thereof, and any common carrier by mail, motor, water, air or express company doing business in or operating within the state which has one or more individuals Disability: any person who has a physical or mental impairment which substantially limits one or more major life activities, has a history or record of such or is regarded as having such Exclusions: no exclusions available Virginia Title 51.5 Persons with Employer: the state or entity Disabilities funded Previous title passed in 1972 Disability: any person who (public employers only) has physical or mental Source: Code of Virginia impairment which 1950 Annotated, Volume 7A, substantially limits one or 1998 Replacement Volume. more major life activities, or having record of such Exclusions: employers covered by the Federal Rehabilitation Act of 1973 206 Hotchkiss Table D.1 (continued) Current covered employer, definitions of disability, and State Legislation exceptions Washington Title 49 Labor Regulations, Employer: any person acting Chapter 60 in the interest of the Discrimination—Human employer, directly or Rights Commission indirectly, who employs eight Added disability section in or more persons 1973 Disability: no definition of Source: West’s Revised Code disability of Washington Annotated Exclusions: nonprofit Titles 49–50 (1990). religious or sectarian organizations, family and domestic employment Washington, D.C. Title 1 Administration, Employer: any person who, Chapter 25 Human Rights for compensation employs an Subchapter II Prohibited Acts individual, any agent of such of Discrimination an employer and any Effective 1994 professional association Source: DC Code Annotated, Disability: a physical or 1981 Edition, Volume 2A, mental impairment that 1999 Replacement. substantially limits one or more of the major life Title 16 Health and Safety, activities of an individual Chapter 17 Rights of the having a record of such an Blind and Physically impairment or being regarded Disabled Persons, Section 5 as having such an impairment Discrimination in Employment Prohibited Exclusions: family and domestic employment Likely in place in 1972 (unable to verify) (pubic employers and employers receiving appropriations for D.C. only) Source: DC Code Annotated, 1981 Edition, Volume 4, 1995 Replacement . State Disability Legislation 207 Table D.1 (continued) Current covered employer, definitions of disability, and State Legislation exceptions West Virginia Chapter 5 General Powers Employer: the state, any and Authority of the political subdivision thereof, Governor, Secretary of State and person employing 12 or and Attorney General, Board more employees, 20 calendar of Public Works; weeks Miscellaneous Agencies, Disability: physical or mental Commissions, Offices, impairment which Programs, Etc., Article 11 substantially limits one or Human Rights Commission more of such person’s major Handicap provisions added in life activities, a record of such 1981 impairment, or being Source: Michie’s West regarded as having such Virginia Code Annotated, Exclusions: private clubs and Volume 2, 1999 Replacement family employment Volume. Wisconsin Chapter 111 Employment Employer: the state and each Relations, Subchapter II Fair agency of the state, and any Employment other person engaging in any Section amended to include activity, enterprise or the word handicap in 1965 business employing at least one individual Source: West’s Wisconsin Statutes Annotated (1997). Disability: physical or mental impairment which makes achievement unusually difficult or limits the capacity to work, has a record of such impairment, or is perceived as having such Exclusions: social club or fraternal society, family employment 208 Hotchkiss Table D.1 (continued) Current covered employer, definitions of disability, and State Legislation exceptions Wyoming Title 27 Labor and Employer: the state or any Employment, Chapter 9 Fair political subdivision or board, Employment Practices commission, department, Language added in 1985 institution, or school district thereof, and every other Source: Wyoming Statutes person employing two or Annotated, 1999 Edition more employees Volume 6. 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Burkhauser, and Monroe Berkowitz, eds. Kalamazoo, Michigan: W.E. Upjohn Institute for Employment Research, pp. 33–58. Zveglich, Joseph E., Jr., and Yana van der Meulen Rodgers. 1996. ‘‘The Impact of Protective Measures for Female Workers: Some Evidence from Taiwan.’’ Working paper, Department of Economics, College of William and Mary, Williamsburg, Virgina. The Author Julie L. Hotchkiss is an Associate Professor of Economics in the Andrew Young School of Policy Studies at Georgia State University. She received her B.A. degree from Willamette University in 1985, and her Ph.D. in Economics from Cornell University in 1989. Hotchkiss has published numerous articles on a variety of topics, including the relationship among state unemployment rates, wage differentials in Jamaica, labor supply behavior and welfare of two- earner families, the impact of unemployment insurance programs on individ- ual job search behavior, and wage determination of part-time workers. She is also co-author of one of the leading Labor Economics textbooks. It is with great enthusiasm that she brings her varied skills and experience to the impor- tant subject of workers with disabilities. In addition to her professional activi- ties, she counts among her greatest accomplishments her marriage of 15 years and her two terrific children. 217 This Page Intentionally Left Blank Index Accommodation costs. See Costs of impact on opportunities in high-wage accommodation occupations and industries, 98–99 ADA. See Americans with Disabilities impact on part-time employment, Act 80–81 Age barriers to education, 149 impact on voluntary job separations, Americans with disabilities 106–111 distribution across disability type, impact on voluntary part-time SIPP data set, 1986–1997, 17f employment, 81–83, 85 impact of disabilities on being impact on wage differentials, 63–64, employed part-time, CPS, 136 1981–2000, 79f impact on wages, 60–61, 70–71, 140 labor force participation rates, 28–29 lack of dramatic impact, 141–142 overreporting of disabilities by litigation, 142 nonworking, 13 long-term trends versus its outcomes, public attitudes toward, 4 11, 66 voluntary part-time employment, new ground broken by, 2 CPS, 1981–2000, 79f relation to social change, 4–5, 132 See also Disabled versus nondisabled unique effects of, 140 workers; Disabled workers Americans with Disabilities Act (ADA), 1 Benefits. See Fringe benefits compliance difficulties, 4 Bivariate probit model conclusions about, 152–154 employment and labor force covered and noncovered workers, 57 participation, 24–25 documenting its impact, 5 part-time and voluntary part-time effect of state legislation on, 125 employment, 86–87t expected impact on wages, 49 part-time employment, 77–79, 80t firm size and compliance with, 42 Coefficient effect, 62, 63, 64–66 impact on composition of the College education assistance, 149 unemployed, 112–115 Compensation, 49–74 impact on employment, 27, 31–33, relative position of disabled workers 37, 44, 139 regarding, 71 impact on fringe benefits, 67–70 Costs of accommodation impact on hours of work, 138, 140 estimates, 37 impact on industrial disparity, 93 and firm size, 44 impact |
on job search spell length, influence on employment outcomes, 115–116 37 impact on labor force participation, and wages, 57, 60, 70, 136 132–133 Covered disabled workers, 57 impact on occupational disparity, 93 CPS. See Current Population Survey impact on opportunities in high- Cross-sectional analyses, 11 growth occupations and See also Pooled, cross-sectional industries, 97–98 analysis 219 220 Index Current Population Survey (CPS), differential, CPS, 1981–2000, 157–158 116f work disability measure, 9–12 average real hourly wages, CPS, 1981–2000, 50f Data sources, 9–10, 15–18 compensation trends, 71 Demographic differences and wage demographic differences, 13–14, 54, differentials 135t-136t among groups of disabled workers, dissimilarity across occupations and 54 industries, compared to nonwhite between disabled and nondisabled versus white, CPS, 1981–2000, workers, 14, 54, 135t-136t 93f Demographic variables, CPS, dissimilarity across occupations and 1981–2000, 14t industries by type of disability, Differences-in-differences methodology, SIPP, 1997, 94f variation of, 46n14 employment levels and trends, 21, Differences-in-differences-in- 22f differences calculation for hours of work, 14–15 disability and firm size across job mobility, 90–95 job search strategies used, CPS, time, 42t, 44 1981–2000, 119f Disability type labor force participation rates, CPS, dummy variables, 35–36 1981–1991, 128f Duncan indices of dissimilarity part-time/full-time wage across occupations and industries differentials, CPS, 1981–2000, for, SIPP, 1997, 94f 90f four basic categories, 16–18 pension plans, 67–70 identification of, 15 percentage employed, CPS, impact on kind of part-time 1981–2000, 22f, 166t employment, 83–85, 86–87t percentage employed part-time, CPS, labor force participation and 1981–2000, 77f employment bivariate probit predicted employment probabilities results for, SIPP, 1981–2000, 36t by firm size, CPS, 1987–1999, 41f SIPP classification, 159, 162t predicted expected job search Social Security Administration duration, 118f, 177t classification, 19n14 predicted joint labor force and wage differentials, 55–57 participation and joint/ Disabled versus nondisabled workers unconditional employment across firm size, CPS, 1987–1999, probability, CPS, 1981–2000, 39f 167t across occupations and industries, proportion employed, CPS, CPS, 1981–2000, 173t 1981–1991, 128f across occupations and industries, proportion employed part-time, CPS, CPS, 2000, 91f 1981–1991, 137f analyses used for comparing, 11 proportion receiving benefits, CPS, average job search spell length 1980–1999, 67f Index 221 similarity in wage declines, 58 time and voluntary part-time unemployment type probabilities, employment, CPS, 1981–2000, 113, 114f 172t voluntary and involuntary job marginalization of, 111, 145 separations, CPS, 1981–2000, policy issues, 3–5 108f, 110, 174t, 175t proportion indicating work-limiting wage differentials, 50–51, 98–99 disabilities, 13, 165t wages and firm size, 58 representation in desirable industries See also Heckman procedure for and occupations, 95–99 controlling self-selection reservation wage, 21 Disabled workers wage variations among demographic covered and noncovered by ADA, 57 groups of, 54 effects of cash payment programs on, See also Americans with disabilities; 2–3 Disabled versus nondisabled entering labor force post-ADA, 64 workers evaluating barriers that face, 27 Disabled Worker Tax Credit, 145 history of legislation for, 1–2 disable X post regressor identification of, 10, 157 employment and labor force industry/occupation wage, CPS, participation probability, from 1981–2000, 99f state legislation subsample, 130, job mobility, 90–95 133 labor force participation rates, 27–29 labor force participation rates, 31 labor market demand issues, 6–9 part-time employment probability, marginal effect of disability on post–state legislation, 138 employer-provided fringe wage differentials, 54, 56 benefits, CPS, 1981–2000, wage differentials, from state legislation subsample, 136 170–171t Discrimination. See Job discrimination; marginal effect of disability on Wage discrimination employment in high-growth Distribution of workers, 90–95 occupation or industry, CPS, 98t Dummy variables marginal effect of disability on fringe existence of a disability, 31 benefit receipt, 68, 69f measure of discrete change in, 45n7 marginal effect of disability on job pre- or post-ADA time period, 31 separation type, CPS, 1981–2000, type of disability, 35–36 110f Duncan Index, 92–94, 173t marginal effect of disability on joint Duration dependence, 118 labor force participation and employment, CPS, 1981–2000, Earned income exclusions, 144, 149 25f EARN. See Employer Assistance marginal effect of disability on labor Referral Network force participation and Education, 147–151 employment probabilities before and employment, 134 and after ADA, 33t higher, 149 marginal effect of disability on part- wage differentials, 65–66 222 Index Employer Assistance Referral Network (ADA); Legislation for (EARN), 152 individuals with disabilities Employers Firm size hiring incentives, 121, 151–152 changes in employment across, 23 tax credits, 70, 145–146, 151 and employment probabilities, 37–43 See also Firm size; Fringe benefits Relative predicted probabilities of Employment, 21–47 working in each firm size, CPS, barriers versus labor supply 1987–1999, 168t decisions, 27 and wages, 57–61 bivariate probit results, CPS, Flexibility in hours, 83, 102n12, 137 1981–2000, 32–33t Flextime, 150 bivariate probit results, SIPP, Fringe benefits, 66–70, 170–171t 1981–2000, 34t Full-time wage premium, 85, 88–90 bivariate probit results by type of disability, SIPP, 1981–2000, 36t effect of state-level disability Health insurance, 67–70, 170–171t legislation on, 129–133 Health-related job quits, 110 growth rates for industry and Heckman procedure for controlling self- occupational classifications, 97t selection, 52, 61–62, 88–89 in high-wage and/or high-growth Higher education assistance, 149 occupations and industries, 95–99 High-growth indicator for occupations incentives, 143–147 and industries, 95–96 percentages of disabled and Hiring incentives for employers, 121, nondisabled, CPS, 1981–2000, 151–152 22f, 166t Hours of work, 14–15, 76–90 quality, 75–103 effect of disability legislation on, See also Employment probabilities; 137–138 Labor force participation; Part- improvements in, 100 time employment; Unemployment ICPSR data. See Inter-University Employment probabilities Consortium for Political and before and after ADA, 33t Social Research data and firm size, 37–43 Incentives for disabled workers, joint versus unconditional, 23–27, 144–145 167t Incentives for employers, 70, 121, state legislation subsample 145–147 determinants of, 133 Industries for workers with mental disabilities, comparing distributions of workers 37 Endogeneity problem with self-reported across various, 92–95 disabilities, 9, 13, 29 dissimilarity across, by type of Endowment effect, 62, 66 disability, SIPP, 1997, 94f Estimation issues, 9–12 dissimilarity across, disabled versus nondisabled and nonwhite versus Federal disability legislation. See white, CPS, 1981–2000, 93f, 173t Americans with Disabilities Act distribution of disabled versus Index 223 nondisabled workers across, CPS, Labor force participation 2000, 91f bivariate probit results, CPS, high-wage and/or high-growth, 1981–2000, 32–33t 95–99 bivariate probit results, SIPP, wage differentials, 65–66 1981–2000, 34t Information dissemination programs, bivariate probit results by type of 146–147 disability, SIPP, 1981–2000, 36t Internal disabilities, 162t declining rates of, 27–29 Inter-University Consortium for Political effect of state legislation on, and Social Research (ICPSR) 129–133 data, 157 factors affecting, 22–23 Involuntary job separation, 107, 108f, incentives for the disabled, 144–145 174t, 175t by new entrants and reentrants, 112, reasons for, 122n6 114f See also Job losers probabilities before and after ADA, IP Index, 102n14 33t See also Employment Job Accommodations Network (JAN), Labor supply decisions of disabled 146, 147 persons, 45n10 Job discrimination versus employment barriers, 27 EEOC’s estimate of, 142 Large firms in hiring, 118 and the Americans with Disabilities at hiring versus separation stage, 107 Act (ADA), 44 mistaking labor supply decisions for, definitions of, 38, 58 27 and wages, 58 from switching jobs, 123n15 Layoffs, 107 See also Wage discrimination Legislation for individuals with Job leavers, 112, 113f, 176t disabilities, 1–2 See also Voluntary job separation federal versus state, 125, 128–140 Job losers, 111, 112, 113f, 115, 176t relation to social change, 4–5, 132 See also Involuntary job separation state-level, 126–127t, 181–208t Job mobility, 90–95 See also Americans with Disabilities Job placement services, 121, 152 Act (ADA) Jobs. See Employment Job search duration, 106, 115 Medicaid for disabled workers, 69, 144, estimation of, 116–119 150 mean difference in expected duration Medicare for disabled workers, 144, 150 and predicted expected duration, Medium firms CPS, 1981–2000, 177t definition of, 38 Job search strategies, 119–120 and wages, 58 Job separation, 105, 106–111, 174t, 175t Mental disabilities See also Involuntary job separation; distribution across industries and Voluntary job separation occupations, 95 Joint probability of employment, 23–27, employment probabilities for 167t workers with, 37 224 Index part-time employment of workers Part-time employment, 76–81 with, 85 bivariate probit, SIPP, 1986–1997, SIPP classification, 162t 86–87t wages of workers with, 72n9 definition of, 76 Mental retardation, 19n14 impact of being disabled on Models. See Research methods probability of, CPS, 1981–2000, Multinomial logit analysis, 47n26 172t employment and firm size, 38 types of, 81–85 unemployment categories, 112 See also Voluntary part-time voluntary job separation analysis, employment 107, 109 Part-time wage penalty, 87–90 Multinomial probit analysis, 122n5 PASS. See Plan for Achieving Self- Musculoskeletal disabilities Support program advantage of college degrees to Pension plans, 67–70, 170–171t workers with, 149 Personal Responsibility and Work definition of, 72n7 Opportunity Reconciliation Act part-time employment of workers (PRWORA), 13 Plan for Achieving Self-Support with, 85 Program (PASS), 148, 149 SIPP classification, 162t Policies before passage of ADA and wage differentials, 56–57 (Americans with Disabilities Act), 2–3 National Easter Seal Society, 152 Policy issues, 3–5 Natural experiments, 140n2 Policy recommendations New entrants to the labor force, 112, education and training, 147–151 114f, 176t employment incentives, 143–147 New Freedom Initiative, 150 job placement of disabled workers, Nondisabled workers. See Disabled 121 versus nondisabled workers reducing wage differentials, 66 Pooled, cross-sectional analysis, 102n7 Occupations employment probabilities before and after ADA, 30–34 comparing distributions of workers part-time employment, 79–81 across various, 92–95 wage differentials over time, 51–57 dissimilarity across, by type of Pooled, cross-sectional bivariate probit disability, SIPP, 1997, 94f model, 129–130 dissimilarity across, disabled versus Project EMPLOY, 152 nondisabled and nonwhite versus PRWORA. See Personal Responsibility white, CPS, 1981–2000, 93f, 173t and Work Opportunity distribution of disabled versus Reconciliation Act nondisabled workers across, CPS, 2000, 91f Real wages high-wage and/or high-growth, average hourly wages for disabled 95–99 versus nondisabled workers, CPS, wage differentials, 65–66 1981–2000, 50f Index 225 estimated regression results for, by Sample versus population percentages of covered firm size, CPS, disabled workers 1984–2000, 59–60t CPS data set, 1981–2000, 12f estimated regression results for, CPS, SIPP data set, 1986–1997, 16, 17f 1984–2000, 53 Search. See Job search estimated regression results for, SIPP, Selectivity-corrected part-time 1986–1997, 55 employment, 78 log real wage OLS estimation, CPS, Selectivity-corrected wage differentials, 1981–1991, 135–136t 62–64, 169t Recession, impact on disabled workers, Selectivity effect, 62 21 Self-employment, 146–147 Reentrants to the labor force, 112, 114f, Self-reported disability status issues, 9, 176t 13, 29 Representation of workers, 95–99 Self-selection Research methods as explanation for post-ADA wage bivariate probit model, 24–25, 77 differentials, 64 cross-sectional analysis, 11 Heckman procedure for controlling, differences-in-differences-in- 52, 61–62, 88–89 differences calculation, 42 in state legislation subsample, 134 Duncan Index, 92 Separation from employment. See Job estimating job search duration, separation 116–118 SIPP. See Survey of Income and estimating the effect of state laws on Program Participation the ADA, 125 Skill certification, 152 estimation issues, 9–12 Small business assistance, 146–147, 148 Heckman procedure for controlling Small firms self-selection, 52, 61–62 definitions of, 38, 58 IP Index, 102n14 and wages, 58 multinomial logit analysis, 38, Social Security Administration 47n26, 107, 112 cash payment programs for natural experiments, 140n2 pooled, cross-sectional analysis, Americans with disabilities, 2–3 102n7 Web site listing of disability pooled, cross-sectional bivariate categories, 19n14 probit model, 129–130 Social Security Disability Insurance steady state assumptions, 122n11 Program (SSDI), 3 universal logit analysis, 122n5 extended period of eligibility, See also Data sources; Dummy 144–145 variables training and rehabilitation programs, 148–149 Sample sizes Trial Work Period (TWP), 144 disabled and nondisabled workers, SSDI. See Social Security Disability CPS data files, 10t Insurance Program disabled and nondisabled workers, SSI. See Supplemental Security Income SIPP data files, 16t Program 226 Index State disability legislation, 1–2, Unemployment, 105, 111–115 126–127t, 181–208t categories, 112 versus federal disability legislation, See also Job separation 125, 128–140 Union Research Corporation data, 157 See also Legislation for individuals Unobservable factors, 24 with disabilities States used for subsample of state Variables. See Demographic variables; Dummy variables; Unobservable legislation, 128 factors State unemployment rate regressor, 30 Vocational rehabilitation programs, Supplemental Security Income Program 148–149 (SSI), 3 Voluntary job separation, 105, 106–111, AFDC participant flow to, 108f, 174t, 175t 1993–1995, 13, 64 health-related, 110 exclusion of earned income, 144, 149 reasons for, 122n6 impact on health insurance for See also Job leavers disabled workers, 69 Voluntary part-time employment reinstatement of payments without bivariate probit, SIPP, 1986–1997, new application, 144–145 86–87t training and vocational rehabilitation definition of, 102n8 programs, 148, 149 effect of state legislation on, 140 Supplemental tables, 165–177 impact of having a disability on, Survey of Income and Program CPS, 1981–2000, 79f, 172t Participation (SIPP), 15–18 linear probability results, CPS, evidence of effect of ADA on labor 1981–2000, 83t force participation and post-ADA, 85 employment, 34–37 evidence |
Handbook of Inpatient Endocrinology Rajesh K. Garg James V. Hennessey Alan Ona Malabanan Je rey R. Garber Editors 123 Handbook of Inpatient Endocrinology https://www.facebook.com/groups/2202763316616203 Rajesh K. Garg James V. Hennessey Alan Ona Malabanan Jeffrey R. Garber Editors Handbook of Inpatient Endocrinology Editors Rajesh K. Garg James V. Hennessey Division of Endocrinology Beth Israel Deaconess Diabetes and Metabolism Medical Center University of Miami Miller Harvard Medical School School of Medicine Division of Endocrinology Coral Gables Diabetes and Metabolism FL Boston USA MA USA Alan Ona Malabanan Beth Israel Deaconess Jeffrey R. Garber Medical Center Beth Israel Deaconess Harvard Medical School Medical Center Division of Endocrinology Brigham and Women’s Hospital Diabetes and Metabolism Harvard Medical School Boston Department of Endocrinology MA Boston USA MA USA ISBN 978-3-030-38975-8 ISBN 978-3-030-38976-5 (eBook) https://doi.org/10.1007/978-3-030-38976-5 © Springer Nature Switzerland AG 2020 This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed. 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This Springer imprint is published by the registered company Springer Nature Switzerland AG The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland https://www.facebook.com/groups/2202763316616203 Dedicated to our fellows. – Rajesh K. Garg, James V. Hennessey, Alan Ona Malabanan, and Jeffrey R. Garber Preface During the last two decades, there has been increasing emphasis on physicians seeing more patients in ambulatory settings. As a result, hospital-based physicians are providing more inpatient care, and fewer endocrinologists, after fellowship training, are caring for their hospitalized patients. Yet managing endocrine dis- eases in the inpatient setting has become more complex, while transitioning that care back to the ambulatory setting is as critical as ever. Examples of complex care and challenges regularly encountered in hospitalized patients abound and include manag- ing diabetes emergencies, those with diabetes mellitus on total parenteral nutrition, insulin treatment protocols for pregnancy in diabetes, and thyroid crises. Additionally, the diagnosis and man- agement of adrenal insufficiency; perioperative care of patients undergoing pituitary, parathyroid, adrenal, and thyroid surgery; and patients with thyroid dysfunction who have heart disease as well as those who cannot take oral medications frequently are encountered. The editors of this handbook, attending endocrinol- ogists in Boston’s Longwood Medical Area at either the Brigham and Women’s Hospital or Beth Israel Medical Center, decided to produce this volume after agreeing that even the most experienced endocrinologist working on a busy inpatient consult service would benefit from an easy-to-navigate and concise text for guidance. Many authors were in their fellowship training when they con- tributed to this book. The book is designed to highlight salient clinical points with more detailed information available on each point. The well-established clinical approaches are emphasized vii https://www.facebook.com/groups/2202763316616203 viii Preface with suggestions for further reading. In addition to serving as a practical, easy-to-navigate reference guide for those taking care of inpatients with endocrine disorders, each section provides guidance about bridging their care from the inpatient to the outpa- tient setting. The audience for this book includes physicians who provide most inpatient consultative care, for example, endocrinology fel- lows, their attending physicians, surgical and obstetrical special- ists, primary care physicians, and hospitalists. We look forward to receiving your feedback so that future editions can remain up-to- date and we can address issues that we have not sufficiently emphasized in this, our first edition. Coral Gables, FL, USA Rajesh K. Garg Boston, MA, USA James V. Hennessey Alan Ona Malabanan Jeffrey R. Garber Contents 1 Pituitary Apoplexy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1 Ana Paula Abreu and Ursula B. Kaiser 2 Panhypopituitarism . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15 Ana Paula Abreu and Ursula B. Kaiser 3 Postoperative Management After Pituitary Surgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27 Anna Zelfond Feldman and Pamela Hartzband 4 Severe Thyrotoxicosis and Thyroid Storm . . . . . . . . . . 33 Melissa G. Lechner and Trevor E. Angell 5 Myxedema Coma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43 Gwendolyne Anyanate Jack and James V. Hennessey 6 Abnormal Thyroid Stimulating Hormone Values That Are Not due to Common Causes of Primary Hypothyroidism or Thyrotoxicosis . . . . . . 55 Zsu-Zsu Chen and James V. Hennessey 7 Management of a Hospitalized Patient with Thyroid Dysfunction . . . . . . . . . . . . . . . . . . . . . . . . 73 Megan Ritter and James V. Hennessey 8 Perioperative Management of Patients with Hyperthyroidism or Hypothyroidism Undergoing Nonthyroidal Surgery . . . . . . . . . . . . . . . . . . . . . . . . . . . 85 Catherine J. Tang and James V. Hennessey ix https://www.facebook.com/groups/2202763316616203 x Contents 9 Thyroid Problems Encountered Specifically in Inpatients with Cardiac Disease . . . . . . . . . . . . . . . 101 Jeena Sandeep and James V. Hennessey 10 Severe Hypercalcemia . . . . . . . . . . . . . . . . . . . . . . . . . . 115 Antonia E. Stephen and Johanna A. Pallotta 11 Hypocalcemia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 123 Alan Ona Malabanan 12 Perioperative Evaluation of Primary Hyperparathyroidism . . . . . . . . . . . . . . . . . . . . . . . . . . 133 J. Carl Pallais 13 Management of Osteoporosis in the Inpatient Setting . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 145 Marcy A. Cheifetz 14 Calcium Disorders in End- Stage Renal Failure Including Those on Dialysis . . . . . . . . . 159 Alan Ona Malabanan 15 Disorders of the Serum Sodium Concentration . . . . . 165 Julian L. Seifter and Hsin-Yun Chang 16 Inpatient Management of Hyperkalemia . . . . . . . . . . 189 Erika R. Drury and Bradley M. Denker 17 Suspected Adrenocortical Deficiency . . . . . . . . . . . . . 199 Anand Vaidya 18 Cushing’s Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . 215 Brandon P. Galm and Nicholas A. Tritos 19 Adrenalectomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 229 Ole-Petter R. Hamnvik 20 Pheochromocytoma and Paraganglioma . . . . . . . . . . 237 Alejandro Raul Ayala and Mark Anthony Jara 21 Primary Aldosteronism . . . . . . . . . . . . . . . . . . . . . . . . 251 Alejandro Raul Ayala and Mark Anthony Jara Contents xi 22 Treatment of Hyperglycemia in a Hospitalized Patient Without Hyperglycemic Emergency . . . . . . . 261 Rajesh K. Garg 23 Hypoglycemia in Patients with Diabetes . . . . . . . . . . . 271 Margo Hudson 24 Hypoglycemia in Patients Without Diabetes . . . . . . . 283 Rajesh K. Garg 25 Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic State . . . . . . . . . . . . . . . . . . . . . . . . . . . 293 Daniela V. Pirela and Rajesh K. Garg 26 Management of Preexisting Diabetes and Gestational Diabetes During Hospitalization . . . 307 Gregory P. Westcott and Florence M. Brown 27 Inpatient Insulin Pump Management . . . . . . . . . . . . . 319 Maria Vamvini and Elena Toschi 28 Severe Hypertriglyceridemia in the Hospitalized Patient . . . . . . . . . . . . . . . . . . . . . . 333 Roselyn Cristelle I. Mateo and Om P. Ganda 29 Hypomagnesemia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 345 Alan Ona Malabanan Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 353 https://www.facebook.com/groups/2202763316616203 Contributors Ana Paula Abreu, MD, PhD Division of Endocrinology, Diabe- tes and Hypertension, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA Trevor E. Angell, MD Keck School of Medicine, University of Southern California, Division of Endocrinology and Diabetes, Los Angeles, CA, USA Alejandro Raul Ayala, MD University of Miami, Miller School of Medicine, Department of Endocrinology and Metabolism, Miami, FL, USA Florence M. Brown, MD Joslin-Beth Israel Deaconess Medical Center Diabetes in Pregnancy Program, Joslin Diabetes Center, Department of Adult Diabetes, Boston, MA, USA Hsin-Yun Chang, MD National Cheng Kung University Hospi- tal, Department of Family Medicine, Tainan City, Taiwan Marcy A. Cheifetz, MD Harvard Vanguard Medical Associates, Atrius Health, Department of Endocrinology, Chestnut Hill, MA, USA Zsu-Zsu Chen, MD Beth Israel Deaconess Medical Center, Department of Endocrinology, Diabetes and Metabolism, Boston, MA, USA xiii xiv Contributors Bradley M. Denker, MD Beth Israel Deaconess Medical Center, Department of Medicine, Nephrology Division and Harvard Medical School, Boston, MA, USA Erika R. Drury, MD Division of Nephrology, Department of Medicine, University of Rochester School of Medicine, Rochester, NY, USA Anna Zelfond Feldman, MD Harvard Medical School, Beth Israel Deaconess Medical Center, Department of Endocrinology, Boston, MA, USA Brandon P. Galm, MD, MPH, FRCPC Neuroendocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA Om P. Ganda, MD Joslin Diabetes Center, Department of Med- icine, Beth Israel Deaconess Medical Center, Boston, MA, USA Jeffrey R. Garber, MD Beth Israel Deaconess Medical Center, Brigham and Women’s Hospital, Harvard Medical School, Department of Endocrinology, Boston, MA, USA Rajesh K. Garg, MD Division of Endocrinology, Diabetes and Metabolism, University of Miami Miller School of Medicine, Coral Gables, FL, USA Ole-Petter R. Hamnvik, MB BCh BAO, MMSc, MRCPI Brigham and Women’s Hospital, Department of Medi- cine, Division of Endocrinology, Diabetes and Hypertension, Boston, MA, USA Pamela Hartzband, MD Harvard Medical School, Beth Israel Deaconess Medical Center, Department of Endocrinology and Metabolism, Boston, MA, USA James V. Hennessey, MD Beth |
Israel Deaconess Medical Cen- ter, Harvard Medical School, Division of Endocrinology, Diabe- tes and Metabolism, Boston, MA, USA Margo Hudson, MD Brigham and Women’s Hospital, Department of Endocrinology, Hypertension and Diabetes, Boston, MA, USA https://www.facebook.com/groups/2202763316616203 Contributors xv Gwendolyne Anyanate Jack, MD, MPH Weill Cornell Medical Center-New York Presbyterian Hospital, Department of Medi- cine, Division of Endocrinology, Diabetes and Metabolism, New York, NY, USA Mark Anthony Jara, MD University of Miami, Miller School of Medicine, Division of Endocrinology and Metabolism, Miami, FL, USA Ursula B. Kaiser, MD Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA Melissa G. Lechner, MD, PhD David Geffen School of Medi- cine, University of California at Los Angeles, Division of Endo- crinology, Diabetes and Metabolism, Los Angeles, CA, USA Alan Ona Malabanan, MD, FACE, CCD Beth Israel Deacon- ess Medical Center, Harvard Medical School, Division of Endo- crinology, Diabetes and Metabolism, Boston, MA, USA Roselyn Cristelle I. Mateo, MD MSc Joslin Diabetes Center, Department of Endocrinology, Beth Israel Deaconess Medical Center, Boston, MA, USA J. Carl Pallais, MD, MPH Brigham and Women’s Hospital, Division of Endocrinology, Department of Medicine, Boston, MA, USA Johanna A. Pallotta, MD Harvard Medical School, Beth Israel Deaconess Medical Center, Department of Medicine, Endocrinol- ogy and Metabolism, Boston, MA, USA Daniela V. Pirela, MD Jackson Memorial Hospital/University of Miami Hospital, Division of Endocrinology, Diabetes and Metabolism, Miami, FL, USA Megan Ritter, MD Weill Cornell Medicine, New York Presbyte- rian, New York, NY, USA Jeena Sandeep, MD St. Elizabeth Medical Center, Department of Medicine, Division of Endocrinology, Brighton, MA, USA xvi Contributors Julian L. Seifter, MD Brigham and Women’s Hospital, Depart- ment of Medicine, Boston, MA, USA Antonia E. Stephen, MD Harvard Medical School, Massachu- setts General Hospital, Department of Surgery, Boston, MA, USA Catherine J. Tang, MD Beth Israel Deaconess Medical Center, Harvard Medical School, Division of Endocrinology, Diabetes and Metabolism, Boston, MA, USA Elena Toschi, MD Adult Clinic, Joslin Diabetes Center, Harvard Medical School, Beth Israel Deaconess Medical Center, Depart- ment of Endocrinology and Diabetes, Boston, MA, USA Nicholas A. Tritos, MD, DSc Harvard Medical School, Massa- chusetts General Hospital, Neuroendocrine Unit and Neuroendo- crine & Pituitary Tumor Clinical Center, Boston, MA, USA Anand Vaidya, MD, MMSc Harvard Medical School, Center for Adrenal Disorders, Division of Endocrinology, Diabetes, and Hypertension, Brigham and Women’s Hospital, Boston, MA, USA Maria Vamvini, MD Adult Clinic, Joslin Diabetes Center, Har- vard Medical School, Beth Israel Deaconess Medical Center, Department of Endocrinology and Diabetes, Boston, MA, USA Gregory P. Westcott, MD Beth Israel Deaconess Medical Cen- ter and Joslin Diabetes Center, Department of Endocrinology, Diabetes and Metabolism, Boston, MA, USA https://www.facebook.com/groups/2202763316616203 Pituitary Apoplexy 1 Ana Paula Abreu and Ursula B. Kaiser Contents Definition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2 Precipitating Factors/Patients at Risk . . . . . . . . . . . . . . . . . . . . . . . . . . . 2 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3 Obtain Detailed Clinical History . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3 Perform Detailed Physical Exam Including Cranial Nerves and Visual Fields . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4 Evaluation of Endocrine Dysfunction/Laboratory Assessment . . . . . . 4 Imaging . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5 Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7 Consider Initiation of Corticosteroid Treatment . . . . . . . . . . . . . . . . . 7 Acute Intervention: Surgery vs. Conservative Treatment . . . . . . . . . . 8 Postoperative Care . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10 Monitor for Signs and Laboratory Abnormalities Suggestive of Diabetes Insipidus (DI) . . . . . . . . . . . . . . . . . . . . . . 10 Assess Pituitary Reserve . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11 Visual Assessment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12 A. P. Abreu (*) · U. B. Kaiser Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA e-mail: apabreu@bwh.harvard.edu; ukaiser@bwh.harvard.edu © Springer Nature Switzerland AG 2020 1 R. K. Garg et al. (eds.), Handbook of Inpatient Endocrinology, https://doi.org/10.1007/978-3-030-38976-5_1 2 A. P. Abreu and U. B. Kaiser Follow-Up After Discharge . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12 Check Electrolytes After 1 Week . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12 Reassess Pituitary Function After 4 to 8 Weeks . . . . . . . . . . . . . . . . . 12 Suggested Reading . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13 Definition Apoplexy means “sudden attack” in Greek. Classical pituitary apoplexy (PA) is a clinical syndrome characterized by abrupt hemorrhage and/or infarction of the pituitary gland. Severe head- ache of sudden onset is the main symptom, sometimes associated with visual disturbances or ocular palsy. Apoplexy usually occurs in patients with preexisting pituitary adenomas and evolves within hours or days. Subclinical PA is defined as asymptomatic or unrecognized pituitary hemorrhage and/or infarction. It may be detected on rou- tine imaging or during histopathological examination. The fre- quency of subclinical hemorrhagic infarction in pituitary tumors is around 25%. Precipitating Factors/Patients at Risk The precise pathophysiology of PA is not completely understood. Since most cases occur in preexisting pituitary adenomas, it has been hypothesized that a reduction in blood flow or abnormal vas- cularity of the tumor could be mechanisms contributing to PA. The underlying process can be simple infarction, hemorrhagic infarc- tion, or mixed hemorrhagic infarction. The pituitary gland is enlarged in pregnancy and prone to infarction from hypovolemic shock. Pituitary necrosis that occurs in the setting of large-volume obstetric hemorrhage post- partum is referred to as Sheehan syndrome. It is a rare but poten- tially life- threatening complication that can result in postpartum hypopituitarism. https://www.facebook.com/groups/2202763316616203 1 Pituitary Apoplexy 3 The clinical symptoms of PA mimic other common neurologi- cal disorders such as subarachnoid hemorrhage, migraine, bacterial meningitis, or stroke, which can lead to delayed or even missed diagnosis. A high degree of clinical suspicion is needed to diagnose pituitary apoplexy, as most patients do not have a previ- ous history of known pituitary adenoma. Precipitating risk factors have been identified in 10–40% of cases of PA, and it is important to recognize them. Hypertension has been considered a precipitat- ing factor for PA, although recent studies question this associa- tion. Surgery, particularly coronary artery surgery, and angiographic procedures have been reported to be associated with PA. Dynamic testing of pituitary function, using growth hormone- releasing hormone, gonadotropin-releasing hormone, thyrotropin- releasing hormone, and corticotrophin-releasing hormone (less commonly), or an insulin tolerance test, is also associated with PA. Initiation or withdrawal of dopamine receptor agonists, estro- gen therapy, radiation therapy, pregnancy, head trauma, and coag- ulopathy are some other factors known to induce pituitary apoplexy. A diagnosis of PA should be considered in all patients with these risk factors who present with acute severe headache, with or without neuro-ophthalmologic signs. Diagnosis Obtain Detailed Clinical History The clinical presentation can be acute or subacute and is highly variable, determined by the extent of hemorrhage, necrosis, and edema. Headache is present in more than 80% of patients. It is usually retro-orbital but can be bifrontal or diffuse. Nausea and vomiting can be associated. As most patients have an underlying macroadenoma, signs and symptoms of hypopituitarism may have been present prior to the episode of PA. As discussed ear- lier, most patients do not have a history of a known prior pitu- itary adenoma and therefore do not carry a diagnosis of hypopituitarism. 4 A. P. Abreu and U. B. Kaiser Sheehan syndrome usually presents with a combination of fail- ure to lactate postdelivery and amenorrhea or oligomenorrhea, but any of the manifestations of hypopituitarism (e.g., hypotension, hyponatremia, hypothyroidism) can occur at any time from the immediate postpartum period to years after delivery. Perform Detailed Physical Exam Including Cranial Nerves and Visual Fields More than half of patients with PA have some degree of visual field impairment, with bitemporal hemianopsia being the most com- mon. About half of patients have oculomotor palsies due to func- tional impairment of cranial nerves III, IV, and/or VI. Cranial nerve III is most commonly affected, resulting in ptosis, limited eye adduction, and mydriasis due to nerve compression. Extravasation of blood or necrotic tissue into the subarachnoid space can result in meningismus and an altered level of consciousness. Evaluation of Endocrine Dysfunction/Laboratory Assessment Most patients will have dysfunction of one or more pituitary hor- mones at the time of initial presentation. The most clinically important hormone deficiency is adrenocorticotrophic hormone (ACTH), which can be life-threatening. It is present in 50–80% of patients and can cause hemodynamic instability and hyponatre- mia. Of note, hyponatremia is a consequence of cortisol deficiency, with loss of feedback inhibition of arginine vasopressin/antidi- uretic hormone (ADH) release despite hypoosmolality and a direct water excretion defect. Additionally, hypothalamic irritation in the setting of PA can result in the syndrome of inappropriate antidi- uretic hormone. Nausea/vomiting and hypoglycemia (secondary to GH and/or ACTH deficiency) are also stimuli for ADH secretion. Secondary hypothyroidism can also contribute to hyponatremia. Patients with suspected PA should have electrolytes, renal function, kidney function, coagulation, and CBC checked to assess for risk factors and for the general condition of the patient. 1 Pituitary Apoplexy 5 Pituitary endocrine evaluation is necessary to diagnose secretory pituitary adenomas as well as hypopituitarism. An initial random cortisol, ACTH, LH, FSH, testosterone or estradiol, FT4, TSH, IGF-1, and prolactin should be measured immediately upon the diagnosis of PA to screen for a hyperfunctioning pituitary ade- noma. Low serum prolactin at presentation is seen in patients with the highest intrasellar pressure, who are less likely to recover pituitary function. It is important to emphasize that blood sam- |
ples for ACTH and cortisol measurements should be obtained prior to the administration of steroids. The hypothalamic-pitu- itary-adrenal axis usually responds to critical illness with an increase in serum cortisol levels, and it is expected that a random cortisol level will similarly be elevated during the acute phase of PA without hypopituitarism. There is no clearly agreed-upon cut- off for random cortisol levels for the diagnosis of adrenal insuf- ficiency during the acute phase of PA, but studies have shown that in patients with PA and proven central adrenal insufficiency, cortisol levels are very low. Approximately 40–70% of patients with PA have thyrotropin or gonadotropin deficiency. Hormone replacement of these defi- ciencies can begin when the patient has recovered from the acute illness. GH deficiency is seen in almost all patients but is not always tested or treated. Diabetes insipidus is present in less than 5% of patients with PA and may be further masked by the development of secondary adrenal failure and/or hypothyroidism. Imaging CT is usually the initial imaging modality performed for patients with sudden onset of headache. CT is useful to rule out subarach- noid hemorrhage and can detect a sellar mass in up to 80% of cases. In 20–30% of cases, the CT scan will detect hemorrhage into the pituitary mass, confirming the diagnosis of PA. Magnetic resonance imaging (MRI) is the imaging procedure of choice and has been found to identify an underlying tumor, if present, in over 90% of the cases. Therefore, MRI is more sensitive for the diag- nosis of PA and should be done in all patients with suspected 6 A. P. Abreu and U. B. Kaiser PA. MRI can detect hemorrhagic and necrotic areas and can show the relationship between a tumor and adjacent structures such as the optic chiasm, cavernous sinus, and hypothalamus (Fig. 1.1). However, conventional MRI sequences may not detect an infarct a b c d Fig. 1.1 MRI of a patient with pituitary apoplexy. Images were obtained approximately 24 hours after onset of symptoms (sudden headache, nausea, vomiting, and fatigue). Images show enlargement of the pituitary gland, which contains a fluid hematocrit level. (a) T1 sagittal, the upper margin of the pituitary gland is contacting and slightly displacing the optic chiasm supe- riorly. (b) Axial pre-contrast. (c) T1 axial post gadolinium. (d) T2 axial 1 Pituitary Apoplexy 7 for up to 6 hours after the acute event. Diffusion-weighted imag- ing (DWI) is a commonly performed MRI sequence for the detec- tion of small infarcts and initial hemorrhage and can be very helpful in the early phases of PA. Thickening of the sphenoid mucosa in the sphenoid sinus beneath the sella turcica has been reported during the acute phase of PA and corresponds with marked mucosal swelling from increased pressure in the venous sinuses draining the sinus area. Such mucosal thickening has been shown to correlate with worse neurological and endocrinological outcomes. Management Patients with PA should be managed by neurosurgeons and endo- crinologists in a hospital with an acute care neurosurgical unit available and with access to ophthalmological evaluation. Consider Initiation of Corticosteroid Treatment PA can be a true medical emergency. The course of PA is variable and management will depend on a patient’s clinical condition. The first intervention is hemodynamic stabilization and correction of electrolyte disturbances. As corticotropin deficiency is present in the vast majority of patients and may be life-threatening, corti- costeroids should be administered intravenously as soon as the diagnosis is confirmed and blood is collected for cortisol and ACTH measurement. A bolus of 100 mg (some studies recom- mend 200 mg) of hydrocortisone followed by 50–100 mg IV every 6–8 hours is given; alternatively, 2–4 mg/h by continuous administration should be given. There are no randomized trials comparing different doses, so the ideal dose of hydrocortisone administration is not known. Dexamethasone may be used instead of hydrocortisone to reduce edema as a part of a conservative approach for treatment of PA. Although the majority of the litera- ture recommends empiric corticosteroid treatment for all patients with diagnosis of PA, the UK guidelines for the management of 8 A. P. Abreu and U. B. Kaiser pituitary apoplexy recommend steroid therapy in patients with hemodynamic instability, altered level of consciousness, reduced visual acuity, and severe visual field defects, or if a 9:00 am corti- sol is less than 18 mcg/dL. Acute Intervention: Surgery vs. Conservative Treatment Most cases of PA improve with either surgical or expectant man- agement, but the most appropriate approach in the acute phase is controversial. Studies comparing the two modalities are retro- spective and suffer from selection bias. The ideal surgical treat- ment is via the transsphenoidal approach. One important factor to consider is the risk of surgery, and in the acute setting, the opera- tion may be performed by the on-call neurosurgeon rather than by skilled pituitary surgeons; this may increase the risk of complica- tions. Studies suggest that the posttreatment prevalence of pitu- itary deficiency is similar after either treatment modality. The endocrine prognosis is poorer in patients with pituitary adenoma and PA than in uncomplicated pituitary adenoma, as pituitary damage more commonly occurs during the acute apoplectic event. Studies suggest that visual field defects improve or normalize in most patients regardless of the treatment modality. However, it is the general consensus – and is the recommendation by the UK guidelines for the management of PA – to consider surgical treat- ment in patients with severe neuro-ophthalmologic signs such as severely reduced visual acuity or severe and persistent or deterio- rating visual field defects. A deteriorating level of consciousness is also an indication for surgical treatment. Studies suggest, although one should keep selection bias in mind, that patients treated conservatively have better outcomes with regard to ocular palsies. Resolution of ocular paresis resulting from involvement of cranial nerve III, IV, or VI is usually seen within days to weeks, and it is not an indication for surgery. Surgery should be per- formed within 7 days of the onset of the symptoms. One study showed that the prognosis of visual defects is less favorable when surgery is done more than a week after onset. A Pituitary Apoplexy 1 Pituitary Apoplexy 9 Table 1.1 Pituitary Apoplexy Score Variable Points Level of consciousness Glasgow Coma Scale 15 0 Glasgow Coma Scale 8–14 2 Glasgow Coma Scale <8 4 Visual acuity Normal 0 Reduced unilateral 1 Reduced bilateral 2 Visual field defects Normal 0 Unilateral defect 1 Bilateral defect 2 Ocular paresis Absent 0 Present unilateral 1 Present bilateral 2 Reprinted with permission from Rajasekaran S, Vanderpump M, Baldeweg S, et al. UK guidelines for the management of pituitary apoplexy. Clin Endocri- nol;74(1):9–20, © 2011, with permission from John Wiley and Sons Score (see Table 1.1) was designed by the UK guidelines for the management of PA to enable more uniform clinical description of PA and enable better comparison between different management options. It is rare to change from conservative treatment to an opera- tive course, but urgent imaging should be done in the presence of a new or deteriorating visual field deficit or neurological dete- rioration. Reduction in tumor size is frequent after apoplexy, and follow- up imaging can show empty sella, partially empty sella, or even normal pituitary. The tumor recurrence rate is similar with both treatment modalities, and it has been shown to be approximately 6%. Therefore, long-term surveillance is recommended. Patients with simple infarction on MRI typically have less severe clinical features and better outcomes than those with hemorrhage or hem- orrhagic infarction. 10 A. P. Abreu and U. B. Kaiser Postoperative Care Postoperative management of patients following surgery for PA is similar to that of elective pituitary surgery for pituitary tumors. In some cases, patients may not have had a complete evaluation prior to surgery, and the pituitary function status will not be known. An early postoperative CT or sellar MRI should be performed in any patient with a new or worsened neurological deficit such as visual deterioration or diplopia and in anyone with significant rhinorrhea and a suspected CSF leak. Monitor for Signs and Laboratory Abnormalities Suggestive of Diabetes Insipidus (DI) Alterations in sodium and fluid balance are relatively common in the early postoperative phase. The classic reported triphasic response, in which patients initially develop DI in the first 24 to 48 hours, followed by transient SIADH developing 4–10 days postoperatively, followed by the return of DI in a matter of weeks, is not the most common pattern seen postpituitary surgery but can occur. More often, patients present with DI within the first days postsurgery and then either recover completely or develop SIADH about 5 days postsurgery or later. Fluid balance, serum electro- lytes, urea, creatinine, and plasma and urine osmolality should be monitored closely during the first week postsurgery. During the first 2 days after surgery, fluid balance, electrolytes, and urine and serum osmolality should be checked every 8–12 hours; thereafter, further monitoring will depend on the patient’s clinical status. DI is present in about 5% of the patients after PA but can be seen in up to 25% of patients undergoing transsphenoidal pitu- itary surgery. In most cases, the patients may develop transient DI but do not require any therapy. They should be allowed to drink to thirst and their serum sodium should be monitored closely. When treatment is needed, desmopressin (DDAVP) should be given sub- 1 Pituitary Apoplexy 11 cutaneously or intravenously (0.5–2 mcg every 24 hours as needed), or alternatively, an oral formulation can be given (often starting with 0.1–0.2 mg orally as a single evening dose, with doses up to 0.3 mg orally three times daily sometimes needed). Intranasal DDAVP is not generally used acutely in patients who have undergone transsphenoidal surgery until after the nose has healed and nasal congestion has improved. SIADH, when it occurs, usually presents 4 to 10 days postoperatively and can often be treated with fluid restriction and close monitoring. Assess Pituitary Reserve As discussed above, most of the patients will receive corticoste- roid treatment during the acute phase of PA. The dose should be tapered to replacement doses when the patient is clinically stable. In patients without a previous diagnosis of adrenal insufficiency, a morning fasting cortisol should be checked on day 2 or 3 after surgery to assess residual postpituitary infarction and post-steroid treatment reserve after the acute event of PA and postoperatively. Hydrocortisone should be held for at least 24 hours prior to mea- suring cortisol levels. In patients with known and documented cortisol deficiency before surgery, a morning cortisol level should be checked within 4 to 8 weeks to determine if they will need long-term steroid treatment. TSH and free T4 (FT4) should be checked on day 3 or 4 post- operatively, and thyroid hormone replacement should be consid- ered if deficient. The interpretation of thyroid function tests postsurgically should be careful as “sick euthyroid syndrome” can alter TSH and FT4 hormone levels and affect the interpretation of these tests. Thyroid deficiency may take several weeks to be diag- nosed given thyroid gland reserve and the half-life of T4, so thy- roid function can be normal in the immediate postoperative period; hence it is important to test it again ~4–8 weeks postop- eratively or if symptoms of hypothyroidism develop. 12 A. P. Abreu and U. B. Kaiser Visual Assessment Visual fields, eye movements, and visual acuity should be exam- ined at the bedside as soon as the patient can cooperate with the examination, ideally within 48 hours. A formal visual field assess- ment using a Humphrey analyzer or Goldmann perimetry should be performed within a few weeks after the acute event. Follow-Up After Discharge Check Electrolytes After 1 Week Patients should be seen in follow-up within 1 week of surgery to have sodium, thyroid function, ACTH, morning cortisol, and urine osmolality tested. As discussed earlier, patients may develop SIADH up to 10 days after surgery or after PA and should be monitored closely. Reassess Pituitary Function After 4 to 8 Weeks Hypopituitarism (discussed separately) is one of the complica- tions of PA and may not be detected during the acute phase of PA. Thyroid deficiency may take several weeks to be diagnosed given thyroid gland reserve and T4 half-life. All patients should be seen 4–8 weeks after presenting with PA for |
evaluation of pitu- itary function. On the other hand, some pituitary hormonal defi- ciencies may recover postoperatively, and such recovery can also be assessed as part of this evaluation. Studies have shown partial or complete recovery of pituitary function in up to 50% of patients. In most cases, patients will be treated with glucocorticoids during the acute episode of PA; the long-term need for glucocorticoid replacement therapy should be determined at this time. Thyroid, adrenal, gonadal, and GH axes may be assessed at this visit. Patients should also have formal visual field, visual acuity, and eye movement assessment. 1 Pituitary Apoplexy 13 Patients treated for apoplexy should have at least annual bio- chemical assessment of pituitary function, which should usually include FT4, TSH, LH, FSH, testosterone in men, estradiol in women, prolactin, IGF-1, and dynamic tests of cortisol and growth hormone secretion if clinically appropriate. Suggested Reading Bonicki W, Kasperlik-Zaluska A, Koszewski W, Zgliczynski W, Wislawski J. Pituitary apoplexy: endocrine, surgical and oncological emergency. Incidence, clinical course and treatment with reference to 799 cases of pituitary adenomas. Acta Neurochir. 1993;120(3–4):118–22. Briet C, Salenave S, Bonneville JF, Laws ER, Chanson P. Pituitary apoplexy. Endocr Rev. 2015;36(6):622–45. https://doi.org/10.1210/er.2015-1042. Briet C, Salenave S, Chanson P. Pituitary apoplexy. Endocrinol Metab Clin N Am. 2015;44:199–209. Loh JA, Verbalis JG. Diabetes insipidus as a complication after pituitary sur- gery. Nat Clin Pract Endocrinol Metab. 2007;3(6):489–94. Rajasekaran S, Vanderpump M, Baldeweg S, et al. UK guidelines for the management of pituitary apoplexy. Clin Endocrinol. 2011;74:9–20. Randeva HS, Schoebel J, Byrne J, Esiri M, Adams CB, Wass JA. Classical pituitary apoplexy: clinical features, management and outcome. Clin Endocrinol. 1999;51:181–8. Semple PL, Jane JA Jr, Laws ER Jr. Clinical relevance of precipitating factors in pituitary apoplexy. Neurosurgery. 2007;61:956–61; discussion 61-2. Sibal L, Ball SG, Connolly V, et al. Pituitary apoplexy: a review of clinical presentation, management and outcome in 45 cases. Pituitary. 2004;7:157–63. Panhypopituitarism 2 Ana Paula Abreu and Ursula B. Kaiser Contents Definition and Significance . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16 Identify Causes of Hypopituitarism . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16 Mass Lesions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16 Traumatic Brain Injury . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18 Medications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18 Hypophysitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18 Systemic Diseases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20 Genetic Causes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20 Vascular . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21 Diagnosis of Hypopituitarism in the Hospital . . . . . . . . . . . . . . . . . . . . 21 Assess Anterior Pituitary Function . . . . . . . . . . . . . . . . . . . . . . . . . . 21 Assess Posterior Pituitary Function . . . . . . . . . . . . . . . . . . . . . . . . . . 24 Imaging . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24 Management of Hypopituitarism in the Hospital . . . . . . . . . . . . . . . . . . 25 Management of Hypopituitarism at the Time of Discharge . . . . . . . . . . 26 Suggested Reading . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26 A. P. Abreu (*) · U. B. Kaiser Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA e-mail: apabreu@bwh.harvard.edu; ukaiser@bwh.harvard.edu © Springer Nature Switzerland AG 2020 15 R. K. Garg et al. (eds.), Handbook of Inpatient Endocrinology, https://doi.org/10.1007/978-3-030-38976-5_2 16 A. P. Abreu and U. B. Kaiser Definition and Significance Hypopituitarism is the inability of the pituitary gland to provide sufficient hormones for the needs of the individual. It is the result of the failure in either the production or secretion in one or more pituitary hormones. The diagnosis of hypopituitarism is important in the hospital because some hormone deficiencies, such as ACTH, pose significant risk to the patient’s life and need to be treated. Also, it is crucial to diagnose and treat diabetes insipidus as it can cause hypernatremia, severe dehydration, coma, and death. The diagnosis of central hypothyroidism is challenging in the hospital, but thyroid hormone should be replaced in patients with secondary hypothyroidism. On the other hand, other pitu- itary hormone deficiencies do not pose acute risk to patient’s life, and replacement may be postponed to the outpatient setting. Identify Causes of Hypopituitarism A high diagnostic suspicion is necessary to identify patients not previously diagnosed with hypopituitarism. Therefore, it is impor- tant to know what causes hypopituitarism in order to detect it (Table 2.1). Insults in the regulation, production, or secretion of any pituitary hormones can result in pituitary insufficiency. Physiological secretion of pituitary hormones relies on intact function of the hypothalamus. Mass Lesions Any structural disruption of the hypothalamic-pituitary region can cause decreased production or secretion of the hormones. Pituitary tumors are the most common cause of hypopituitarism, but any other tumor occupying the region can also cause pituitary dysfunc- tion (Table 2.1). Mechanical compression of portal vessels and the 2 Panhypopituitarism 17 Table 2.1 Causes of hypopituitarism Structural causes: Mass lesions Pituitary adenoma Craniopharyngioma Rathke’s cleft cyst Metastatic disease Lymphomas, germinomas, and other tumors Infiltrative diseases Hypophysitis (lymphocytic and others) Sarcoidosis Hemochromatosis Tuberculosis and other infections Syphilis Vascular events Pituitary apoplexy Sheehan’s syndrome (infarction of the pituitary gland after postpartum hemorrhage) Intra-sellar carotid artery aneurysm Traumatic injury Traumatic brain injury Perinatal trauma Neurosurgery Radiation Functional causes: Medications Glucocorticoids Megestrol acetate Immunotherapy – CTLA-4 inhibitors/PDL1 antibodies Opioids GnRH agonists Systemic diseases Chronic illness Anorexia nervosa Developmental and Several genetic defects can cause isolated or inherited genetic causes combined pituitary deficiency pituitary stalk, with resulting ischemic necrosis, is thought to be the predominant mechanism by which mass lesions cause hypo- pituitarism. Hyperprolactinemia in non-prolactin producing tumors is common with pituitary macroadenomas, given the dis- ruption of the normal suppressive effects of dopamine from the hypothalamus. https://www.facebook.com/groups/2202763316616203 18 A. P. Abreu and U. B. Kaiser Traumatic Brain Injury This is an underestimated cause that can cause hypopituitarism even years after the trauma. Given the frequency of traumatic brain injury in the general population, it is important not to over- look this important cause of hypopituitarism. Medications Several medications can cause hypopituitarism. Chronic use of systemic corticosteroids inhibits the hypothalamic-pituitary- adrenal axis and is a common cause of central adrenal insuffi- ciency. This is very relevant for patients admitted to the hospital for acute disorders or for procedures, as they will need to receive higher doses of steroids (usually called stress doses of steroids) to compensate for the lack of an endogenous increase in the amount of cortisol production during stress. Chronic administration of some opioids such as fentanyl and hydromorphone has the poten- tial to cause secondary adrenal insufficiency as well as secondary hypogonadism. Immunotherapy causes hypopituitarism second- ary to hypophysitis that is discussed below. Hypophysitis Autoimmune hypophysitis and medication-induced hypophysitis can cause pituitary deficiency. Lymphocytic hypophysitis is more common in females, and more than half of the cases (57%) pres- ent during pregnancy or postpartum. Immunotherapy, used to treat melanoma, renal cell carcinoma, and other malignancies, can also cause hypophysitis. The pathophysiology and clinical pre- sentation of immunotherapy-induced hypophysitis are different from those of lymphocytic hypophysitis. The monoclonal anti- bodies, ipilimumab and tremelimumab, which bind and inhibit cytotoxic T-lymphocyte antigen-4 (CTLA-4), are reported to cause hypophysitis in 1–18% of treated patients. Most cases are caused by ipilimumab. The anti-programmed cell death protein 2 Panhypopituitarism 19 antibodies (anti-PD-1 Abs), nivolumab and pembrolizumab, rarely cause hypophysitis. Patients with hypophysitis present with headache, pituitary enlargement, and hypopituitarism (Fig. 2.1). In most patients, the pituitary enlargement eventually resolves, a b c d Fig. 2.1 MRI of a patient with lymphocytic hypophysitis. A pregnant woman presented to the emergency room at 30 weeks of gestational age with a 2-week history of worsening headaches and blurred vision in the last 24 hours: (a) coronal and (b) sagittal images without contrast showing enlargement of the pituitary gland, which measures approximately 1.4 cm in craniocaudal dimension. The gland has a convex superior border and is protruding into the suprasellar cistern. Since patient was pregnant, no contrast was given. Coro- nal images 3 months after the initial images and 1 month postpartum: (c) pre-gadolinium and (d) post-gadolinium. Images show interval decrease in size of anterior pituitary, which is no longer enlarged and now measures approximately 6 to 7 mm and demonstrates a flat superior surface 20 A. P. Abreu and U. B. Kaiser but hypopituitarism is usually permanent. The most common hor- mone deficiency in classical autoimmune lymphocytic hypophysi- tis is ACTH deficiency, seen in approximately 32% of the patients. Eighteen percent present with hyperprolactinemia and 31% develop diabetes insipidus. In anti-CTLA-4-induced hypophysitis, around 85% of the patients presented thyrotroph and gonadotroph deficiency, while 73% had corticotroph deficiency. In these cases, pituitary function recovered in approximately 25% of cases only. Systemic Diseases Infiltrative systemic diseases such as sarcoidosis, hemochromato- sis, and rarely infiltrative infections such as tuberculosis can cause hypopituitarism. Neurosarcoidosis typically presents with DI. Systemic diseases can also cause functional hypopituitarism, but the significance of the disruption of pituitary function in this context is not always completely understood. Functional hypopi- tuitarism in some cases is thought to be an appropriate response of the organism to insults. It is important to understand that some hormonal changes seen in admitted patients do not require treat- ment. One example frequently seen in the hospital is euthyroid sick syndrome, in which critically ill patients have functional sec- ondary hypothyroidism with low TSH, T4, and T3 levels. Based on current knowledge, there is no indication for thyroid hormone replacement in these patients, and the thyroid hormone levels nor- malize when they recover from the acute phase of their illness. Chronically ill and malnourished patients frequently have central hypogonadism that also does not require treatment in the acute setting. For these reasons, it is not |
useful to measure gonadal and thyroid function in acutely ill patients. Similarly, the growth hor- mone axis is not assessed in hospitalized patients. Genetic Causes Mutations in several genes involved in pituitary development and differentiation, and hormone production and secretion are 2 Panhypopituitarism 21 associated with isolated or combined pituitary hormone defi- ciency. Genetic defects in genes associated with pituitary gland development can also cause pituitary hypoplasia, aplasia, or other midline defects. Most of these patients have a known diagnosis of hypopituitarism upon admission to the hospital. Vascular Vascular events, including pituitary apoplexy and Sheehan’s syn- drome as discussed elsewhere, can also disrupt pituitary function. Diagnosis of Hypopituitarism in the Hospital The clinical manifestations of hypopituitarism can vary greatly depending on the axis affected, age, gender, and clinical status of the patient. Symptoms of hypopituitarism in acutely ill patients can be particularly challenging to recognize, given the masking of some subtle symptoms by other complications. Assess Anterior Pituitary Function Adrenal Axis As stated above, central adrenal insufficiency must not be missed in a hospitalized patient given the risk that it poses to the patient’s life. Patients with adrenal insufficiency may have longstanding nonspecific symptoms. In comparison with primary adrenal insuf- ficiency, patients with central adrenal insufficiency have relative sparing of aldosterone secretion due to the preservation of renin and angiotensin control of aldosterone production. With this resid- ual aldosterone production, severe hypotension and hyperkalemia are less common. Nonetheless, they can still present with hemody- namic instability despite adequate fluid resuscitation, most often associated with a hyperdynamic circulation and decreased systemic vascular resistance. This is an important diagnostic clue and should trigger investigation for adrenal insufficiency. 22 A. P. Abreu and U. B. Kaiser The combined occurrence of hypoglycemia, hyponatremia, and eosinophilia should alert the clinician to the possibility of hypoad- renalism. Patients with central adrenal insufficiency do not have the characteristic hyperpigmentation that classically occurs in patients with primary adrenal insufficiency, resulting from accu- mulation of proopiomelanocortin (POMC). The diagnosis of adrenal insufficiency in the hospitalized patients is challenging not only because of the lack of specific symptoms or clinical signs but also due to the difficulties estab- lishing cutoff values for cortisol levels in acutely ill patients. Expected cortisol levels vary with the type and severity of disease, making it difficult to define normal ranges. Patients admitted to the hospital do not have the classical circadian rhythms with higher cortisol levels early in the morning and lower levels at night. Many threshold levels have been proposed for the definition of an insufficient cortisol level (measured at any time of day) dur- ing acute illness, but none is entirely satisfactory. In critically ill patients, cortisol levels are usually elevated, and a serum cortisol value of ≥18 mcg/dL (497 nmol/L) effectively rules out adrenal insufficiency. Patients with central adrenal insufficiency have low cortisol levels with inappropriately normal or low ACTH levels. Given the lack of a cutoff value for random cortisol levels, an ACTH stimulation test can be performed to confirm the diagnosis of adrenal insufficiency if basal levels are equivocal. Cosyntropin, a synthetic ACTH corresponding to amino acids 1–24 of ACTH that has full biologic potency, is used to evaluate the capacity of the adrenal gland to produce cortisol. The ACTH stimulation or cosyntropin test consists of measuring serum cortisol immedi- ately before and 30 and 60 minutes after intravenous or intramus- cular injection of 250 mcg (85 nmol or 40 international units) of cosyntropin. Serum cortisol concentration ≥18 to 20 mcg/dL (500 to 550 nmol/L) after the injection indicates normal adrenal func- tion. It is important to highlight that patients with new onset of central adrenal insufficiency may have an appropriate response to cosyntropin stimulation because the adrenal gland will respond to an ACTH stimulus normally. Therefore, a normal response to 2 Panhypopituitarism 23 cosyntropin test does not rule out central adrenal insufficiency, and physicians will have to rely on basal cortisol and ACTH levels and clinical judgment. Patients with adrenal atrophy resulting from chronically low stimulation by endogenous ACTH will have an abnormal response in the cosyntropin test. It is also important to note that hydrocortisone, prednisone, and several other corticosteroids cross-react with the assays used to measure cortisol and interfere with the assay results. Dexamethasone is not measured by the cortisol assays, but it is a strong inhibitor of the hypothalamic-pituitary axis and has a bio- logical effect for almost 54 hours. For these reasons, cortisol lev- els should be interpreted with caution in patients who are currently receiving or recently received corticosteroids. Thyroid Axis As discussed above, the diagnosis of central hypothyroidism is challenging in the hospital, but thyroid hormone should be replaced in patients with secondary hypothyroidism in the hospi- tal. If there is a clinical suspicion of pituitary dysfunction, TSH and FT4 should be measured. Patients with central hypothyroid- ism have low FT4 levels combined with inappropriately normal TSH levels. While this scenario can be seen in patients with “sick euthyroid syndrome,” the presence of any known cause of hypo- pituitarism (see Table 2.1) would corroborate the diagnosis of central hypothyroidism. Other Axes Growth hormone and gonadotropin deficiencies usually do not pose risk to the patient’s life, and thus there is usually no indica- tion for testing these axes in hospitalized patients. Prolactin mea- surement can help diagnosing hypophysitis, as the levels can be low in this condition. All individuals with mechanical compres- sion of the pituitary stalk can present with elevated prolactin lev- els; however, levels above 100 ng/dL are more suggestive of a prolactinoma. It is also important to keep in mind that several medications can increase prolactin levels. 24 A. P. Abreu and U. B. Kaiser Assess Posterior Pituitary Function Patients with central DI are unable to concentrate urine. The diag- nosis is particularly challenging in the hospital when patients fre- quently receive significant amounts of intravenous fluids for resuscitation and have increased volumes of dilute urine when fluid is being redistributed. True hypernatremia (plasma sodium concentration greater than 150 meq/L) is rare in adults with DI and no cognitive impairment, because the initial loss of water stimulates thirst, resulting in an increase in fluid intake to match the urinary losses. However, debilitated patients may not have free access to water, and some patients may have impaired thirst mechanisms. In this setting, the plasma sodium concentration can be elevated. Elevated serum sodium associated with low urine osmolality, particularly when urine osmolality is less than the plasma osmolality, is indicative of DI. The response to DDAVP treatment will differentiate between central and nephrogenic DI. Imaging Unless the patient has an unequivocal cause for a specific hor- monal deficiency, patients should have imaging of the hypothalamic- pituitary region. Pituitary adenomas do not usually cause diabetes insipidus; this is usually caused by suprasellar lesions. Pituitary microadenomas do not usually cause hypopitu- itarism. Empty sella is a radiological term. It can be seen in asso- ciation with pituitary hypoplasia/aplasia or can be a consequence of a previous insult to the pituitary gland such as apoplexy or hypophysitis. However, it can also be seen in patients with normal pituitary function. Absence of the posterior white spot may have no clinical significance or may be secondary to absence of ADH storage in the posterior hypophysis in patients with diabetes insip- idus. Hypophysitis can present as enlargement of the pituitary gland and thickening of the stalk. However, normal imaging of the pituitary does not rule out hypophysitis. 2 Panhypopituitarism 25 Management of Hypopituitarism in the Hospital Patients with a known diagnosis of hypopituitarism should continue their hormone replacement when admitted to the hospital, but some adjustments to the therapy are frequently necessary. The most important treatment is corticosteroid therapy. Critically ill patients should receive stress dose steroids. A bolus of 100 mg of hydrocortisone followed by 50–100 mg IV every 6–8 hours is given; alternatively, 2–4 mg/h by continuous admin- istration should be given. Dose should be tapered down to main- tenance oral dose as the clinical condition improves. Patients undergoing surgical procedures or immobilized patients at higher risk of deep venous thrombosis should discon- tinue estrogen therapy. Growth hormone and testosterone therapy are often discontinued during hospitalization, depending on spe- cific situations. Thyroid replacement should be given to patients in the hospital, and special attention should be given to patients on enteral diets, given the need for it to be taken on an empty stom- ach for proper absorption. Patients with significant edema may have impaired absorption, and patients with proteinuria have increased wasting of thyroid hormones and may need adjustments in their dose of levothyroxine. Patients on DDVAP treatment should receive it while in the hospital and should be carefully monitored. Mental status alterations due to anesthesia or current disease can affect the thirst mechanism and interfere with appro- priate water intake, requiring adjustment of the DDAVP dose. Patients are often NPO or have nasal tubes, and the DDAVP route of administration may need to be adjusted. If DDAVP cannot be administered intranasally or orally, it can be given subcutaneously or intravenously. A usual antidiuretic dose is 0.5 to 2 mcg admin- istered subcutaneously or intravenously; the duration of action, as judged by increased urine osmolality, will be 12 hours or more. Some patients do not respond well to subcutaneous DDAVP due to inadequate absorption. 26 A. P. Abreu and U. B. Kaiser Management of Hypopituitarism at the Time of Discharge Patients with hypopituitarism should be discharged on hormone replacement therapy. Patients on stress doses of steroids should be tapered to a replacement dose (around 3–4 mg of prednisone or 15 mg of hydrocortisone daily) as soon as they are clinically sta- ble. Those with a new diagnosis of hormone deficiency should be reevaluated for the need of replacement therapy. If the diagnosis of hypopituitarism was made in an acute setting, after brain trauma or surgery, for example, patients may recover pituitary function and may not need long-term replacement or may need adjustment of dose of hormonal replacement. The appropriate time for post-discharge follow-up will depend on the specific hor- monal deficiency and the cause of hypopituitarism. A follow-up visit 6 weeks after discharge to evaluate pituitary status may be ideal in most cases. Suggested Reading Benvenga S, Campenni A, Ruggeri RM, Trimarchi F. Clinical review 113: Hypopituitarism secondary to head trauma. J Clin Endocrinol Metabol. 2000;85:1353–61. Caturegli P, Newschaffer C, Olivi A, Pomper MG, Burger PC, Rose NR. Autoimmune hypophysitis. Endocr Rev. 2005;26:599–614. Schneider HJ, Aimaretti G, Kreitschmann-Andermahr I, Stalla GK, Ghigo E. Hypopituitarism. Lancet. 2007;369:1461–70. Thodou E, Asa SL, Kontogeorgos G, Kovacs K, Horvath E, Ezzat S. Clinical case seminar: lymphocytic hypophysitis: clinicopathological findings. J Clin Endocrinol Metabol. 1995;80:2302–11. Postoperative Management 3 After Pituitary Surgery Anna Zelfond Feldman and Pamela Hartzband Contents Assess Hormone Status Before Surgery if Possible . . . . . . . . . . . . . . . . 28 Intraoperative/Postoperative Steroids . . . . . . . . . . . . . . . . . . . . . . . . . . . 28 Patient with Unknown Adrenal Function Prior to Surgery . . . . . . . . . 28 Patients Known to Have Preexisting Adrenal Insufficiency . . . . . . . . 29 Patients Known to Have Normal Adrenal Function Preoperatively and Patients with Cushing’s Disease . . . . . . . . . . . . . . . . . . . . . . . 29 Diabetes Insipidus/Sodium Management . . . . . . . . . . . . . . . . . . . . . . . . 30 Arrange Endocrine Follow-Up Within 1–2 Weeks of Discharge . . . . . . 31 Suggested Reading . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 32 A. Z. Feldman (*) Harvard Medical School, Beth Israel Deaconess Medical Center, Department of Endocrinology, Boston, MA, USA e-mail: afeldma1@bidmc.harvard.edu P. Hartzband Harvard Medical School, Beth Israel Deaconess Medical Center, Department of Endocrinology and Metabolism, Boston, MA, USA e-mail: phartzba@bidmc.harvard.edu © Springer Nature Switzerland AG 2020 27 R. |
K. Garg et al. (eds.), Handbook of Inpatient Endocrinology, https://doi.org/10.1007/978-3-030-38976-5_3 28 A. Z. Feldman and P. Hartzband Assess Hormone Status Before Surgery if Possible – Ideally patient should be seen by endocrinology as outpatient prior to surgery. Intraoperative/Postoperative Steroids Patient with Unknown Adrenal Function Prior to Surgery – Day of surgery (pre- or intra-op): Hydrocortisone 100 mg IV q 8 h (alternative methylprednisolone 60 mg IV × 1). – POD 1: Hydrocortisone 100 mg IV × 1 at 8 am and hydrocor- tisone 50 mg IV × 1 at 4 pm (alternative methylprednisolone 30 mg IV × 1), and then hold steroids. – POD 2: Draw 8 am fasting cortisol level. After blood is drawn (while results pending), give hydrocortisone 50 mg IV q 12 h (alternative methylprednisolone 20 mg IV × 1). – POD 3: If a.m. cortisol drawn on POD 2 is >/= 10, stop steroids. If a.m. cortisol drawn on POD 2 is <10 (or results pending, or patient received steroids within 12 hours prior to cortisol assessment), start oral hydrocortisone 15 mg morning and 5 mg afternoon (alternative prednisone 5 mg morning). Higher doses of steroids may be needed depending on clinical status. – Discharge: Discharge patient on hydrocortisone or prednisone if indicated as above. – Additional outpatient assessment of HPA axis should be done in approximately 2 weeks at endocrine follow-up. 3 Postoperative Management After Pituitary Surgery 29 Patients Known to Have Preexisting Adrenal Insufficiency – Day of surgery (pre-op): hydrocortisone 100 mg IV q 8 h (alternative methylprednisolone 60 mg IV × 1). – POD 1: Hydrocortisone 50 mg IV × q 8 h (alternative methyl- prednisolone 30 mg IV × 1). – POD 2: Hydrocortisone 50 mg IV q 12 h (alternative methyl- prednisolone 20 mg IV × 1). – POD 3: Start oral hydrocortisone 15 mg morning and 5 mg afternoon (alternative prednisone 5 mg morning). Higher doses of steroids may be needed depending on clinical status. – Discharge: No assessment of adrenal function in the hospital; patient should be discharged on steroids as above. Patients Known to Have Normal Adrenal Function Preoperatively and Patients with Cushing’s Disease – Day of surgery: Do not give pre-, peri-, or postoperative glucocorticoids. – Monitor patient closely for adrenal insufficiency. – POD 1: Check 8 a.m. fasting cortisol. After blood is drawn (while results pending), give hydrocortisone 50 mg IV × q 8 h (alternative methylprednisolone 30 mg IV × 1). – POD 2: If a.m. cortisol drawn on POD 2 is >/= 10, stop steroids. If a.m. cortisol drawn on POD 2 is <10 (or results pending or patient received steroids within 12 hours prior to cortisol assessment), give hydrocortisone 50 mg IV q 12 hours (alter- native methylprednisolone 20 mg IV × 1). 30 A. Z. Feldman and P. Hartzband – POD 3: If patient still on steroids: Start oral hydrocortisone 15 mg morning and 5 mg afternoon (alternative prednisone 5 mg morning). Higher doses of steroids may be needed depending on clinical status. – Discharge: Endocrinologist to follow up 8 a.m. cortisol drawn on POD1 prior to discharge and decide on steroid management. Diabetes Insipidus/Sodium Management – Day of surgery: Check serum Na and urine osmolality or spe- cific gravity post-op. – POD 1–2: Check serum Na and urine osmolality or specific gravity bid. Increase frequency if clinically indicated. Reduce to daily if clinically stable. – Strict ins/outs with special attention to urine output (UOP): Urine output should be measured hourly (if cathe- ter) or Q 2 hours (if no catheter) postoperatively. – If UOP is >250 cc/h × 2 or more hours: Send serum Na and urine osmolality or specific gravity. – If labs consistent with DI with Na >145 with urine specific gravity <1.005 or osmolality <300: – Give DDAVP 1 mcg IV × 1. – If patient getting NS IVF, change IVF to one-half NS (alter- native D5W). – Monitor serum Na, urine osmolality, or specific gravity q 4–6 hours until either DI resolves or Na normalizes and is stable, and then decrease frequency of labs. – Repeated doses of DDAVP IV may be needed. However, DI post-transsphenoidal surgery is often transient. If DI is per- sistent, patient may need oral daily, BID, or rarely TID doses of DDAVP. Intranasal DDAVP is contraindicated in the immediate postoperative period. 3 Postoperative Management After Pituitary Surgery 31 – If discordant labs with Na >145 with urine specific gravity >1.005 or osmolality >300 or Na normal with urine specific gravity <1.005 or osmolality <300: – Monitor closely, but DDAVP is not necessarily indicated. – Clinical judgment must be used in these cases about DDAVP administration. – Discontinue IVF as quickly as possible and allow patient to drink to thirst. – If thirst mechanism is not intact, match PO intake to urine output. – Discharge: If DI is persistent and patient is discharged on oral DDAVP, a serum Na level should be checked within 1–2 days of discharge, as some patients will develop transient syndrome of inappropriate diuretic hormone secretion (SIADH). – These patients need close follow-up postoperatively, ideally within 1 week of discharge. Arrange Endocrine Follow-Up Within 1–2 Weeks of Discharge – Order 8 a.m. cortisol and Na to be done fasting 1–2 days prior to endocrine follow-up. – If the patient is discharged on hydrocortisone, advise patient to hold this medication the afternoon prior and the morning of the lab draw and to take it immediately after labs are drawn that morning. – If the patient is discharged on prednisone, advise patient to hold this medication on day of lab draw and take it immedi- ately after labs are drawn that morning. – Urine osmolality or specific gravity may also be ordered if clinically indicated. 32 A. Z. Feldman and P. Hartzband Suggested Reading Fleseriu M, Hashim IA, Karavitaki N, Melmed S, Murad MH, Salvatori R, Samuels MH. Hormonal replacement in hypopituitarism in adults: an endocrine society clinical practice guideline. J Clin Endocrinol Metabol. 2016;101(11):3888–921. Woodmansee WW, Carmichael J, Kelly D, Katznelson L. AACE Neuroendocrine and Pituitary Scientific Committee. American Association of Clinical Endocrinologists and American College of Endocrinology Disease State Clinical Review: Postoperative Management Following Pituitary Surgery. Endocr Pract. 2015;21(7):832–8. Ziu M, Dunn IF, Hess C, Fleseriu M, Bodach ME, Tumialan LM, et al. Congress of neurological surgeons systematic review and evidence-based guideline on posttreatment follow-up evaluation of patients with nonfunc- tioning pituitary adenomas. Neurosurgery. 2016;79(4):E541–3. Severe Thyrotoxicosis 4 and Thyroid Storm Melissa G. Lechner and Trevor E. Angell Contents Performing the History for Thyrotoxicosis . . . . . . . . . . . . . . . . . . . . . . 34 Assess Symptoms of Thyrotoxicosis . . . . . . . . . . . . . . . . . . . . . . . . . 34 Assess for the Etiology of Thyrotoxicosis . . . . . . . . . . . . . . . . . . . . . 34 Assess for Medications That Affect Thyroid Status . . . . . . . . . . . . . 35 Performing the Physical Exam for Thyrotoxicosis . . . . . . . . . . . . . . . . 35 Key Findings in Thyrotoxicosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 35 Specific Exam Findings in Different Causes of Thyrotoxicosis . . . . 35 Assessing for Thyroid Storm . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 36 Making a Diagnosis of Thyroid Storm . . . . . . . . . . . . . . . . . . . . . . . . . 36 Obtain Thyroid Function Tests . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 37 Biochemical Findings in Thyrotoxicosis . . . . . . . . . . . . . . . . . . . . . . . . 37 M. G. Lechner David Geffen School of Medicine, University of California at Los Angeles, Division of Endocrinology, Diabetes and Metabolism, Los Angeles, CA, USA e-mail: mlechner@mednet.ucla.edu T. E. Angell (*) Keck School of Medicine, University of Southern California, Division of Endocrinology and Diabetes, Los Angeles, CA, USA e-mail: trevor.angell@med.usc.edu © Springer Nature Switzerland AG 2020 33 R. K. Garg et al. (eds.), Handbook of Inpatient Endocrinology, https://doi.org/10.1007/978-3-030-38976-5_4 34 M. G. Lechner and T. E. Angell Obtain Testing to Identify Underlying Illnesses . . . . . . . . . . . . . . . . . . 37 Initial Emergent Therapy for Thyroid Storm or Severe Thyrotoxicosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38 Provide Aggressive Supportive Care . . . . . . . . . . . . . . . . . . . . . . . . . 38 Order β-Blocker Therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 39 Order Antithyroid Drug Therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . 39 Order Iodine Therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 40 Order Steroid Therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 40 Use of Adjunct Treatments in Refractory Cases . . . . . . . . . . . . . . . . 40 Treatment of Thyrotoxic Patients Without Thyroid Storm . . . . . . . . . . 41 Monitoring Clinical Response . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41 Planning Outpatient Follow-Up . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 42 Suggested Reading . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 42 Performing the History for Thyrotoxicosis Assess Symptoms of Thyrotoxicosis Symptoms of thyrotoxicosis frequently include sweating, heat intolerance, palpitations, fatigue, and dyspnea on exertion. Cognitive symptoms may include anxiety, hyperactivity, or diffi- culty with concentration. Reported weight loss may be modest or substantial. Note any previous history of Graves’ disease, other thyroid disorders, thyroid surgery, and radioactive iodine treat- ment. In apathetic hyperthyroidism, overt symptoms are absent or often limited to weight loss, failure to thrive, fatigue, or lethargy. In patients already taking β-blockers, thyrotoxic symptoms may be blunted. Assess for the Etiology of Thyrotoxicosis Patients with longer duration of symptoms (>3 months) likely have persistent hyperthyroidism such as Graves’ disease or auton- omous nodule(s). Patients may report diffuse thyroid enlargement 4 Severe Thyrotoxicosis and Thyroid Storm 35 in Graves’ disease, a tender thyroid in subacute (painful) thyroid- itis, or a history of thyroid nodules suggesting possible autono- mous function. Eye complaints (protrusion, inflammation, or visual changes) are seen only in Graves’ disease. Assess for Medications That Affect Thyroid Status Note use of |
thyroid hormone preparations, antithyroid medication (methimazole or propylthiouracil [PTU]), exposure to iodinated contrast or iodine supplements, weight loss supplements, or other medications, including amiodarone, lithium, tyrosine kinase inhib- itors, and immune checkpoint inhibitors for cancer treatment. Performing the Physical Exam for Thyrotoxicosis Key Findings in Thyrotoxicosis Findings include sweating, skin warmth, fine tremor, low body weight and loss of muscle mass, hyperactivity, and poor attention. Heart rate (HR) may be mildly elevated (80–100 bpm) or clearly tachycardic. Supraventricular tachyarrhythmias, particularly atrial fibrillation, or signs of heart failure may be present. There is often mild systolic hypertension with widened pulse pressure. Patients may be mildly tachypneic from thyrotoxicosis alone. Rarely, patients may present with episodes of paralysis (termed paroxysmal periodic paralysis), affecting the lower before the upper extremities, proximal more than distal muscle groups, and usually sparing the diaphragm. Specific Exam Findings in Different Causes of Thyrotoxicosis A diffusely enlarged non-tender thyroid gland suggests Graves’ disease, and the presence of a thyroid bruit in combination with ophthalmopathy, pretibial myxedema, or digital clubbing is 36 M. G. Lechner and T. E. Angell pathognomonic. Exquisite thyroid tenderness indicates subacute (painful) thyroiditis. The presence of a large thyroid nodule on palpation may suggest an autonomously functioning nodule. The presence of a normal or small thyroid gland without any abnormal characteristics in the appropriate clinical setting may suggest accidental or surreptitious patient use of thyroid hormones. Assessing for Thyroid Storm The critical physical exam findings include hyperthermia, altered mentation (e.g., confusion, lethargy, seizures, coma), tachyar- rhythmias (most commonly atrial fibrillation), or congestive heart failure (e.g., elevated jugular venous pressure, lower extremity swelling, pulmonary edema, congestive hepatopathy). Other features of thyrotoxicosis described above will often be present in patients with thyroid storm but are not specific and frequently present in thyrotoxic patients without thyroid storm as well. Making a Diagnosis of Thyroid Storm Thyroid storm is a clinical diagnosis. Thyroid storm has been recognized traditionally as a clinical syndrome of thyrotoxicosis, hyperthermia, altered mentation, and a precipitating event. Other manifestations of thyrotoxicosis are often present but are not spe- cific for thyroid storm. The Burch-Wartofsky Score assigns points for dysfunction of the thermoregulatory, central nervous, gastrointestinal (GI)-hepatic, and cardiovascular systems. A score of >45 is considered highly suspicious for thyroid storm. However, this cutoff is not specific, indicating that some thyro- toxic patients without thyroid storm have a score greater than 45. The numerical score should not supplant physician judgment in making the diagnosis. 4 Severe Thyrotoxicosis and Thyroid Storm 37 Obtain Thyroid Function Tests Biochemical assessments of thyroid function are the most perti- nent laboratory results to consider. A suppressed thyroid- stimulating hormone (TSH) helps establish thyrotoxicosis. Thyroid hormone measurement, such as free thyroxine (FT4), should also be performed to confirm thyroid hormone excess, since mild TSH suppression in hospitalized patients occurs with non-thyroidal illnesses. Biochemical confirmation of thyrotoxico- sis is not necessary to diagnose and begin treatment for thyroid storm. The degree of thyroid hormone elevation or other tests are not helpful in determining which thyrotoxic patients have thyroid storm. Biochemical Findings in Thyrotoxicosis Mild hyperglycemia, hypercalcemia, normocytic anemia, and elevation in alkaline phosphatase and transaminase concentra- tions are all commonly seen in thyrotoxicosis. Serum creatinine is lower in thyrotoxicosis, leading to overestimating glomerular fil- trate rate. An elevated bilirubin is a particularly important finding since it has been correlated with adverse outcomes in thyroid storm. Obtain Testing to Identify Underlying Illnesses It is most critical to identify concurrent illnesses that may compli- cate thyrotoxicosis or be precipitants of thyroid storm. In addition to a thorough physical exam, pregnancy test should be performed if relevant, and sources of infection should be assessed through urinalysis, blood cultures, and chest imaging. Consideration of concomitant adrenal insufficiency should be assessed with a ran- dom serum cortisol, but doing so should not delay delivery of ste- https://www.facebook.com/groups/2202763316616203 38 M. G. Lechner and T. E. Angell roid treatment (discussed below). If adrenal insufficiency is suspected, more formal evaluation, such as a cosyntropin (ACTH 1–24) stimulation test, may need to be deferred until recovery from the patient’s acute presentation. Further testing, such as abdominal imaging or lumbar puncture, should be performed when clinically indicated. Other testing should evaluate for poten- tial acute coronary syndrome, hyperglycemia and diabetic keto- acidosis, and drug use (especially cocaine and methamphetamines). Initial Emergent Therapy for Thyroid Storm or Severe Thyrotoxicosis The treatment of thyroid storm should be initiated as early as pos- sible after recognition of the diagnosis. For patients with severe thyrotoxicosis who are considered to have “impending” thyroid storm based on clinical evaluation or a BWS of 25–45, similar treatment to thyroid storm may be considered. Provide Aggressive Supportive Care • Hemodynamic stabilization is critical. Management in the intensive care unit (ICU) is usually needed for patients with thyroid storm. Invasive hemodynamic monitoring is often appropriate. Intravenous fluid is typically necessary to improve perfusion in the setting of absolute or effective hypovolemia. If hypotension is not responsive to fluid resuscitation, vasopres- sors should be used. • Sedatives, narcotics, and diuretics should be used carefully because they may lower blood pressure and worsen hypoperfu- sion. • Hyperthermia can initially be treated with cooling measures and acetaminophen. Salicylates may increase free hormone levels by lowering protein binding. 4 Severe Thyrotoxicosis and Thyroid Storm 39 • Underlying illnesses should be treated. Specifically, broad- spectrum empiric antibiotics should be considered given the frequency with which infections precipitate thyroid storm. Order β-Blocker Therapy β-Adrenergic blockade improves tachycardia, cardiac workload, oxygen demand, and thyrotoxic symptoms. The HR goal is approximately 90–110 bpm rather than slower rates until thyro- toxicosis resolves. Carefully monitoring and use of shorter-acting agents may reduce the risk of cardiovascular insufficiency arising from excess β-blockade. Initial regimens include the following: • Intravenous propranolol 0.5–1.0 mg and then continuous infusion (5–10 mg/hour) • Oral propranolol 60–80 mg every 4 hours • Intravenous esmolol 0.25–0.50 mg/kg loading dose and then continuous infusion (0.05–0.1 mg/kg/minute) Order Antithyroid Drug Therapy Start antithyroid drugs at least 1 hour before iodides to prevent iodine incorporation into additional thyroid hormone. Initial regi- mens include the following: • PTU (oral loading dose of 500–1000 mg and then 250 mg every 4 hours) is favored for thyroid storm, because it decreases peripheral conversion of T4 to T3. • Methimazole (oral 60–80 mg daily) is an alternative when there is endogenous hyperthyroidism (e.g., Graves’ disease), but does not inhibit peripheral convention. 40 M. G. Lechner and T. E. Angell • When a patient is unable to take medication orally, nasogastric tube (NGT) administration may be employed. If there are con- traindications to NGT use or other issues that limit upper GI function, an intravenous reconstitution of methimazole in 0.9% saline solution given as a slow IV push has been reported. Per rectum regimens also have been employed (see also Chap. 7). Order Iodine Therapy Because thyroidal exposure to excess iodine acutely attenuates thyroid hormone secretion, consideration should be given to initi- ating an inorganic iodine preparation, such as saturated solution of potassium iodide [SSKI] (250 mg [0.25 ml/drop] every 6 hours). Iodines produce rapid decrease in thyroidal hormone release and can lower circulating thyroid hormone levels to near normal within 4–5 days. Again, to prevent incorporation of iodine in newly formed thyroid hormone and potentially prolong or exacerbate hyperthyroidism, antithyroid medication should be given before initiation of iodine therapy (see above). Order Steroid Therapy Give glucocorticoid therapy (intravenous hydrocortisone 300 mg and then 100 mg every 8 hours) to reduce T4 to T3 conversion and potentially treat coexisting adrenal insufficiency. Use of Adjunct Treatments in Refractory Cases Other treatments have been used in cases where patients are unable to receive traditional treatment or remain critically ill despite therapy. The data supporting these measures are limited. • Calcium channel blockers. Verapamil and diltiazem, which are not dihydropyridines and therefore do not cause vasodilator- 4 Severe Thyrotoxicosis and Thyroid Storm 41 induced reflex tachycardia, have been used for rate control in lieu of, but not in combination with, β-blockers. • Cholestyramine. When used with thionamides and a β-blocker, serum T4 and T3 levels drop faster during the first 2 weeks of therapy. • Lithium carbonate (300 mg every 6 hours and titration to lith- ium level of 0.8–1.2 mEq/L) causes inhibition of thyroid hor- mone release from the thyroid. • Plasmapheresis (2.5– 3 L volume of combined fresh-frozen plasma and 5% albumin) can remove excess thyroid hormone from circulation. • L-carnitine (1–2 g twice daily) may inhibit T3 action in the nucleus. • Thyroidectomy may be necessary in rare patients to treat hyperthyroidism when medical therapy does not adequately control thyrotoxicosis. Treatment of Thyrotoxic Patients Without Thyroid Storm • Hospitalized thyrotoxic patients usually require prompt but not emergent therapy. Providing β-blockers, such as propranolol (orally 10–40 mg every 8 hours), ameliorates adrenergic symp- toms. Initial dosing should be based on blood pressure and heart rate tolerability and the presence of CHF. Initiation of methimazole for patients diagnosed with Graves’ disease dur- ing hospitalization may be appropriate. Monitoring Clinical Response After initiation of therapy, supportive care measures should be adjusted to treat hemodynamic status as needed. Titration of β-blocker therapy should be performed to goal heart rates while avoiding hypotension. Repeat assessment of circulating thyroid hormone levels may be helpful to assure improvement starting 2–3 days after treatment initiation. 42 M. G. Lechner and T. E. Angell Planning Outpatient Follow-Up Discharge plans should include a timely follow-up visit with an endocrinologist for continued treatment. In Graves’ disease, inter- ruption of therapy can result in recurrence of symptoms. Patients should be advised about common adverse effects, which are most often rash, itching, GI upset, taste change, and joint pain. Agranulocytosis, vasculitis, hepatic inflammation, and cholestasis are rare but potentially life-threatening complications of antithy- roid drugs, and patients should be informed to report relevant symptoms. Repeat thyroid hormone testing should be performed 2–4 weeks after discharge to assure improvement in thyrotoxico- sis. Once stable, definitive treatment (radioactive iodine ablation or thyroidectomy) may be warranted for patients with Graves’ dis- ease to prevent recurrent hospitalization for thyrotoxicosis. Disclosure Statement All authors have no financial disclosures. Suggested Reading Alfadhli E, Gianoukakis AG. Management of severe thyrotoxicosis when the gastrointestinal tract is compromised. Thyroid. 2011;21(3):215–20. Angell TE, Lechner MG, Nguyen CT, Salvato VL, Nicoloff JT, LoPresti JS. Clinical features and hospital outcomes in thyroid storm: a retrospec- tive cohort study. J Clin Endocrinol Metab. 2015;100(2):451–9. Burch HB, Wartofsky L. Life-threatening thyrotoxicosis. Thyroid storm. Endocrinol Metab Clin North Am. 1993;22(2):263–77. Klein I, Danzi S. Thyroid disease and the heart. Curr Probl Cardiol. 2016;41(2):65–92. Klubo-Gwiezdzinska J, Wartofsky L. Thyroid emergencies. Med Clin North Am. 2012;96(2):385–403. Ross DS, Burch HB, Cooper DS, Greenlee MC, Laurberg P, Maia AL, Rivkees SA, Samuels M, Sosa JA, Stan MN, Walter MA. American thyroid association guidelines for diagnosis and management of hyperthyroidism and other causes of thyrotoxicosis. Thyroid. 2016; 26(10):1343–421. Myxedema Coma 5 Gwendolyne Anyanate Jack and James V. Hennessey Contents Assess Preadmission Thyroid Status and Thyroid Treatment . . . . . . . . . 44 Evaluate for Risk Factors Associated with Myxedema Coma . . . . . . . . 45 Identify Cardinal Features of Myxedema Coma . . . . . . . . . . . . . . . . . . . 45 Use a Systems-Based Approach to Identify Multi-organ Dysfunction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 46 General . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 46 Neurologic . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 46 Cardiovascular . . . . . . . . . . . . . |
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 46 Respiratory . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 47 Gastrointestinal . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 48 Genitourinary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 48 Order Thyroid Function Tests. Do Not Wait for Results . . . . . . . . . . . . 48 Order Cortisol for Adrenal Insufficiency Evaluation. Do Not Wait for Results . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 49 G. A. Jack (*) Weill Cornell Medical Center-New York Presbyterian Hospital, Department of Medicine, Division of Endocrinology, Diabetes and Metabolism, New York, NY, USA e-mail: gwj9003@med.cornell.edu J. V. Hennessey Beth Israel Deaconess Medical Center, Harvard Medical School, Division of Endocrinology, Diabetes and Metabolism, Boston, MA, USA e-mail: jhenness@bidmc.harvard.edu © Springer Nature Switzerland AG 2020 43 R. K. Garg et al. (eds.), Handbook of Inpatient Endocrinology, https://doi.org/10.1007/978-3-030-38976-5_5 44 G. A. Jack and J. V. Hennessey Admit Critically Ill Patients to Intensive Care Unit for Close Monitoring . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 49 Provide Emergency Supportive Care . . . . . . . . . . . . . . . . . . . . . . . . . . . 49 Administer Stress Dose Glucocorticoids . . . . . . . . . . . . . . . . . . . . . . . . 50 Manage Underlying Precipitating Factors . . . . . . . . . . . . . . . . . . . . . . . 50 Administer Levothyroxine +/− LT3 . . . . . . . . . . . . . . . . . . . . . . . . . . . . 51 Follow Up the Results of Thyroid Function Tests and Cortisol . . . . . . . 51 Reassess Clinical Status of Patient . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 52 Hospital Discharge Plan . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 52 Suggested Reading . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 52 Abbreviations AST aspartate aminotransferase ATA American Thyroid Association GCS Glasgow Coma Scale GFR glomerular filtration rate LDH Lactate dehydrogenase LDL Low-density lipoprotein LT3 Liothyronine LT4 Levothyroxine MC Myxedema coma NTI Nonthyroidal illness T3 Triiodothyronine T4 Thyroxine TSH Thyroid-stimulating hormone Assess Preadmission Thyroid Status and Thyroid Treatment Since patients present with altered mentation, obtaining a history may be difficult. Therefore, it is also important to obtain collateral information from family, friends, and outpatient medical records. 5 Myxedema Coma 45 A detailed history may reveal underlying hypothyroidism, previ- ous history of thyroidectomy (with thyroidectomy scar on exam), radioactive iodine ablation (RAI), and medication noncompli- ance/inappropriate discontinuation of thyroid hormone therapy. Signs and symptoms such as lapses in memory, slowness of thoughts, disorientation, fatigue, cold intolerance, weight gain, edema, constipation, brittle nails, and thin/coarse hair may be present. Vital signs may show hypothermia, hypotension, and bra- dycardia. Some patients may have undiagnosed hypothyroidism; therefore, other physical exam findings typical of hypothyroidism may provide clues such as the presence of a goiter, cold dry skin, delayed reflex relaxation phase, periorbital edema, facial puffi- ness, non-pitting edema in the upper and lower extremities, and enlarged tongue. Evaluate for Risk Factors Associated with Myxedema Coma In addition to determining if the patient has not been taking thy- roid hormone or taking it improperly, it is important to evaluate for other precipitating factors such as infection, cold exposure, heart failure, myocardial infarction, cerebrovascular accident, trauma, surgery, gastrointestinal bleed, substantial iodine intake such as from chronic raw bok choy consumption, and several cul- prit medications such as amiodarone, lithium, phenytoin, seda- tives, antidepressants, and anesthetics. Identify Cardinal Features of Myxedema Coma Myxedema coma should be suspected in a patient with decreased mental status, hypothermia (which can be as low as core tempera- ture < 80 °F), and bradycardia, in addition to clinical signs/symp- toms of hypothyroidism, especially in older women during the winter months. 46 G. A. Jack and J. V. Hennessey Use a Systems-Based Approach to Identify Multi-organ Dysfunction General As discussed, hypothermia is one of the key features of myx- edema coma. It is important to note that in the setting of underly- ing infection, patients may be normothermic due to blunted ability to mount a febrile response in the setting of thermal dysregula- tion. Typical signs of infection (fever, tachycardia, diaphoresis) may not be evident. Therefore in a patient with suspected myx- edema coma, normal temperature should warrant more in-depth investigation for underlying infection. Complete blood count with differential, urinalysis, urine culture, and blood culture should be obtained (Table 5.1). Neurologic Neurocognitive disturbances observed in myxedema include a reduced level of consciousness, confusion, psychomotor slowing, cerebellar ataxia, memory deficits, dementia, depression, seizure, lethargy that devolves into stupor, and ultimately coma. Sensory and motor peripheral neuropathy, psychosis, and hallucinations (“myxedema madness”) have also been described. Cardiovascular Cardiovascular disturbances include reduction in myocardial con- tractility, low cardiac output, hypotension, cardiogenic shock, and bradycardia. Mucopolysaccharide accumulation in the pericar- dium can lead to pericardial effusions and subsequent cardiac tam- ponade physiology. Patients may endorse dyspnea. Physical exam would reveal jugular venous distention, muffled heart sounds, tachycardia, and pulsus paradoxus and can be further confirmed by chest X-ray, EKG, and cardiac echocardiogram. Confirmatory tests include chest X-ray, EKG, and cardiac echocardiogram. 5 Myxedema Coma 47 Table 5.1 Signs and symptoms of myxedema coma Signs/symptoms General Fatigue, weakness Hypothermia without shivering Neurologic Memory deficits Delayed relaxation phase of DTR Seizure Psychomotor slowing Decreased level of consciousness (lethargy, stupor, coma) Cardiac Bradycardia (tachycardia if cardiac tamponade is present) Hypotension Diastolic dysfunction Tamponade Respiratory Dyspnea Renal Decreased urine output Bladder atony Increased creatinine Decreased GFR Metabolic Hypoglycemia Hyponatremia Elevated creatine kinase, elevated LDH Elevated LDL Gastrointestinal Constipation, fecal impaction Paralytic ileus, megacolon Ascites Elevated AST Dermatologic Puffy face and extremities Cool, dry skin Cold intolerance Brittle nails Thin, sparse, dry hair Musculoskeletal Myalgia, easy fatigability Respiratory Respiratory manifestations including hypoventilation, hypoxia, and hypercapnia can also occur in myxedema coma patients. An arterial blood gas analysis to assess for hypercapnia and hypoxemia should be considered. Also, laryngeal edema and macroglossia, resulting 48 G. A. Jack and J. V. Hennessey in airway narrowing, can pose a challenge during endotracheal tube placement. Pleural effusions and underlying pneumonia can also contribute to diminished respiratory function. Chest X-ray should be obtained to evaluate for underlying pneumonia and pleu- ral effusion. Gastrointestinal Bowel wall edema can result in reduced intestinal motility, atony, paralytic ileus, and toxic megacolon. Patients may present with nausea/vomiting, abdominal distension, constipation, and fecal impaction. Also, absorption of medications can be diminished, and dose adjustment of oral medications may be needed. Impaired gluconeogenesis, infection, and concomitant adrenal insuffi- ciency may contribute to hypoglycemia; therefore, serum blood sugar should be obtained. Genitourinary Severe hypothyroidism results in a decrease in renal glomerular filtration rate and renal perfusion and rhabdomyolysis. Obtain a complete metabolic panel, which may reveal hyponatremia, elevated creatinine kinase, creatinine, and aspartate aminotrans- ferase. Urine output should also be monitored for decreased urine output from acute renal injury and bladder atony. Order Thyroid Function Tests. Do Not Wait for Results The diagnosis of myxedema coma is in large part based on clin- ical suspicion and confirmed with biochemical testing. Thyroid function tests including thyroid-stimulating hormone (TSH), free T4 (fT4), should be obtained prior to administration of thy- roid replacement therapy. Initial evaluation includes an assess- ment of underlying precipitating factors; however, if a high 5 Myxedema Coma 49 index of suspicion is obvious, do not wait until the results of the evaluation are definitive before initiating treatment. Order Cortisol for Adrenal Insufficiency Evaluation. Do Not Wait for Results Given the overlap in the presentation of MC with adrenal insuffi- ciency such as fatigue, hyponatremia, hypothermia, and hypogly- cemia, evaluation for adrenal insufficiency is prudent. Adrenal insufficiency can be from hypopituitarism or can be part of poly- endocrine syndrome in a patient with underlying Hashimoto’s thyroiditis with autoimmune primary adrenal insufficiency (i.e., Schmidt syndrome). Also, after starting thyroid replacement ther- apy, there is concern for increased metabolism of cortisol leading to adrenal crisis; therefore, obtaining baseline serum cortisol level is essential. In a stressed patient with normal serum albumin lev- els, a serum cortisol level greater than 18 mg/dl would rule out adrenal insufficiency and would permit rapid taper of hydrocorti- sone after limited initial exposure. Admit Critically Ill Patients to Intensive Care Unit for Close Monitoring Myxedema crisis is an emergency that warrants frequent monitor- ing of patient’s clinical status; therefore, it should be managed in a critical care setting. Provide Emergency Supportive Care Maintain a low threshold for intubation and mechanical ventila- tion in the setting of worsening hypoxemia and hypercapnia and concern for airway protection in the setting of reduced Glasgow Coma Scale, macroglossia, or suspicion for laryngeal edema. Cardiovascular collapse and hypotension may require volume resuscitation with isotonic normal saline or 5–10% dextrose in 50 G. A. Jack and J. V. Hennessey half-normal saline if hypoglycemia is also present. Hypotension might be refractory to intravenous fluids without thyroid replace- ment therapy and in the setting of adrenal insufficiency. Vasopressors may be added if fluid resuscitation is inadequate in providing cardiovascular support; however, it should be weaned off as soon as clinically indicated. Regarding management of hypothermia, external warming techniques with blankets are suitable, though this may worsen hypotension through vasodilation. Aggressive external rewarming and central warming can potentiate cardiovascular collapse; therefore, it is generally not recommended. Treatment with thy- roid hormone should restore thermoregulation. Administer Stress Dose Glucocorticoids Due to the concern for underlying adrenal insufficiency, and the risk of inciting adrenal crisis with initiation of thyroid hormone therapy, it is recommended that stress dose steroids be adminis- tered prior to thyroid supplementation. Hydrocortisone 50–100 mg can be administered intravenously every 6–8 hours until clinical improvement and quickly tapered off if labs obtained prior to glu- cocorticoid initiation ultimately do not demonstrate adrenal insuf- ficiency. Manage Underlying Precipitating Factors Based on clinical presentation, laboratory analysis, and imag- ing studies, treat for any precipitants such as myocardial infarc- tion, gastrointestinal bleeding, and other underlying medical conditions. If suspicious for infection, draw cultures and start empiric antibiotics. Metabolic derangements such as hypo- glycemia and hyponatremia should be monitored and treated accordingly. Caution must be exercised to not rapidly correct serum sodium, given the risk for osmotic demyelination syn- drome. This is focused on the classic definition; however, a similar approach can be adopted in patients with features of profound hypothyroidism. 5 Myxedema Coma 51 Administer Levothyroxine +/− LT3 Controversy exists regarding optimal thyroid hormone regimens including the |
type, dose, route, frequency of administration, and duration of therapy. An approach adopted by earlier studies is administration of an intravenous L-thyroxine 300–600 μg loading dose to replete the deficit in the total body thyroid hormone pool, followed by maintenance doses of 50–100 μg LT4 daily by intra- venous or oral route (if mentally alert). The ATA 2014 guideline recommends an intravenous loading dose of 200–400 μg of L- thyroxine, followed by daily oral L-thyroxine dose of 1.6 μg/kg body weight or 75% of this dose if intravenous route. The under- lying principle behind levothyroxine monotherapy is that it allows for restoration to near-normal levels. In myxedema coma, T3 is low and concomitant nonthyroidal illness further decreases T4 to T3 conversion. Therefore, another strategy is the addition of LT3 to L-thyroxine therapy. LT3 has a quicker onset on action, crosses the blood-brain barrier readily, increases core temperature within 2–3 hours (as opposed to 14 hours from LT4 intravenously), and possibly improves neuropsychiatric manifestations more rapidly. According to the ATA 2014 guide- lines, clinicians can consider coadministration of LT3, with an ini- tial intravenous loading dose of LT3 5–20 μg, followed by a maintenance dose of LT3 IV 2.5–10 μg every 8 hours, which can be continued until patient’s clinical status has improved and mainte- nance oral LT4 can be administered. Alternatively, LT3 therapy can be added if clinical status does not improve after 24–48 hours of L-thyroxine alone. Due to the potential risk of cardiac arrhythmias and myocardial infarction, especially in older patients, it is recom- mended to use lower doses of L-thyroxine and LT3. Follow Up the Results of Thyroid Function Tests and Cortisol Marked TSH elevation is consistent with primary hypothyroid- ism. In patients with central hypothyroidism, TSH is not a reliable measure. Also, TSH may not be substantially elevated in the set- ting of nonthyroidal illness (NTI) and glucocorticoid or dopamine 52 G. A. Jack and J. V. Hennessey administration. In myxedema coma, free T4 is low, and with con- comitant nonthyroidal illness, these parameters may be even lower. In those known to be hypothyroid or with well-established hypothyroidism, if thyroid function tests and cortisol are normal, glucocorticoids can be promptly discontinued, and depending on clinical status, one may consider transitioning to the preadmission LT4 dose. Reassess Clinical Status of Patient It is important to monitor the patient frequently for clinical improvement. Once stabilized, frequent monitoring is no longer necessary, and patient can be transferred to medical floors for fur- ther management. Hospital Discharge Plan Patients with underlying hypothyroidism should be instructed to administer levothyroxine on an empty stomach and wait at least 1 hour before eating/drinking, in order to optimize absorption of LT4. If dose adjustments of LT4 were done during hospitalization, repeat TSH can be obtained in 6–8 weeks to determine if further dosage adjustments are needed. Outpatient follow-up with the patient’s endocrinologist and primary care physician should be arranged to reassess thyroid status at an appropriate interval. Suggested Reading Chiong YV, Bammerlin E, Mariash CN. Development of an objective tool for the diagnosis of myxedema coma. Transl Res. 2015;166(3):233–43. Fliers E, Wiersinga WM. Myxedema coma. Rev Endocr Metab Disord. 2003;4(2):137–41. Holvey DN, Goodner CJ, Nicoloff JT, Dowling JT. Treatment of myxedema coma with intravenous thyroxine. Arch Intern Med. 1964;113(1):89–96. Jordan RM. Myxedema coma: pathophysiology, therapy, and factors affect- ing prognosis. Med Clin N Am. 1995;79(1):185–94. 5 Myxedema Coma 53 Kasid N, Hennessey JV. Myxedema Coma. In: Endocrine and metabolic medical emergencies: a clinician’s guide; 2018. p. 252–61. Klubo-Gwiezdzinska J, Wartofsky L. Thyroid emergencies. Med Clin N Am. 2012;96(2):385–403. Liamis G, Filippatos TD, Liontos A, Elisaf MS. Management of endocrine disease: Hypothyroidism-associated hyponatremia: mechanisms, implica- tions and treatment. Eur J Endocrinol. 2017;176(1):R15–r20. Mathew V, Misgar RA, Ghosh S, Mukhopadhyay P, Roychowdhury P, Pandit K, et al. Myxedema coma: a new look into an old crisis. J Thyroid Res. 2011;2011:493462. Osborn LA, Skipper B, Arellano I, MacKerrow SD, Crawford MH. Results of resting and ambulatory electrocardiograms in patients with hypothyroid- ism and after return to euthyroid status. Heart Dis. 1999;1(1):8–11. Popoveniuc G, Chandra T, Sud A, Sharma M, Blackman MR, Burman KD, et al. A diagnostic scoring system for myxedema coma. Endocr Pract. 2014;20(8):808–17. Sorensen JR, Winther KH, Bonnema SJ, Godballe C, Hegedus L. Respiratory manifestations of hypothyroidism: a systematic review. Thyroid. 2016;26(11):1519–27. Wartofsky L. Myxedema coma. Endocrinol Metab Clin N Am. 2006;35(4):687–98, vii-viii. Abnormal Thyroid 6 Stimulating Hormone Values That Are Not due to Common Causes of Primary Hypothyroidism or Thyrotoxicosis Zsu-Zsu Chen and James V. Hennessey Contents Physiologic Causes of Variations in TSH Levels in Asymptomatic Patients . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 56 Laboratory Detection of Isoforms or Assay Interference Leading to Abnormal TSH Values in Patients Who Are Asymptomatic . . . . . . . . 58 Medications That Can Affect TSH Levels . . . . . . . . . . . . . . . . . . . . . . . 59 Medications Associated with Low TSH Levels . . . . . . . . . . . . . . . . . 61 Medications Associated with High TSH Levels . . . . . . . . . . . . . . . . . 62 Z.-Z. Chen (*) Beth Israel Deaconess Medical Center, Department of Endocrinology, Diabetes and Metabolism, Boston, MA, USA e-mail: zchen5@bidmc.harvard.edu J. V. Hennessey Beth Israel Deaconess Medical Center, Harvard Medical School, Division of Endocrinology, Diabetes and Metabolism, Boston, MA, USA e-mail: jhenness@bidmc.harvard.edu © Springer Nature Switzerland AG 2020 55 R. K. Garg et al. (eds.), Handbook of Inpatient Endocrinology, https://doi.org/10.1007/978-3-030-38976-5_6 56 Z.-Z. Chen and J. V. Hennessey Immune Checkpoint Inhibitor Effects on TSH in Patients Treated with These Therapies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 63 Tyrosine Kinase Inhibitor Effects on TSH in Patients Treated with These Therapies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 63 Nonthyroidal Illness . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 64 Thyroid Function Tests That Are Consistent with Nonthyroidal Illness . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 64 Treatment Considerations in a Patient with Nonthyroidal Illness . . . 65 Central Hypothyroidism Is Associated with Variable TSH Levels . . . . . 65 Consider Genetic Causes of Central Hypothyroidism . . . . . . . . . . . . 67 Consider Acquired Causes of Central Hypothyroidism . . . . . . . . . . . 68 Rare Causes of Abnormal TSH Levels . . . . . . . . . . . . . . . . . . . . . . . . . . 69 Resistance to TSH Causes High TSH Levels . . . . . . . . . . . . . . . . . . . 69 Resistance to TRH Is a Rare Cause of Central Hypothyroidism . . . . 69 Resistance to Thyroid Hormone Is a Rare Cause of Abnormal TSH Levels . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 70 Consider TSH Secreting Tumor as a Rare Cause of High TSH and High Peripheral Thyroid Hormones . . . . . . . . . . . . . . . . . . . . 70 Suggested Reading . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 71 Physiologic Causes of Variations in TSH Levels in Asymptomatic Patients Thyroid stimulating hormone (TSH) levels can vary up to 40–50% within a single day. Levels are typically lowest in the late afternoon and highest at bedtime. Normal ranges for TSH laboratory values are also determined based on where 95% of TSH values fall within a carefully screened population of healthy euthyroid volunteers. This means that 5% of people with normal thyroid function could still have TSH values that are considered abnormal. Also, these normal ranges can differ based on which reference population was studied. This chapter will give an over- view of the different causes of abnormal serum TSH values not due to primary thyroid dysfunction (several of which are outlined in Fig. 6.1). 6 Abnormal Thyroid Stimulating Hormone Values That Are Not… 57 Variable TSH Genetic mutations Physiologic Variation (Euthyroid) Laboratory Artifact (Euthyroid) - Isolated or combined congenital hypothyroidism - - - Resistance to TRH, TSH Central hypothyroidism Diurnal variation Detection of biologically inactive TSH (variable TSH and T4/T3, TSH is not an - Normal population outliers isoformsAcquired hypothyroidism appropriate surrogate marker of - Age - Antibodies- Mass lesion thyroid function in these cases) - Ethnicity - Heterophile antibodies - latrogenic - IgG complexes - Traumatic brain injury/cerebral vascular event - Biotin - Infiltrative/infectious process - Autoimmunity ↑ TSH ↓TSH TSH secreting pituitary adenoma Medications - Dopamine Hypothalamus ↑ TSH secretion Medications - Dopamine agonist TRH - Dopamine receptor blockers - Bromocriptine - Amphetamines - Cabergoline (+) Nonthyroidal Illness - Somatostatin analogues Pituitary - Octreotide ↓ TSH TSH Antiepiletic medications - - Pasireotide secretion - Valproate ↓T3, nl/↓T4,nl/↓TSH Unknown etiology Carbamazepine - - Lanreotide - Sometimes transient ↑ - High dose glucocorticoids (-) - OxcarbazepineTSH with recovery - Opiates Failure to - Metformin lodine/lodine contrast escape Wolff- (+) - Retinoid × receptor (Bexarotene) Amiodarone Chaikoff (-) lodine/lodine Contrast ↑ T3/T4 Ritonavir Amiodarone production St. John’s Wort Possibly Negative feedback Positive feedback Selective serotonin reuptake alters T3/T4 to hypothalamus inhibitors (SSRIs) ClearanceThyroid hormone analogues to hypothalamus - Levothyroxine and pituitary and pituitary (↓ T3/T4, ↑ TSH) lodine/lodine Contrast - Liothyronine (↑ T3/T4, ↓ TSH) Interferon alpha Amiodarone Lithium ↓ T3/T4 Tyrosine Kinase Inhibitors Acute thyroiditis Thyroid Thionamides production Immune checkpoint inhibitors - initial ↑ T3/T4, ↓ TSH, - Propyllthiouracil or secretion - Pembrolizumab - subsequent ↓ T3/T4, ↑ TSH - Methimazole - Nivolumab - resolution or chronic - lpilimumab hypothyroidism with ↑ TSH T3/T4 ↑ T3/T4, Thyroid Hormone Resistance Autoimmunity nl/↑ TSH 58 Z.-Z. Chen and J. V. Hennessey Fig. 6.1 Causes of abnormal serum TSH values not due to primary thyroid dysfunction. This figure demonstrates the normal hypothalamic-pituitary- thyroid axis. Thyrotropin-releasing hormone (TRH) is secreted by the hypo- thalamus that provides positive feedback to the pituitary that secretes thyroid stimulating hormone (TSH). TSH provides positive feedback to the thyroid gland causing increased production of thyroxine (T4) and triiodothyronine (T3) that both in turn provide negative feedback to the hypothalamus and pitu- itary. Causes of TSH abnormalities discussed in this book chapter are grouped as those that cause elevated TSH, decreased TSH, and variable TSH levels Age can also affect TSH values with an estimated 0.3 mIU/L increase in value for every 10-year increase in age after 30–39 years old. TSH normal ranges can also vary based on eth- nicity. In the NHANES III reference population study, African Americans aged 30–39 years old had the lowest TSH values, while Mexican Americans that were 80 years or older had the highest TSH values. Laboratory Detection of Isoforms or Assay Interference Leading to Abnormal TSH Values in Patients Who Are Asymptomatic Issues with laboratory detection of TSH |
levels can lead to abnor- mal values in a euthyroid patient. Several TSH isoforms can be expressed in humans that are not biologically active. Some labo- ratory assays may detect these isoforms leading to the reporting of abnormal TSH values that, however, do not correlate with hypothalamic- pituitary-thyroid dysfunction. Antibodies can also interfere with immunoassays used for the detection of TSH levels. Patients with high heterophile antibodies (HAb) can have falsely elevated levels. Manufactures have refined their assays to over- come this issue, but a small percentage of patients can still have high enough titers to cause interference. The most common het- erophile antibodies in humans are those targeting animal antigens, specifically human anti-mouse antibodies (HAMA). Human anti- bodies targeting human antigens, such as rheumatoid factor, can also interfere. Suspicion should be raised in patients that have a 6 Abnormal Thyroid Stimulating Hormone Values That Are Not… 59 clinical picture inconsistent with their lab values. People at high risk for development of these antibodies are those who have had recent vaccines, blood transfusions, and monoclonal antibody treatments, veterinarians, or those who have jobs that require fre- quent animal contact. If there is suspicion that there is a hetero- phile antibody, the TSH can be measured with a different manufacturer’s assay. The presence of TSH autoantibodies can cause TSH immuno- globulin G (IgG) complexes that also interfere with TSH immu- noassays. This could lead to either falsely elevated or lower TSH values. These autoantibodies are immunoreactive, causing the erroneous lab values, but are not biologically active and therefore do not cause pituitary-thyroid axis dysfunction. There are assays available for removal of these IgG complexes prior to processing the serum sample. High-dose oral biotin supplementation (>5000–10,000 μg daily) can also cause interference with the detection assays of TSH, total thyroxine (T4), and total triiodothyronine (T3). It can have a negative effect on TSH and positive effect on T3 and T4, biochemically mimicking thyrotoxicosis. Clinicians should ask about biotin supplementation so that biotin interference can be considered if the labs are inconsistent with the clinical picture. Biotin supplementation can be held prior to the blood draw to prevent interference, and the literature regarding the duration of holding biotin varies from at least 2 days to 7 days. Medications That Can Affect TSH Levels Medications, some of which are detailed in Table 6.1, can also affect TSH secretion and/or interrupt the hypothalamic-pituitary- thyroid axis. Often, abnormal TSH levels due to medications will normalize once the offending agent is stopped. However, some patients may require long-term antithyroidal treatment or thyroid hormone replacement therapy due to persistent thyroid dysfunc- tion. Of note, there are several medications including iodine, iodine contrast agents, and amiodarone that can cause both hypo- thyroidism and thyrotoxicosis. These medications typically cause 60 Z.-Z. Chen and J. V. Hennessey Table 6.1 Medications that affect thyroid stimulating hormone (TSH) Low TSH Dopamine Dopamine agonists Bromocriptine Cabergoline Somatostatin analogues Octreotide Pasireotide Lanreotide Glucocorticoids Opiates Retinoid X receptor (i.e., bexarotene) Metformin Thyroid hormone analogues High TSH Dopamine receptor blockers Amphetamines Ritonavir St. John’s wort Selective serotonin reuptake inhibitors (SSRIs) Thionamides (i.e., antithyroid medications) Propylthiouracil Methimazole Lithium Antiepileptic medications Valproate Carbamazepine Oxcarbazepine Interferon alpha High or low TSH Immune checkpoint inhibitors Pembrolizumab Nivolumab Ipilimumab 6 Abnormal Thyroid Stimulating Hormone Values That Are Not… 61 Table 6.1 (Continued) Tyrosine kinase inhibitors Amiodarone Iodine/iodine contrast agents Table derived in part from Table 10 of Garber JR, Cobin RH, Gharib H, Hen- nessey JV, Klein I, Mechanick JI, et al. Clinical practice guidelines for hypo- thyroidism in adults: cosponsored by the American Association of Clinical Endocrinologists and the American Thyroid Association. Endocr Pract Off J Am Coll Endocrinol Am Assoc Clin Endocrinol. 2012:18(6);988–1028. See Suggested Reading thyroid dysfunction in patients who already have underlying thy- roid disease or who have the propensity to develop dysfunction (i.e., antithyroid antibody positivity or nodular goiter). The devel- opment of hypo- or hyperfunction is dictated by the underlying thyroid disorder. Medications Associated with Low TSH Levels Dopamine infusions and agonists, high-dose glucocorticoids, somatostatin analogues including octreotide, oral bexarotene (a retinoid X receptor-selective ligand used to treat cutaneous T-cell lymphoma), metformin, and opiates have been linked to inhibi- tion of TSH release and therefore low TSH levels. Thyroid hor- mone medications, including liothyronine (LT3) and levothyroxine (LT4), also lower TSH due to hypothalamic-pituitary suppression. Iodine, iodine contrast agents, and amiodarone (which is rich in iodine) can cause hyperthyroidism due to increased thyroid hor- mone synthesis resulting in a low TSH. The normal thyroid gland has mechanisms to prevent increased thyroid hormone production when there is excess substrate (i.e., iodine) and prevent hyperthy- roidism. However, in patients who have autonomous function of the whole or part of the thyroid gland (i.e., with Graves’ disease 62 Z.-Z. Chen and J. V. Hennessey or toxic nodule), these mechanisms may be bypassed and lead to hyperthyroidism with exposure to increased iodine. Amiodarone can also cause hyperthyroidism through the mechanism outlined above due to its high iodine content. This is known as type 1 amiodarone-i nduced thyrotoxicosis (AIT). Type 2 AIT is a destructive thyroiditis that leads to excessive release of T3 and T4. The thyrotoxicosis can resolve or persist and eventually lead to long-term hypothyroidism. Medications Associated with High TSH Levels Medications including dopamine receptor blockers and amphet- amines have been linked with increased TSH secretion and therefore a high TSH. Other medications such as ritonavir, St. John’s wort, and selective serotonin uptake inhibitors (SSRIs) could affect the clearance of T3 and T4 leading to elevated TSH levels. Patients on long-term lithium are also at increased risk for development of hypothyroidism. This increased risk is thought to be due to decreased T4 and T3 secretion or due to a thyroiditis that may be transient. Other antiepileptic medications including valproate, carbamazepine, and oxcarbazepine have been associated with increased risk of hypothyroidism but with unclear mechanism. Interferon alpha, a treatment for hepatitis C, has been associated with hypothyroidism likely due to a destructive thyroiditis that can lead initially to transient hyper- thyroidism, then to hypothyroidism, and eventually to either resolution or permanent hypothyroidism. Thionamides, used as antithyroid therapy in acute thyrotoxicosis, also causes hypothy- roidism and an elevated TSH due to the blocking of thyroid hor- mone synthesis. Iodine, iodine contrast agents, and amiodarone can enhance the inhibitory effect iodine has on the thyroid gland and cause hypothyroidism. As discussed above, the thyroid gland can tran- siently decrease thyroid hormone synthesis when there is excess iodine. This prevents the development of hyperthyroidism and is known as the Wolff-Chaikoff effect. Eventually, however, the thyroid gland will return to normal function and “escape” the Wolff- Chaikoff effect. In thyroid glands that are already dam- 6 Abnormal Thyroid Stimulating Hormone Values That Are Not… 63 aged by preexisting autoimmune thyroiditis, the gland may not escape from the Wolff-Chaikoff effect leading to persistent hypothyroidism. Immune Checkpoint Inhibitor Effects on TSH in Patients Treated with These Therapies Immune checkpoint inhibitors used for cancer therapy, including anti-programed cell death protein 1 (anti PD-1) immunotherapy pembrolizumab and nivolumab and cytotoxic T-lymphocyte- associated antigen (CTLA-4) therapy with ipilimumab, have been linked with thyroid dysfunction. Clinically, patients can present with thyrotoxicosis due to thyroiditis (initially low TSH and ele- vated T4 that can resolve or progress to overt hypothyroidism). Patients who already have hypothyroidism can develop worsening of their hypothyroidism (elevated TSH with low T4) requiring higher doses of thyroid hormone replacement. Patients can also develop centrally mediated hypothyroidism that usually occurs with panhypophysitis. This diagnosis is made with a low free T4 levels. TSH levels can be low, inappropriately normal, or elevated. Patients with transient thyroiditis typically do not require treat- ment therapy. A short course of beta-blockers can be considered when there are significant clinical symptoms of thyrotoxicosis, but this is typically not required. Patients who develop overt hypothy- roidism or panhypophysitis will need long-term thyroid hormone supplementation. Tyrosine Kinase Inhibitor Effects on TSH in Patients Treated with These Therapies Tyrosine kinase inhibitors (TKI) have been linked to hypothyroid- ism in euthyroid patients causing an elevated TSH. In patients who already have hypothyroidism, there can be increasing thyroid hormone replacement therapy requirements. This could be due to a transient destructive thyroiditis similar to the immune check- point inhibitors or possibly due to altered set points in the hypothalamic- pituitary-thyroid axis. 64 Z.-Z. Chen and J. V. Hennessey Nonthyroidal Illness Serum TSH can be suppressed in patients with acute illnesses, especially those that are hospitalized and in the intensive care units. There is a distinctive pattern of serum thyroid hormone level derangements that is known as nonthyroidal illness syn- drome. It is also referred to in the literature as sick euthyroid and low T3 syndrome. This entity has been described in healthy fasting patients as well as in a wide range of patients with acute and chronic illnesses including starvation, infec- tion, trauma, surgery, sepsis, heart disease, cerebral vascular accidents, renal failure, and malignancy. It is believed that these changes help reduce energy expenditure and cellular catabolism which could have protective effects while fasting. It is unclear if these changes are an adaptive or maladaptive process in acute i llness. Thyroid Function Tests That Are Consistent with Nonthyroidal Illness The diagnosis of nonthyroidal illness is usually obvious in acutely ill patients. Thyroid function tests show low T3 levels. T4 levels can be normal or low. TSH is typically normal but can be low. If TSH is undetectable (<0.01 mU/L), there is an increased likelihood that the patient has true hyperthyroidism. TSH levels can rise in parallel with normalization of serum T4 and T3 levels and could suggest recovery from the pituitary- thyroid axis suppression of nonthyroidal illness. If the TSH is very elevated (> 20 mU/L), there is a far higher likelihood that the patient will have persistent hypothyroidism. Serum rT3 levels can occasionally be used to help differentiate central hypothyroidism from nonthyroidal illness since it is elevated in the latter. However, its diagnostic utility is limited since it can also be slightly elevated in patients with mild hypothy- roidism. 6 Abnormal Thyroid Stimulating Hormone Values That Are Not… 65 Treatment Considerations in a Patient with Nonthyroidal Illness Several small randomized controlled trials studied treatment of nonthyroidal illness with LT3 and/or LT4 but did not show benefit in patient outcomes. Also, theoretically, if these thyroid hormone changes are adaptive, then attempts to correct the transient low T3 state could cause harm. Current recommendations are not to treat thyroid function test abnormalities likely due to nonthyroidal ill- ness with thyroid hormone replacement unless the patient has overt clinical signs of hypothyroidism. Thyroid function tests should be checked after sufficient time has elapsed following resolution of the illness to confirm normalization of thyroid hormone levels. Central Hypothyroidism Is Associated with Variable TSH Levels Central hypothyroidism is characterized by an impaired TSH response. This can be caused by defects in thyrotropin-releasing hormone (TRH) – including defects in the TRH receptor – or in defects in TSH. These defects can either be due to congenital or acquired causes. Most congenital causes are due to genetic muta- tions and can lead to isolated central hypothyroidism or combined pituitary hormone deficiencies. With the advent of newborn screen- ing, these are usually diagnosed during infancy. Acquired causes are typically due to processes that disrupt or destroy TRH produc- ing cells in the hypothalamus or TRH sensing cells in the pituitary due to invasive or compressive lesions, trauma, vascular accidents, autoimmune or infectious diseases, infiltrative processes, or iatro- genic causes. Acquired causes typically lead to combined pituitary hormone deficiencies, and isolated central hypothyroidism is less common. Some of the causes of central hypothyroidism are detailed in Table 6.2. In these patients, the TSH level can either be high or low or even appear normal. However, the peripheral thy- roid hormone levels (including free T4 and total T3) will be low. 66 Z.-Z. Chen and J. V. Hennessey Table 6.2 Causes of central hypothyroidism Genetic causes (gene mutations) Isolated central hypothyroidism TSHB TRHR TSHR IGSF1 TBL1X Combined congenital hypothyroidism LHX3, LHX4 HESX1 SOX3 OTX2 PROP1 POU1F1 LEPR Acquired causes Mass lesion Pituitary adenoma (functional/nonfunctional) Craniopharyngioma Meningioma Rathke’s cleft cyst Empty sella Metastasis Iatrogenic Intracranial surgery Radiation Traumatic brain injury Cerebral vascular events Cerebral infarct Intracranial hemorrhage Sheehan’s syndrome Autoimmune disease Lymphocytic hypophysitis Polyglandular autoimmune disease Infiltrative |
process Sarcoidosis 6 Abnormal Thyroid Stimulating Hormone Values That Are Not… 67 Table 6.2 (Continued) Histiocytosis X Iron overload (hemochromatosis, blood transfusions) Infectious diseases Tuberculosis Toxoplasmosis Fungal infections Table derived in part from Table 2 of Beck-Peccoz P, Rodari G, Giavoli C, Lania A. Central hypothyroidism - a neglected thyroid disorder. Nat Rev. Endocrinol. 2017:13;588–598. See Suggested Reading Consider Genetic Causes of Central Hypothyroidism The most frequent cause of inheritable isolated central hypothy- roidism are mutations of the TSHB gene that encodes for the β-subunit of the TSH molecule. This leads to decreased levels of functional TSH and increased circulating levels of the glycopro- tein hormone α-subunit (α-GSU). The α-GSU is also a subunit for follicle stimulating hormone (FSH), luteinizing hormone (LH), and human chorionic gonadotropin (hCG) and is frequently referred to as the α-subunit. A loss of function mutation in the immunoglobulin superfamily member 1 (IGSF1) gene leads to central hypothyroidism and macroorchidism. A missense m utation in the TBL1X gene is associated with central hypothyroidism and hearing loss. Mutations in pituitary transcription factors (includ- ing LHX3, LHX4, HESX1, SOX3, OTX2, PROP1, POU1F1, and LEPR genes) are the most common genetic causes of combined congenital hypothyroidism. For both genetic causes of either isolated or combined congeni- tal hypothyroidism, TSH levels can be low or normal in the setting of low free T4. These patients should be treated with l evothyroxine hormone replacement. Free T4 levels should be used to monitor the adequacy of hormone replacement since TSH levels can be unreli- able. Goal free T4 levels in these individuals are the same as those with central hypothyroidism, which are to be in the upper half of the normal laboratory free T4 range. It is important to remember that 68 Z.-Z. Chen and J. V. Hennessey free T4 should be checked in the morning prior to the ingestion of a patient’s levothyroxine dose because that can cause transient eleva- tion in the free T4 level. In the case of combined congenital hypo- thyroidism, hormone replacement should also be initiated for any other identified pituitary hormone deficiencies. Consider Acquired Causes of Central Hypothyroidism Masses in the hypothalamus and/or pituitary are the most com- mon cause of acquired central hypothyroidism. These lesions can lead to both qualitative and quantitative dysfunction of TSH. The most common masses found are nonfunctioning pituitary mac- roadenomas. Other lesions include craniopharyngiomas, menin- giomas, Rathke’s cleft cysts, metastases, as well as empty sella syndrome. Intracranial surgeries, especially for resection of a pituitary lesion, can lead to panhypopituitarism with associated central hypothyroidism. The risk of developing hypothyroidism is associated with the size and position of the tumor as well as the experience of the surgeon. Radiation therapy, especially in or around the sella, can also cause hypopituitarism with associated central hypothyroidism. Patients with traumatic brain injury are also at risk for central hypothyroidism with an estimated disease prevalence of 15–68%. Vascular events including cerebral infarcts, subarachnoid hemor- rhage, as well as Sheehan’s syndrome are more rare causes of central hypothyroidism. Other less common causes of acquired central hypothyroidism include autoimmune diseases (such as lymphocytic hypophysitis which may be associated with poly- glandular autoimmune disease), infiltrative processes (such as sarcoidosis, histiocytosis X, or iron overload from hemochroma- tosis or blood transfusions), and infectious diseases (tuberculosis, toxoplasmosis, and fungal infections). Patients with acquired central hypothyroidism typically have low free T4. TSH can be low, inappropriately normal, or even high. High TSH levels likely reflect a qualitative defect in the cir- culating TSH, hence the development of hypothyroidism despite elevated TSH levels. Treatment should be with thyroid hormone https://www.facebook.com/groups/2202763316616203 6 Abnormal Thyroid Stimulating Hormone Values That Are Not… 69 replacement. Free T4 levels should be measured to monitor ade- quacy of hormone replacement since the TSH is unreliable. Of note, adrenal insufficiency should be ruled out in any cases where there is concern for hypopituitarism. Adrenal insufficiency should be treated prior to initiation of thyroid hormone replacement to prevent precipitation of an adrenal crisis. Rare Causes of Abnormal TSH Levels Resistance to TSH Causes High TSH Levels Several point mutations in the TSH receptor gene can cause resis- tance to TSH. These patients typically have elevated levels of TSH with low or normal T4 and T3 concentrations. They are usually iden- tified with newborn screens. Unlike other causes of congenital hypo- thyroidism, these patients do not have goiters due to the lack of TSH stimulation of the thyroid gland. Clinical symptoms and treatment are dependent on the type of mutation and percentage of functional TSH receptors present. Some patients may be euthyroid with hyperthyro- tropinemia alone. Others develop severe congenital hypothyroidism requiring thyroid h ormone replacement. Patients who have hyperthy- rotropinemia can be differentiated from patients with autoimmune hypothyroidism because their TSH levels remain stable over time while the TSH levels change over time in autoimmune hypothyroid- ism. TSH levels will normalize with thyroid hormone replacement. Resistance to TRH Is a Rare Cause of Central Hypothyroidism A mutation in the thyrotropin-releasing hormone receptor (TRHR) has also been identified as a cause of isolated central hypothyroid- ism. However, this TRH resistance typically does not clinically manifest until childhood or early adulthood with delayed growth. Of note, the diagnosis of TRH resistance was made in a 33-year- old woman after her second successful pregnancy. She had nor- mal height and IQ and had no difficulties breastfeeding, and her children had normal pre- and postnatal growth without thyroid 70 Z.-Z. Chen and J. V. Hennessey hormone supplementation. TSH levels are typically normal, but there is a blunted TSH response to an infusion of thyrotropin- releasing hormone (TRH). Resistance to Thyroid Hormone Is a Rare Cause of Abnormal TSH Levels There are also mutations associated with dysfunction of thyroid hormone action. This resistance to thyroid hormone can be caused by malfunction of the thyroid hormone nuclear receptors, cell membrane transport of the hormone, or hormone metabolism. The most common mutation is associated with THRB which encodes for thyroid hormone receptor β. There is phenotypic variability even in patients with the same mutation. Typically in these syn- dromes, free T4 and T3 are high with normal or slightly elevated TSH. Patients can have goiters or develop attention deficit disor- der and tachycardia. However, some may not have obvious symp- toms of clinical thyrotoxicosis. Patients typically do not require thyroid hormone treatment because they will compensate for the insensitivity with increased T4 and T3 production. The most important thing to avoid in these patients is surgical thyroidec- tomy or radioactive iodine ablation of the thyroid. Mutation of the THRA gene that encodes for thyroid hormone receptor alpha is associated with low free T4, normal or slightly elevated T3, and normal TSH. The TSH is normal because the beta receptors that control TSH output remain intact. Clinically, patients exhibit signs of hypothyroidism in the peripheral tissues. These can lead to significant bony abnormalities, gastrointestinal tract dysmotil- ity, bradycardia, and mental disabilities. Consider TSH Secreting Tumor as a Rare Cause of High TSH and High Peripheral Thyroid Hormones TSH secreting tumors are a very rare cause of hyperthyroidism. They represent 0.5–3% of functional pituitary adenomas, even though this could be an underestimation, and they are typically 6 Abnormal Thyroid Stimulating Hormone Values That Are Not… 71 benign. Patients are usually diagnosed in their fifth to sixth decades. The majority of the lesions only secrete intact TSH, but they can also secrete growth hormone or prolactin. Sometimes there is also increased α-GSU (α-subunit). Patients develop clinical symptoms of hyperthyroidism. If it is a mac- roadenoma, compressive symptoms including headache and visual field defects can develop as well as adrenal and gonadal axis dysfunction. In patients who co-secrete growth hormone or prolactin, the development of acromegaly or galactorrhea may be seen. Labs are consistent with elevated levels of T4 and T3. TSH can be inappropriately normal or mildly elevated. Patients should also be screened for hyper- and hyposecretion of other pituitary hor- mones, and α-GSU levels should be checked. MRI of the pituitary is recommended for imaging. Once the diagnosis of a mass is made, the patient should be evaluated by neurosurgery for resec- tion. Interval treatment prior to surgery for hyperthyroid symp- toms can include the use of beta-blockers. Somatostatin analogues or dopamine agonists can also be used for lesions that co-secrete growth hormone and prolactin. Suggested Reading Barroso-Sousa R, Barry WT, Garrido-Castro AC, Hodi FS, Min L, Krop IE, et al. Incidence of Endocrine Dysfunction Following the Use of Different Immune Checkpoint Inhibitor Regimens: A Systematic Review and Meta- analysis. JAMA Oncol. 2018;4(2):173–82. Beck-Peccoz P, Rodari G, Giavoli C, Lania A. Central hypothyroidism - a neglected thyroid disorder. Nat Rev Endocrinol. 2017;13:588–98. Bonomi M, Busnelli M, Beck-Peccoz P, Costanzo D, Antonica F, Dolci C, et al. A Family with Complete Resistance to Thyrotropin-Releasing Hormone. N Engl J Med. 2009;360(7):731–4. Demir K, van Gucht ALM, Büyükinan M, Çatlı G, Ayhan Y, Baş VN, et al. Diverse Genotypes and Phenotypes of Three Novel Thyroid Hormone Receptor-α Mutations. J Clin Endocrinol Metab. 2016;101(8):2945–54. Estrada JM, Soldin D, Buckey TM, Burman KD, Soldin OP. Thyrotropin iso- forms: implications for thyrotropin analysis and clinical practice. Thyroid. 2014;24(3):411–23. Fliers E, Bianco AC, Langouche L, Boelen A. Endocrine and metabolic con- siderations in critically ill patients 4. Lancet Diabetes Endocrinol. 2015;3(10):816–25. 72 Z.-Z. Chen and J. V. Hennessey Garber JR, Cobin RH, Gharib H, Hennessey JV, Klein I, Mechanick JI, et al. Clinical practice guidelines for hypothyroidism in adults: cosponsored by the American Association of Clinical Endocrinologists and the American Thyroid Association. Endocr Pract. 2012;18(6):988–1028. Piketty M-L, Polak M, Flechtner I, Gonzales-Briceño L, Souberbielle J-C. False biochemical diagnosis of hyperthyroidism in streptavidin- biotin- based immunoassays: the problem of biotin intake and related interferences. Clin Chem Lab Med. 2017;55(6):780–8. Refetoff S, Weiss RE, Usala SJ. The syndromes of resistance to thyroid hor- mone. Endocr Rev. 1993;14(3):348–99. Tenenbaum-Rakover Y, Almashanu S, Hess O, Admoni O, Hag-Dahood Mahameed A, Schwartz N, et al. Long-term outcome of loss-of-function mutations in thyrotropin receptor gene. Thyroid. 2015;25(3):292–9. Management 7 of a Hospitalized Patient with Thyroid Dysfunction Megan Ritter and James V. Hennessey Contents Hyperthyroidism 74 Antithyroid Medications 74 Beta-Adrenergic-Blocking Drugs 75 Glucocorticoids 80 Iodine 80 Hypothyroidism 80 Suggested Reading 83 Abbreviations MMI Methimazole NPO Nil per os PO Per os M. Ritter (*) Weill Cornell Medicine, New York Presbyterian, New York, NY, USA e-mail: mer9114@med.cornell.edu J. V. Hennessey Beth Israel Deaconess Medical Center, Harvard Medical School, Division of Endocrinology, Diabetes and Metabolism, Boston, MA, USA e-mail: jhenness@bidmc.harvard.edu © Springer Nature Switzerland AG 2020 73 R. K. Garg et al. (eds.), Handbook of Inpatient Endocrinology, https://doi.org/10.1007/978-3-030-38976-5_7 74 M. Ritter and J. V. Hennessey PTU Propylthiouracil T3 Triiodothyronine T4 Thyroxine TSH Thyroid stimulating hormone Hyperthyroidism Antithyroid Medications Thyroid hormone affects virtually all organ systems. Thyroxine, or T4, can be viewed as the prohormone, while triiodothyro- nine, or T3, is the active form of thyroid hormone. Thyrotoxicosis can be manifested in many ways, including atrial fibrillation, weight loss, neuropsychiatric symptoms, or muscle weakness. The consequences of untreated hyperthyroidism include osteo- porosis as well as frank thyroid storm which can lead to cardio- vascular collapse and death. Further, untreated hyperthyroidism is associated with an increase in mortality, whereas treated hyperthyroidism negates this increase in risk. Longer duration of TSH suppression is associated with an increased hazard of mortality as well. Thus, it is prudent in both the outpatient and inpatient setting to establish the etiology of and to manage hyperthyroidism. The 2016 American Thyroid Association guidelines recom- mend methimazole (MMI) as the first-line antithyroid drug except during the first trimester of a hyperthyroid woman’s pregnancy when propylthiouracil (PTU) should be considered. PTU can also be used in select situations including MMI allergy or thyroid storm. Additional options for the treatment of hyperthyroidism include radioactive iodide or thyroidectomy and are tailored to patient preference in addition to concurrent medical conditions, including pregnancy or heart failure. It is reasonable to continue ambulatory doses of MMI or PTU upon hospital admission in patients who can continue to take medications orally, have no contraindications to continuing the medication, and are well- controlled outside the hospital. 7 Management of a Hospitalized Patient with Thyroid Dysfunction 75 Situations may arise where oral medications cannot be contin- ued upon a patient’s admission to the inpatient setting. The table reviews alternative methods physicians |
have used to administer antithyroid medications. Studies range from healthy volunteers without thyroid dysfunction to case reports of critically ill patients with thyroid disease (Tables 7.1 and 7.2). These studies show that rectal administration of PTU and MMI in either enema or suppository is readily absorbed and well- tolerated for up to several days’ duration. Several options exist for making a rectal application of MMI or PTU. Pharmacy availabil- ity of the different materials will determine which formulation is ultimately used to treat an individual patient. Further, although suppositories might be better tolerated based on smaller size and potentially higher degree of retention, enemas have been shown to have more rapid and robust absorption. Intravenous (IV) medications can be advantageous when both oral and rectal administrations of medications are not possible. Given PTU’s properties, methimazole has more commonly been used as an intravenous medication. Although the use of these medications IV is not widespread, the above case studies support that they can be administered IV in a safe and an effective manner. Beta-Adrenergic-Blocking Drugs Beta-blockers are useful in managing symptoms related to hyper- thyroidism and are important initial tools in the treatment of all forms of hyperthyroidism, while diagnosis is established and con- trol of thyroid hormone levels is being established. Atenolol, esmolol, propranolol, and metoprolol are commonly used beta- blockers but others exist. Intravenous formulations of beta- blockers are generally readily available. No studies have been found comparing efficacy of IV propranolol, IV esmolol, or IV metoprolol in hyperthyroid patients. Pharmacokinetics of both IV esmolol and IV propranolol have been studied. IV esmolol has an elimination half-life of 2 minutes and a duration of action of 9 minutes. IV propranolol has an elimi- nation half-life of 10 minutes and a duration of action of 2.3 hours. 76 M. Ritter and J. V. Hennessey Table 7.1 Alternative strategies for methimazole administration Patient and study Dose Preparation characteristics Source (a) Intravenous administration 10–30 mg q 6–12 hours 500 mg of MMI USP powder 1. A 76-year-old man with Hodak SP, Huang C, Clarke D, reconstituted with pH-neutral biochemical Burman KD, Jonklaas J, 0.9% sodium chloride to attain hyperthyroidism and an ileus Janicic-Kharic N. Intravenous 10 mg MMI/mL was filtered and Clostridium difficile methimazole in the treatment through a 0.22 μm filter. Two diarrhea treated with IV of refractory hyperthyroidism. mL aliquots were transferred MMI 10 mg every 12 hours, Thyroid. 2006;16(7):691–695 into 10 mL sterile vials and increased to 10 mg every refrigerated. MMI was pushed 8 hours. Serum FT4 intravenously over 2 minutes decreased from 2.9 ng/dL to then followed by a normal 2.1 ng/dL saline flush 2. A 42-year-old male with end-stage liver disease had recurrent gastrointestinal bleeding. He was treated with IV MMI for 1 week (tapered from 30 mg IV MMI every 6 hours to 2.5 mg IV MMI every 12 hours); serum FT4 decreased from 5.6 ng/dL to 1.6 ng/dL 7 Management of a Hospitalized Patient with Thyroid Dysfunction 77 10 mg, one-time dose MMI powder was dissolved in Normal and hyperthyroid Okamura Y, Shigemasa C, 1 mL physiologic salt solution. patients were given a one-time Tatsuhara T. Pharmacokinetics Solution was enclosed in dose of methimazole in normal ampule and autoclaved to There was no difference in subjects and hyperthyroid sterilize pharmacokinetics of MMI patients. Endocrinol Jpn. between normal and 1985;33(5):605–615 hyperthyroid patients (b) Rectal administration 60 mg (one-time dose) Suppository: 1200 mg MMI One suppository was Nabil N, Miner DJ, Amatruda dissolved in 12 mL of water. administered to euthyroid JM. Methimazole: an Two drops Span 80® added to volunteers alternative route of 52 mL cocoa butter. Solution Peak serum MMI levels were administration. J Clin placed in 2.6 mL suppository not statistically different Endocrinol Metab. molds among groups. No thyroid 1982;54(1):180–181 outcomes were measured 78 M. Ritter and J. V. Hennessey Table 7.2 Alternative strategies for PTU administration Dose Preparation Patient characteristics Source (a) Intravenous 50 mg PTU tablets were dissolved in A 27-year-old woman, with a Gre Gregoire, G. Presented at the alkalinized 0.9% normal saline and history of multiple small bowel 77th annual meeting of the then administered in 50 mg/mL resections, developed Endocrine Society doses hyperthyroidism secondary to Graves’ disease (b) Rectal 400 mg (one- time Suppository: 200 mg of PTU Patients with biochemical Jongjaroenprasert W, Akarawut W, dose) dissolved into an unspecified hyperthyroidism were given a Chantasart D, Chailurkit L, amount of polyethylene glycol one-time dose of either Rajatanavin R. Rectal base suppository or enema before Administration of Propylthiouracil Enema: eight, 50 mg tablets of transition to PO medication in hyperthyroid patients: ground PTU dissolved in 90 mL Enema group was found to have comparison of suspension Enema sterile water higher peak levels of and suppository form. Thyroid. PTU. Concentration rT3 increased 2004;12(7):627–631 and serum FT3 decreased 7 Management of a Hospitalized Patient with Thyroid Dysfunction 79 400 mg q 6 hours Suppository: 50 mg PTU tablets A 47-year-old male with Zweig S, Schlosser JR, Thomas solubilized in light mineral oil. thyrotoxicosis and a perforated SA, Levy CJ, Fleckman This was mixed in 36 g of cocoa gastric ulcer AM. Rectal administration of butter solid suppository base. One Serum FT4 levels decreased from propylthiouracil in suppository gram suppository molds were 5.6 to 2.5 ng/dL during 5 days of form in patients with made administration thyrotoxicosis and critical illness: case report and review of literature. Endocr Pract. 2006;12(1):43–47 400 mg q 6 hours Suppository: eight, 50 mg PTU A 49-year-old woman with thyroid Walter RM Jr., Bartle WR. Rectal tables were dissolved in 60 mL storm and perforated viscus treated administration of propylthiouracil Fleets’ mineral oil or 60 mL with IV methylprednisolone, IV in the treatment of graves’ disease. Fleet’s phospho soda propranolol, and rectal PTU Am J Med. 1990;88(1):69–70 Serum thyroxine decreased from 26 μg/dL to 8.1 μg/dL after 3 days PTU is largely insoluble at physiologic pH, so its use intravenously is limited but has been reported 80 M. Ritter and J. V. Hennessey Onset of drug action is similar. Given the rapidly changing clinical course that often accompanies thyrotoxicosis, IV esmolol may be beneficial since effects wear off rapidly; however, caution should be observed since a drop in blood pressure may occur. Propranolol does have the effect of reducing plasma T3 concentrations. However, the clinical relevance of this is uncertain as the doses of propranolol that cause reductions in T3 are larger than doses used clinically. Metoprolol can be dosed intravenously every 4–6 hours for heart rate control and is beta-1 selective, which can be beneficial in patients with heart failure. Ultimately, esmolol, propranolol, and metoprolol are all viable options in managing hyperthyroidism, and the dose will be titrated according to the patient’s hemodynamics. Glucocorticoids Glucocorticoids decrease peripheral conversion of thyroxine (T4) to triiodothyronine (T3) and can be used to treat thyrotoxicosis and thyroid storm. Hydrocortisone, methylprednisolone, and dexamethasone are available in intravenous forms and a review of their characteristics is discussed below (Table 7.3). Iodine SSKI and Lugol’s solution can be used to treat thyrotoxicosis and are indicated in the treatment of thyroid storm. Inorganic iodine reduces release of preformed T3 and T4. Five drops of SSKI, 0.25 mL, is equivalent to 250 mg iodine and can be dosed every 6–8 hours. Five to seven drops of Lugol’s solution can be used every 6–8 hours as well. SSKI has been administered rectally after diluting with 20 to 60 mL of sterile water. Hypothyroidism Upon admission to an inpatient setting, levothyroxine (LT-4) ther- apy should be continued in order to maintain a patients’ euthyroid state. It is commonly known that LT-4 absorption is impaired by 7 Management of a Hospitalized Patient with Thyroid Dysfunction 81 Table 7.3 Characteristics of glucocorticoids Equivalent dose (mg) Anti-inflammatory activity Mineralocorticoid activity Duration of action (hours) Hydrocortisone 20 1 1 8–12 Prednisone∗ 5 4 0.8 12–36 Prednisolone 5 4 0.8 12–36 Methylprednisolone 4 5 0.5 12–36 Dexamethasone 0.75 25 0 36–72 ∗Prednisone is administered orally and there is no intravenous form Adapted From: Goodman LS, Brunton LL, Chabner B, Knollmann BC, editors. Goodman & Gilman’s pharmacological basis of therapeutics. 13th ed. New York: McGraw-Hill; 2017 82 M. Ritter and J. V. Hennessey food and that the ideal way to ensure a stable degree of absorption from day-to-day is to take LT-4 fasting, at least 60 minutes prior to eating or 3–4 hours after eating. There are several medications known to impair levothyroxine absorption. Clinically, this can be manifested as an increase in TSH and development of a frank hypothyroid state after previously being euthyroid. Medications that can reduce PO LT-4 absorption include calcium carbonate, cholestyramine, aluminum hydroxide, sevelamer, raloxifene, and ferrous sulfate. The data regarding proton pump inhibitor (PPI) impact on PO LT-4 absorption is mixed. But, LT-4 dosing should be separated from any PPI administration since increases in TSH with initiation of PPI therapy have been reported. During a patient’s hospitalization, LT-4 should not be combined with any other medications at time of administration and should be given while the patient is fasted (i.e., first thing in the morning or 3–4 hours after the last PO intake). In contrast to treating NPO hyperthyroid patients, treating NPO hypothyroid patients is simpler. Options for treating NPO patients with hypothyroidism include intravenous LT-4 or sublin- gual LT-4, or subcutaneous and intramuscular LT-4 injections have been reported in the literature, but these are not approved routes for administration. Pharmacokinetic studies of intramuscu- lar LT-4 have not been done, so it is difficult to determine if a dose change is required. The absorption of oral LT-4 is incomplete; thus, transitioning to intravenous dosing can be challenging. Understanding oral absorption can help better tailor intravenous LT-4 dosing. Hays and Nielson (1994, see suggested readings) analyzed LT-4 absorp- tion in patients based on age. In subjects between 21-year-olds and 69-year-olds, PO LT-4 absorption did not differ with age and was 69.3 ± 11.9%. In subjects over 70 years, PO LT-4 absorption was reduced at 62.8 ± 13.5% with p < 0.001. When transitioning to intravenous LT-4, a dose reduction of 30% for patients less than 70 years and 40% in patients over 70 years is reasonable. The American Thyroid Association recommends a dose reduction of 25% in a patient’s LT-4 dose in hospitalized patients with compro- mised enteral absorption. If intravenous LT-4 therapy is pro- longed, reassessing thyroid function may be indicated. 7 Management of a Hospitalized Patient with Thyroid Dysfunction 83 Levothyroxine can be prepared in liquid and soft gel forms. The liquid form of LT-4 is LT-4 dissolved in glycerol and etha- nol, while soft gel formulation LT-4 is dissolved in glycerin sur- rounded by a layer of gelatin. Both formulations have been used to treat hypothyroidism, particularly in patients with mal- absorption. Some patients with hypothyroidism are treated with a combi- nation of levothyroxine and liothyronine. It is reasonable to con- tinue an oral outpatient regimen in a euthyroid patient with an intact gastrointestinal tract and no impairments in absorption. Liothyronine is also available intravenously and can be used in the treatment of myxedema coma. There is extremely limited data on intravenous liothyronine in hospitalized patients who are NPO, so it would be reasonable to continue an outpatient regimen or tran- sition to LT-4 monotherapy at an appropriate increased dose. Suggested Reading Burch HB, Cooper DS. Management of graves disease: a review. JAMA. 2015;314(23):2544. Carroll R, Matfin G. Review: endocrine and metabolic emergencies: thyroid storm. Ther Adv Endocrinol Metab. 2010;1(3):139–45. De Leo S, Lee SY, Braverman LE. Hyperthyroidism. Lancet. 2016;388(10047):906–18. Goodman LS, Brunton LL, Chabner B, Knollmann BC, editors. Goodman & Gilman’s pharmacological basis of therapeutics. 13th ed. New York: McGraw-Hill; 2017. Hays MT, Nielsen KRK. Human thyroxine absorption: age effects and meth- odological analyses. Thyroid. 1994;4(1):55–64. Hodak SP, Huang C, Clarke D, Burman KD, Jonklaas J, Janicic-Kharic N. Intravenous methimazole in the treatment of refractory hyperthyroid- ism. Thyroid. 2006;16(7):691–5. Jongjaroenprasert W, Akarawut W, Chantasart D, Chailurkit L, Rajatanavin R. Rectal Administration of propylthiouracil in hyperthyroid patients: comparison of suspension enema and suppository form. Thyroid. 2004;12(7):627–31. Jonklaas J, Bianco AC, Bauer AJ, Burman KD, Cappola AR, Celi FS, et al. Guidelines for the treatment of hypothyroidism: prepared by the american thyroid association task force on thyroid hormone replacement. Thyroid. 2014;24(12):1670–751. 84 M. Ritter and J. V. Hennessey Liwanpo L, Hershman JM. Conditions and drugs |
interfering with thyroxine absorption. Best Pract Res Clin Endocrinol Metab. 2009;23(6):781–92. Nabil N, Miner DJ, Amatruda JM. Methimazole: an alternative route of administration. J Clin Endocrinol Metab. 1982;54(1):180–1. Okamura Y, Shigemasa C, Tatsuhara T. Pharmacokinetics of methimazole in normal subjects and hyperthyroid patients. Endocrinol Jpn. 1985;33(5):605–15. Reilly CS, Wood M, Koshakji RP, Wood AJ. Ultra-short-acting beta-b lockade: a comparison with conventional beta-blockade. Clin Pharmacol Ther. 1985;38(5):579–85. Ross DS, Burch HB, Cooper DS, Greenlee MC, Laurberg P, Maia AL, et al. American thyroid association guidelines for diagnosis and management of hyperthyroidism and other causes of thyrotoxicosis. Thyroid. 2016;26(10):1343–421. Walter RM Jr, Bartle WR. Rectal administration of propylthiouracil in the treatment of graves’ disease. Am J Med. 1990;88(1):69–70. Wiersinga WM. Propranolol and thyroid hormone metabolism. Thyroid. 1991;1(3):273–7. Zweig S, Schlosser JR, Thomas SA, Levy CJ, Fleckman AM. Rectal admin- istration of propylthiouracil in suppository form in patients with thyro- toxicosis and critical illness: case report and review of literature. Endocr Pract. 2006;12(1):43–7. Perioperative 8 Management of Patients with Hyperthyroidism or Hypothyroidism Undergoing Nonthyroidal Surgery Catherine J. Tang and James V. Hennessey Contents Assess the Preoperative Patient 86 Evaluate the Type of Surgery 86 The Hypothyroid Patient Undergoing Nonthyroid Surgery 86 Elective Surgery 89 Urgent Surgery 91 The Hyperthyroid Patient Undergoing Nonthyroid Surgery 93 Elective Surgery 94 Urgent Surgery 95 References 98 C. J. Tang (*) · J. V. Hennessey Beth Israel Deaconess Medical Center, Harvard Medical School, Division of Endocrinology, Diabetes and Metabolism, Boston, MA, USA e-mail: ctang@bidmc.harvard.edu; jhenness@bidmc.harvard.edu © Springer Nature Switzerland AG 2020 85 R. K. Garg et al. (eds.), Handbook of Inpatient Endocrinology, https://doi.org/10.1007/978-3-030-38976-5_8 86 C. J. Tang and J. V. Hennessey Assess the Preoperative Patient • History and physical: Focus on comorbid cardiopulmonary disease and other endocrine disorders. • Labs: thyroid function test (TFT) including TSH and free T4 if hypothyroid or TSH, free T4, and total T3 if hyperthyroid; complete blood count (CBC) and basic metabolic panel (BMP). • Radiology: chest X-ray to look for tracheal deviation and com- pression. • Other testing: indirect laryngoscopy if thyroid gland is enlarged to look for vocal cord dysfunction (if present may indicate a difficult intubation). • Anesthesia: airway management. Evaluate the Type of Surgery Once a patient is determined to have a thyroid function abnormal- ity, the next step is to assess the urgency of the surgery. If the surgery can wait until thyroid hormone levels become normal, which may take several weeks or longer, then it is considered elective. If the surgery must be done within a few days, then it is considered urgent (see Table 8.1). The Hypothyroid Patient Undergoing Nonthyroid Surgery Thyroid hormone acts on nearly every tissue in the body and regu- lates essential metabolic pathways, including energy balance, thermogenesis, normal growth, and development [1, 2]. About 90% of free thyroid hormone circulating in the blood is in the form of thyroxine (T4), which is converted to the more potent triiodothyronine (T3) by deiodinase enzymes in the target tissues. The effect of thyroid hormone on the cardiopulmonary system is the primary concern in surgical outcomes, including decreases in 8 Perioperative Management of Patients with Hyperthyroidism… 87 Table 8.1 Summary table Elective surgery Urgent surgery Postoperative Hypothyroidism Subclinical Proceed Proceed Reassess thyroid hypothyroidism status as clinically indicated Moderate Wait until Age <60 years and no CVD: Start PO Continue PO LT4 hypothyroidism euthyroid LT4 at 1.6 mcg/kg daily at time of diagnosis Age >60 years or CVD: Start PO LT4 at 12.5–75 mcg daily at time of diagnosis Severe Wait until Immediately start IV LT4 200–400 mcg Switch to PO LT4 hypothyroidism euthyroid loading dose, followed by maintenance monotherapy IV given at 75% of oral dose 1.6 mcg/kg Taper glucocorticoid daily. If patient not responding, optional as tolerated addition of IV T3 at a loading dose of Reassess pituitary- 5–20 mcg, followed by a maintenance adrenal axis dose of 2.5–10 mcg every 8 h) to outpatient normalize thyroid function If hemodynamically unstable or pituitary-adrenal axis is unknown, start IV hydrocortisone 50–100 mg every 6–8 h before the administration of thyroid hormone (continued) 88 C. J. Tang and J. V. Hennessey https://www.facebook.com/groups/2202763316616203 Table 8.1 (continued) Elective surgery Urgent surgery Postoperative Hyperthyroidism Subclinical Start a BB Start a BB (preferably beta-1 selective Can stop BB hyperthyroidism (preferably blocker such as atenolol or metoprolol beta-1 selective succinate) and proceed blocker such as atenolol or metoprolol succinate) and proceed Overt hyperthyroidism Wait until BB + ATD ± inorganic iodine (add at Continue BB euthyroid least 1 h after thionamide is given) Continue thionamide GD and unable to tolerate ATD: Stop inorganic BB + inorganic iodine iodine TNG and unable to tolerate ATD: BB Taper glucocorticoid alone over 3 postoperative If high risk for thyroid storm regardless days of underlying thyroid etiology, also add Stop cholestyramine glucocorticoid ± cholestyramine Abbreviations: CVD cardiovascular disease, LT4 levothyroxine, T3 triiodothyronine or liothyronine, BB beta-blocker, ATD antithyroid drug (thionamide), GD Graves’ disease, TNG toxic nodular goiter, inorganic iodine – iopanoic acid, SSKI, or Lugol’s solution 8 Perioperative Management of Patients with Hyperthyroidism… 89 systemic vascular resistance, cardiac output, cardiac contractility, heart rate, blood volume, and blood pressure. Clinically, this may present as hypotension, bradycardia, hypoventilation, narrowed pulse pressure, cardiomyopathy, pericardial effusion, and tam- ponade. Other systems can also be adversely affected, resulting in constipation (decreased gastrointestinal motility), hyponatremia (increased antidiuretic hormone), anemia, hypoglycemia, and drug toxicity (reduced renal and hepatic clearance). However, there are no randomized controlled studies that eval- uated the surgical outcomes of hypothyroid versus euthyroid patients in nonthyroidal surgeries, though there are data from ret- rospective and observational studies. Clinical judgment pertain- ing to each individual case is thus crucial. Elective Surgery Subclinical Hypothyroidism Generally, if the surgery is elective, patients should be rendered euthyroid before proceeding to surgery. The exception may be sub- clinical hypothyroidism, where the thyroid-stimulating hormone (TSH) is elevated above reference range but typically lower than 10 μIU/ml and a normal free thyroxine level (FT4). A South Korean observational study found that subclinical hypothyroidism was associated with an increased incidence of transient postopera- tive atrial fibrillation (45.5% vs. 29%) in patients who underwent coronary artery bypass grafting (CABG) [3]. However, the sample size was small (N = 36 subclinical hypothyroid patients), and the subclinical hypothyroid group had a higher rate of preoperative acute myocardial infarction (within 3 months of CABG) compared with the euthyroid group, raising the possibility of acute myocar- dial damage that predisposed to atrial fibrillation. The study did not find any other differences in cardiopulmonary outcomes, including other types of arrhythmias, myocardial infarction, stroke, or respiratory complications. A Boston, Massachusetts, retrospec- tive study found that patients with subclinical hypothyroidism who underwent percutaneous transluminal angioplasty (PTCA) showed no differences in success of the procedure, hospital discharge 90 C. J. Tang and J. V. Hennessey destination, hospital costs, or in-hospital mortality [4]. Given the lack of strong evidence that subclinical hypothyroidism has a sig- nificant negative impact on surgical outcomes, the clinician must consider the patient’s other comorbidities and anticipate possible minor surgical complications. Thus, the decision to proceed with an elective surgery should be individualized, but generally it is rea- sonable to do so. Overt Hypothyroidism In contrast, in patients with overt hypothyroidism, where the TSH is above and the FT4 is below the reference range, elective sur- gery should be deferred until euthyroidism has been achieved. A retrospective study at Massachusetts General Hospital in Boston, MA, compared surgical outcomes in 40 hypothyroid patients matched with 80 euthyroid controls [5]. The hypothyroid patients had a median TSH of 99 (reference 0.5–3.5 μIU/ml) and T4 of 2.0 (reference 4.0–12.0 μg/dl). The study found that in noncardiac surgery, hypothyroid patients were more likely to have intraopera- tive hypotension, though it was corrected quickly with no associ- ated myocardial infarction or cerebrovascular accident. There was no difference in rate of intraoperative arrhythmias or the amount of blood loss. Among patients undergoing cardiac surgery, hypo- thyroid patients were more likely to have perioperative heart fail- ure, but no differences in myocardial infarction or arrhythmias were observed. The authors acknowledged that there might be an inherent bias in these observations in a retrospective study. Other notable findings in the hypothyroid patients included greater prev- alence of postoperative gastrointestinal (constipation, ileus) and neuropsychiatric (confusion, psychosis) occurrences in hypothy- roid patients. Hypothyroid subjects were also more likely to have experienced a difficult endotracheal intubation and were less likely to manifest postoperative fever in response to infection. However, there was no difference in pulmonary complications, hyponatremia, length of hospitalization, or death rates. Another retrospective study at the Mayo Clinic in Rochester, MN, compared surgical outcomes in 59 hypothyroid patients and 59 matched euthyroid controls [6]. The study found that hypothyroid patients had more preoperative risk factors including 8 Perioperative Management of Patients with Hyperthyroidism… 91 lower hemoglobin levels and a higher rate of hypertension, but no difference in surgical outcomes were observed, including intraop- erative blood pressure, arrhythmias, fluid and electrolyte imbal- ances, myocardial infarction, pulmonary complications, bleeding complications, sepsis, or length of hospitalization. There was a trend toward longer time to extubation in hypothyroid patients, though it was not statistically significant. Postoperative gastroin- testinal and neuropsychiatric outcomes were not assessed in this study. Admittedly, these studies are older, had small sample sizes, and may therefore not conclusive. Nonetheless, if a surgery is elective, it is prudent to render the overtly hypothyroid patient euthyroid to avoid any potential perioperative complications such as intraoperative hypotension and prolonged time to extubation. In addition to medical management, careful attention should also be paid to airway management. Obstructive goiters may be present in either hypo- or hyperthyroidism and can cause mechan- ical difficulties for the anesthesiologist. Retrosternal goiters may obstruct the inferior vena cava, and vocal cord dysfunction may cause a difficult intubation. For these reasons, patients with a goi- ter may need additional preoperative assessment including a chest X-ray to look for tracheal compression and deviation, as well as an indirect laryngoscopy to look for vocal cord dysfunction [7]. Urgent Surgery Subclinical Hypothyroidism In patients with subclinical hypothyroidism, it is generally fine to proceed with an urgent surgery, for the reasons stated above in “elective surgery.” Overt Hypothyroidism However, overtly hypothyroid patients should initiate thyroxine (T4) replacement as soon as possible as to minimize the delay in proceeding with an urgent surgery. Both the American Thyroid Association (ATA) and the American Association of Clinical Endocrinologists (AACE) recommend levothyroxine (LT4) to be the drug of choice in the treatment of hypothyroidism [8, 9], 92 C. J. Tang and J. V. Hennessey which has largely replaced the previously favored desiccated thy- roid. Due to the variable bioequivalence of several levothyroxine tablet and one gelatin formulations on the market, it is best to maintain the same preparation, whether brand or generic, in order to minimize fluctuations in thyroid hormone levels. The initial LT4 dosage depends on the severity of the hypothyroidism, etiol- ogy of the hypothyroidism, age, and comorbidities. In general, a full replacement dose of 1.6 mcg/kg of actual body weight per day can be initiated in younger patients (<60 years old) who are oth- erwise healthy with no cardiovascular comorbidities. On the other hand, older patients (>60 years) or those with known cardiovascu- lar disease should start at a lower dose, from 12.5 to 75 mcg daily, erring on the lower range in patients with cardiovascular disease and higher range if TSH >12 mIU/L [8, 9]. Repeat TSH monitor- ing should be done every 4–6 weeks. However, given that it usu- ally takes several weeks for the TSH to normalize, it is not always necessary to wait until euthyroidism if surgery must be done urgently. As such, the surgery and anesthesia teams should antici- pate possible mild to moderate perioperative complications as detailed above under “elective surgery” and prepare accordingly. In the case of severe hypothyroidism where the patient has or is suspected to have myxedema coma, surgery should be delayed until patient is adequately treated. However, if surgery is urgent and cannot be delayed, then intravenous (IV) replacement with LT4 should be instituted immediately, at a loading dose of 200– 400 mcg, with the lower end of the range for patients who are older and have smaller body habitus and in the presence of cardio- vascular comorbidities. Maintenance levothyroxine should be given intravenously at 75% |
(approximately the fraction of oral LT4 that is absorbed) of the oral dosing at 1.6 mcg/kg of body weight per day. The administration of intravenous liothyronine (T3) in addition to IV LT4 is optional. The rationale is that periph- eral T4 to T3 conversion is decreased in acutely ill patients, and IV T3 may accelerate clinical improvement. If used, the loading dose of IV T3 is 5–20 mcg, followed by a maintenance dose of 2.5–10 mcg every 8 h. Again, one should aim for the lower end of the range for patients who are older and have smaller body habitus and in the presence of cardiovascular comorbidities [9]. 8 Perioperative Management of Patients with Hyperthyroidism… 93 Concurrent adrenal insufficiency must be considered in myx- edematous patients, and if they are hemodynamically unstable or the function of their pituitary-adrenal axis is unknown, IV stress dose corticosteroids should be given before the administration of thyroid hormones, to avoid the precipitation of an adrenal crisis. A typical regimen is hydrocortisone 50–100 mg every 6–8 h. Once clinical improvement ensues, LT4 can be switched to an oral formulation. Generally, T3 is not continued orally and LT4 mono- therapy is preferred for maintenance. Note that even with immedi- ate treatment, patients in myxedema coma remain high surgical risk and should have close perioperative hemodynamic monitor- ing. Thus, a multidisciplinary approach with the surgeon, anesthe- siologist, and endocrinologist is crucial in caring for these patients who must undergo urgent surgery. The Hyperthyroid Patient Undergoing Nonthyroid Surgery Excess thyroid hormone produces classic features of hyperthy- roidism such as weight loss, tremor, heat intolerance, and hyper- activity. In the cardiovascular system, too much thyroid hormone increases cardiac contractility, heart rate, cardiac output, and sys- tolic blood pressure, while decreases in diastolic blood pressure and systemic vascular resistance are observed. In the pulmonary system, excess thyroid hormone increases oxygen consumption, respiratory rate, and minute ventilation while decreasing vital capacity and lung compliance. Cardiovascular symptoms can include palpitations, shortness of breath, tachycardia, widened pulse pressure, cardiac murmurs, and chest pain. Of particular interest to the anesthesiologist are atrial fibrillation, ischemic heart disease, and congestive heart failure [7]. Surgery in patients with poorly controlled thyrotoxicosis has been associated with a mortality rate as high as 20% [10], primar- ily due to the precipitation of thyroid storm. However, the actual surgical risk is probably lower in recent decades due to better perioperative management. Again, as in hypothyroidism, there are few randomized controlled studies that have evaluated the surgi- 94 C. J. Tang and J. V. Hennessey cal outcomes of hyperthyroid versus euthyroid patients in nonthy- roidal surgeries. Clinical judgment pertaining to each individual case is thus crucial. Elective Surgery Subclinical Hyperthyroidism Patients with subclinical hyperthyroidism, where the TSH may be slightly suppressed but the levels of T3 and T4 are normal, can generally proceed with an elective surgery, after the initiation of a beta-blocker if no contraindications are evident. A randomized, prospective Swedish study compared surgical outcomes in 30 hyperthyroid patients undergoing thyroid surgery (hemithyroid- ectomy or subtotal resection) and preoperatively managed with either methimazole and thyroxine or metoprolol alone [11]. The methimazole and thyroxine group was treated for 12 weeks and was rendered clinically and biochemically euthyroid prior to thy- roid surgery. The metoprolol group was treated for 5 weeks and remained biochemically hyperthyroid but appeared clinically euthyroid prior to thyroid surgery. The two groups did not differ in anesthetic or cardiovascular complications, nor did anyone suf- fer from thyroid storm. The authors’ conclusion was that meto- prolol alone may be a reasonable choice for preoperative management for hyperthyroid patients needing thyroid surgeries, with the advantage of a shorter preoperative treatment period and without suffering any apparent serious complications. One limita- tion of the study was that the dose of metoprolol was 200–400 mg per day in divided doses, which is much higher than is typically used today. But it is worth noting that this study particularly looked at overtly hyperthyroid patients who underwent thyroid surgeries to treat their hyperthyroidism, so it is likely that the dose of beta-blocker requirement is actually much lower in subclinical hyperthyroid patients. Although some clinicians still prefer pro- pranolol for its reduction of peripheral T4 to T3 conversion, a beta-1 selective blocker such as atenolol or metoprolol succinate is probably better given its longer duration of action and greater safety in patients with obstructive pulmonary disease. A starting 8 Perioperative Management of Patients with Hyperthyroidism… 95 dose may be atenolol or metoprolol succinate 25–50 mg daily and uptitrate as needed for a target heart rate of less than 80 bpm. Overt Hyperthyroidism Because of the risk of precipitating thyroid storm, elective surger- ies should always be postponed in patients with overt hyperthy- roidism, until the patient is rendered euthyroid [10, 12]. Moreover, atrial fibrillation occurs in 10–15% of patients with overt hyper- thyroidism with the prevalence higher in older individuals [12]. Urgent Surgery Subclinical Hyperthyroidism Patients with subclinical hyperthyroidism may proceed with urgent surgeries after the initiation of a beta-blocker, for reasons as discussed above. Overt Hyperthyroidism Overtly hyperthyroid patients should wait until euthyroid before proceeding with surgery. However, if surgery cannot wait and is urgent or emergent, immediate action must be taken to stabilize thyrotoxicosis to reduce the risk of perioperative mortality. For all thyrotoxic patients regardless of etiology, beta-blockers should be initiated immediately. Calcium channel blockers such as diltia- zem and verapamil can be used if beta-blockers are contraindi- cated. There is no general consensus on the superiority of any particular beta-blocker, though each may offer its advantages. Nonspecific beta-blocker propranolol has the additional benefit of blocking 5′-mono deiodinase activity, thus decreasing peripheral T4 to T3 conversion at higher doses, and can be started at 40–80 mg PO every 4–8 h and titrated for a target heart rate less than 80 bpm [10]. Alternatively, beta-1 selective blocker such as atenolol or metoprolol succinate may be used, at an initial dose of 25–50 mg. Though they are longer acting than propranolol and the conventional once daily dosing is more convenient, realistically they may still need to be given twice daily due to the accelerated clearance seen in hyperthyroidism [12]. IV administration may be 96 C. J. Tang and J. V. Hennessey achieved through metoprolol tartrate, propranolol, or esmolol. Esmolol has the shortest half-life of only a few minutes and thus the advantage of fast adjustment of hemodynamic parameters; an initial loading dose is 250–500 mcg/kg, followed by maintenance infusion of 50–100 mcg/kg/min [10, 13]. Beta- blockers should be continued postoperatively in nonthyroidal surgeries, possibly in lower doses, for as long as the patient remains clinically thyro- toxic or until the underlying cause of the hyperthyroidism is addressed. If the underlying etiology of hyperthyroidism is Graves’ dis- ease or toxic nodular goiter, thionamide therapy should be insti- tuted as soon as an urgent nonthyroid surgery is deemed necessary. Thionamide is a class of antithyroid drugs (ATD) which includes propylthiouracil (PTU), methimazole (MMI), and carbimazole. Only PTU and MMI are available in the United States, whereas carbimazole is available in Europe and elsewhere. PTU and MMI can be given either orally or rectally. They block new thyroid hor- mone synthesis by inhibiting the enzyme thyroid peroxidase, which is responsible for the organification of iodine and the cou- pling of mono- and diiodotyrosines to make T3 and T4. Since thionamides largely affect new thyroid hormone synthesis but not secretion of preformed thyroid hormones, they usually take 3–8 weeks to achieve euthyroidism [12]. In the case of an urgent surgery that may take place within a matter of days or hours, thi- onamide therapy alone is not adequate, and additional treatment should be instituted to stabilize the thyrotoxicosis, which are dis- cussed below. PTU is shorter acting and has the additional benefit of decreased T4 to T3 conversion. A typical starting dose of PTU is 100–150 mg every 6–8 h [12]. However, if the patient is severely hyperthyroid or if thyroid storm is suspected, the 2016 ATA guidelines recommend a PTU loading dose of 500–1000 mg, fol- lowed by 250 mg every 4 h [14]. MMI is longer acting and is generally preferred over PTU for its lesser degree of toxicities, except during the first trimester of pregnancy, when PTU is less teratogenic. A typical starting dose of MMI is 20–40 mg daily, though in a severely hyperthyroid patient, the dose is increased to 60–80 mg per day [14], which may be divided into two to three doses daily due to the increased clearance seen in hyperthyroid- 8 Perioperative Management of Patients with Hyperthyroidism… 97 ism. Both PTU and MMI have similar side effect profiles and have 50% cross-reactivity. Minor toxicities include rash, urticaria, and arthralgia, which occur in 1–5% of patients [10, 12]. A more seri- ous complication is hepatotoxicity, which is more common in PTU (2.7%) than in MMI (0.4%), though liver failure remains rare in either (0.03–0.05%) [14]. Perhaps the most dreaded toxic- ity is agranulocytosis, which occurs in 0.1–0.5% of patients [10, 14], with the vast majority of cases occurring within 60–90 days of starting therapy. Although the effect is conventionally thought to be dose-related in MMI (rare at doses below 40 mg daily) but not in PTU, a more recent Danish study demonstrated that the average dose of MMI at the onset of agranulocytosis was 25 mg daily in patients with Graves’ disease [15]. Postoperatively, ATD should be continued at the same dose until thyroid hormone levels are no longer elevated. As mentioned earlier, since ATD takes 3–8 weeks to achieve euthyroidism, it alone is not sufficient in preparing a patient for urgent surgery. In such cases, inorganic iodine should be added to ATD to decrease the production of new thyroid hormone, which is also known as the Wolff-Chaikoff effect and can be seen within 24 h of administration. In addition, inorganic iodine also decreases the release of preformed thyroid hormone. A normal thyroid gland will eventually escape the Wolff-Chaikoff effect and resume thy- roid hormone production, but the effect may persist in those with autoimmune thyroid disease. In contrast, a toxic nodular goiter (TNG) may use the excess iodine as substrate to make more thy- roid hormone (known as the Jod-Basedow effect), further exacer- bating the thyrotoxicosis [10, 12]. For this reason, while iodine can be used as monotherapy in Graves’ disease, it should never be used as monotherapy in TNG. In fact, it is crucial that iodine should be given at least an hour after the administration of a thionamide. In this setting where thyrotoxicosis must be urgently stabilized, iodine can be administered as saturated solution of potassium iodide (SSKI) five drops (50 mg of iodide per drop) every 6 h [12, 14]. Inorganic iodine should be stopped after surgery. Other agents that may be used in the acutely thyrotoxic patient regardless of the underlying cause in preparation of urgent surgery include glucocorticoids and cholestyramine. Glucocorticoids 98 C. J. Tang and J. V. Hennessey reduce peripheral T4 to T3 conversion within hours and can be tapered over 72 h postoperatively [10, 12]. Choice of glucocorti- coids includes hydrocortisone 100 mg every 8 h, dexamethasone 2 mg every 6 h, or betamethasone 0.5 mg every 6 h, which all can be given either IV or PO (betamethasone can also be given as IM) [10, 12]. Postoperatively, glucocorticoids should be tapered over the course of 72 h [10, 12]. Cholestyramine, a bile acid seques- trant, binds to thyroid hormone in the intestine and reduces its reabsorption, thus decreasing its enterohepatic circulation. It is not a first- or second-line agent but is potentially useful in situations where it is not possible to render the patient completely euthyroid prior to surgery or if the patient is intolerant of ATD [14]. A typical dose of cholestyramine used in this setting is 4 g four times daily [12]. Cholestyramine is generally stopped postoperatively. Patients who are intolerant of ATD and those who have Graves’ disease as the underlying etiology may be treated with beta- blockers and iodine, with the addition of glucocorticoid and pos- sibly cholestyramine if hyperthyroidism is severe. In ATD-intolerant patients whose underlying etiology is TNG, preoperative manage- ment may consist of beta-blockers alone, with the addition of glu- cocorticoid and possibly cholestyramine if hyperthyroidism is severe. Iodine is not used in this |
scenario due to concern of exacer- bating thyrotoxicosis, for the reasons stated previously. As in the case of severe hypothyroidism, patients with severe hyperthyroidism remain high surgical risk despite optimal periop- erative management. A multidisciplinary approach with the sur- geon, anesthesiologist, and endocrinologist is vital in the caring of these patients who require urgent surgeries, and careful attention must be paid to airway management (due to goiters, as discussed in the previous section) and hemodynamic monitoring. References 1. Lin JZ, Martagón AJ, Cimini SL, Gonzalez DD, Tinkey DW, Biter A, et al. Pharmacological activation of thyroid hormone recep- tors elicits a functional conversion of white to brown fat. Cell Rep. 2015;13(8):1528–37. 8 Perioperative Management of Patients with Hyperthyroidism… 99 2. Mullur R, Liu YY, Brent GA. Thyroid hormone regulation of metabolism. Physiol Rev. 2014;94(2):355–82. 3. Park YJ, Yoon JW, Kim KI, Lee YJ, Kim KW, Choi SH, et al. Subclinical hypothyroidism might increase the risk of transient atrial fibrillation after coronary artery bypass grafting. Ann Thorac Surg. 2009;87(6):1846–52. 4. Mantzoros CS, Evagelopoulou K, Moses AC. Outcome of percutaneous transluminal coronary angioplasty in patients with subclinical hypothy- roidism. Thyroid. 1995;5(5):383–7. 5. Ladenson PW, Levin AA, Ridgway EC, Daniels GH. Complications of surgery in hypothyroid patients. Am J Med. 1984;77(2):261–6. 6. Weinberg AD, Brennan MD, Gorman CA, Marsh HM, O’Fallon WM. Outcome of anesthesia and surgery in hypothyroid patients. Arch Intern Med. 1983;143(5):893–7. 7. Farling PA. Thyroid disease. Br J Anaesth. 2000;85(1):15–28. 8. Garber JR, Cobin RH, Gharib H, Hennessey JV, Klein I, Mechanick JI, Pessah-Pollack R, Singer PA, Woeber KA, American Association of Clinical Endocrinologists and American Thyroid Association Taskforce on Hypothyroidism in Adults. Clinical practice guidelines for hypothy- roidism in adults: cosponsored by the American Association of Clinical Endocrinologists and the American Thyroid Association. Endocr Pract. 2012;18(6):988–1028. 9. Jonklaas J, Bianco AC, Bauer AJ, Burman KD, Cappola AR, Celi FS, et al. Guidelines for the treatment of hypothyroidism: prepared by the American Thyroid Association task force on thyroid hormone replace- ment. Thyroid. 2014;24(12):1670–751. 10. Langley RW, Burch HB. Perioperative management of the thyrotoxic patient. Endocrinol Metab Clin North Am. 2003;32(2):519–34. 11. Adlerberth A, Stenstrom G, Hasselgren PO. The selective beta 1-blocking agent metoprolol compared with antithyroid drug and thyroxine as preop- erative treatment of patients with hyperthyroidism. Results from a pro- spective, randomized study. Ann Surg. 1987;205(2):182–8. 12. Palace MR. Perioperative management of thyroid dysfunction. Health Serv Insights. 2017;10:1178632916689677. 13. Buget MI, Sencan B, Varansu G, Kucukay S. Anaesthetic management of a patient with thyrotoxicosis for nonthyroid surgery with peripheral nerve blockade. Case Rep Anesthesiol. 2016;2016:9824762. 14. Ross DS, Burch HB, Cooper DS, Greenlee MC, Laurberg P, Maia AL, et al. 2016 American Thyroid Association guidelines for diagnosis and management of hyperthyroidism and other causes of thyrotoxicosis. Thyroid. 2016;26(10):1343–421. 15. Andersen SL, Olsen J, Laurberg P. Antithyroid drug side effects in the population and in pregnancy. J Clin Endocrinol Metab. 2016;101(4): 1606–14. Thyroid Problems 9 Encountered Specifically in Inpatients with Cardiac Disease Jeena Sandeep and James V. Hennessey Contents Hyperthyroidism/Thyrotoxicosis 102 Hypothyroidism 103 Hyperthyroidism/Thyrotoxicosis 104 Effects on the Cardiovascular System 104 Management of Thyrotoxicosis in the Hospitalized Patient 105 Establishing the Etiology of Thyrotoxicosis 105 Treatment Recommendations Based on Etiology 106 Subclinical Hyperthyroidism 107 Treatment with Amiodarone in Patients with Cardiac Arrhythmias 108 J. Sandeep (*) St. Elizabeth Medical Center, Department of Medicine, Division of Endocrinology, Brighton, MA, USA e-mail: jeena.sandeep@steward.org J. V. Hennessey Beth Israel Deaconess Medical Center, Harvard Medical School, Division of Endocrinology, Diabetes and Metabolism, Boston, MA, USA e-mail: jhenness@bidmc.harvard.edu © Springer Nature Switzerland AG 2020 101 R. K. Garg et al. (eds.), Handbook of Inpatient Endocrinology, https://doi.org/10.1007/978-3-030-38976-5_9 102 J. Sandeep and J. V. Hennessey Hypothyroidism and Cardiac Disease 108 Impact of Hypothyroidism on Cardiovascular Risk Factors 108 Cardiovascular Hemodynamics in Hypothyroidism 109 Heart Failure and Arrhythmias in Hypothyroidism 109 Diagnosis of Hypothyroidism 110 Treatment of Overt Hypothyroidism 111 Thyroid Hormone Treatment in Cardiac Failure and Patients Undergoing Cardiac Surgery 112 Suggested Reading 113 Hyperthyroidism/Thyrotoxicosis • Thyrotoxicosis – excessive thyroid hormone regardless of eti- ology – affects the cardiovascular system resulting in cardiac arrhythmias, EKG changes, congestive heart failure (CHF) and angina, and/or myocardial infarction. • Patients with subclinical thyrotoxicosis may be asymptomatic, manifest resting tachycardia, or may develop atrial fibrillation and be at risk for embolic stroke. • Establishing the etiology of thyrotoxicosis is critical in deter- mining appropriate therapeutic interventions. The most com- mon conditions are Graves’ disease, toxic multinodular goiter (toxic MNG) or toxic adenoma (TA), iatrogenic thyrotoxico- sis, and subacute thyroiditis (SAT). • Amiodarone can cause either hypothyroidism or thyrotoxico- sis. There are two types of amiodarone-induced thyrotoxico- sis (AIT) which may be difficult to differentiate from one another. • Diagnostic evaluation includes the history, medication (iatro- genic) and supplement ingestion (factitia), viral infection, neck pain [suggestive of subacute thyroiditis]), presence of eye and pretibial symptoms (Graves’ disease), and presence of thyroid nodules (toxic nodular goiter or adenoma). Lab testing includes TSH, assessment of free thyroxine, T3 testing, thyrotropin receptor antibodies (TRab), and 123-I uptake and/or scanning. 9 Thyroid Problems Encountered Specifically in Inpatients… 103 • Treatments include beta-blockers, antithyroid drugs (methima- zole generally preferred), 131-I ablation, and/or surgery. Treatment for type 1 AIT includes antithyroid drugs, potas- sium perchlorate (not available in the United States), or sur- gery, and type 2 AIT may either be observed, or if mild, may be treated with glucocorticoids, and if inadequately controlled, may require surgery. Hypothyroidism • Hypothyroidism may affect cholesterol metabolism and other CV risk factors such as C-reactive protein and homocysteine that may promote CAD and can also predispose patients to atrial fibrillation (Afib). • Hypothyroidism increases systemic vascular resistance (SVR) and diminishes cardiac output, stroke volume, and heart rate resulting in lower cardiac output. • Diminished erythropoietin production results in blood volume decrease. Capillary permeability allows pericardial and pleural effusions further compromising cardiac (tamponade) and pul- monary function. • Prolongation of the QT interval predisposes to ventricular arrhythmia and AV nodal dysfunction. • Diagnosis requires measurement of TSH and free T4 (FT4) levels. Overt hypothyroidism is recognized when TSH is clearly elevated (over 10 mIu/L) and FT4 is low, while sub- clinical hypothyroidism is characterized by a sustained TSH level between the upper reference range and 10 mIu/L and a normal FT4. • Treatment with levothyroxine (LT4) in overt hypothyroidism improves LDL cholesterol metabolism, diastolic hypertension, and cardiac dysfunction while accelerating heart rate and delaying progression of atherosclerosis. Due to potential underlying CAD, caution in reestablishing euthyroidism may be warranted. Gradual increasing doses at intervals of 6–8 week allow equilibration of thyroid hormone levels before retesting. 104 J. Sandeep and J. V. Hennessey • Coronary bypass surgery is generally considered safe in patients with hypothyroidism. Concerns regarding periopera- tive care and the risk of postoperative atrial fibrillation in hypothyroid patients undergoing cardiac surgery have been raised. Hyperthyroidism/Thyrotoxicosis Effects on the Cardiovascular System Increased levels of circulating thyroid hormones alter the function of the cardiovascular system and produce significant clinical effects. Increased systolic blood pressure due to increased con- tractile ventricular force and decreased diastolic pressure due to lower peripheral vascular resistance result in wide pulse pressure and enhanced cardiac output. Tachycardia reflects a positive chro- notropic action of thyroid hormone on the heart. Increased stroke volume and volume expansion result in increased circulating blood volume. The drop in DBP leads to activation of renin angio- tensin aldosterone system increasing sodium reabsorption and consequent volume expansion. Thyroid hormone directly increases erythropoietin synthesis increasing the red cell mass increasing the preload. Resting tachycardia results from thyroid hormone acting on the sinus node to increase heart rate. The net result of decreased afterload, increased left ventricular contractil- ity, increased preload, wide pulse pressure, and increased heart rate is an overall increase in cardiac output. Cardiac Arrhythmias and EKG Changes Arrhythmias include resting tachycardia and atrial fibrillation which may convert to sinus rhythm within 8–12 weeks after effec- tive antithyroid treatment in the absence of valvular heart disease and of recent onset. EKG changes include the supraventricular arrhythmias and nonspecific ST segment and T-wave changes as well as a short PR interval due to an increased rate of conduction through the AV node. 9 Thyroid Problems Encountered Specifically in Inpatients… 105 Congestive Heart Failure (CHF) and Angina Hyperthyroidism may cause or worsen preexisting cardiac dis- ease by increasing myocardial oxygen demand, contractility, and heart rate. These changes may lead to silent ischemia, angina, or compensated heart failure and even endothelial dysfunction. Heart failure in the thyrotoxic patient occurs in the setting of underlying coronary heart disease and/or atrial fibrillation. Cardiac failure can occur even in young patients without known underlying heart disease suggesting a cardiomyopathy associated with thyrotoxicosis which may well be reversible. Recent reports suggest an increased prevalence of pulmonary hypertension in the setting of thyrotoxicosis suggesting that thyroid hormones increase pulmonary vascular resistance in contrast to its effects on systemic vascular resistance. Management of Thyrotoxicosis in the Hospitalized Patient Establishing the Etiology of Thyrotoxicosis Symptomatic patients with thyrotoxicosis, especially patients with heart rates above 90 beats per minute, elderly patients, and patients with underlying cardiovascular disease should be treated with beta-blockers while determining the etiology of thyrotoxicosis. The most frequent endogenous diagnoses of thy- rotoxicosis include Graves’ disease, toxic multinodular goiter (toxic MNG) or toxic adenoma (TA), and subacute thyroiditis (SAT). Graves’ disease patients may be recognized by the pres- ence of pretibial myxedema and eye involvement. Those with toxic MNG and toxic adenoma may have a prior history of thy- roid nodules. The history may point to thyroiditis as the etiol- ogy. Some may report recent viral infection followed by pain and tenderness over the thyroid or have recently given birth prior to developing thyrotoxicosis. A radioactive iodine uptake is useful to distinguish exogenous sources of thyrotoxicosis and thyroiditis from Graves’ disease and toxic nodular disorders. 106 J. Sandeep and J. V. Hennessey Iodine uptake may be near zero in exogenous thyrotoxicosis, painless, postpartum or painful subacute (deQuervains) thyroid- itis. In addition, low or near zero uptake can also be seen in cases of ectopic thyroid disorders such as Struma Ovarii and after iodine contamination such as post CT with iodine contrast or while on treatment with medications such as amiodarone. Radioactive iodine uptake is typically elevated and diffuse in Graves’ disease while focal nodular patterns are seen in patients with toxic nodular goiters. Treatment Recommendations Based on Etiology Thyrotoxicosis due to exogenous thyroid hormone application is best treated with beta-blocker and discontinuation of the thyroid hormone source. Severely toxic individuals may respond quickly to plasmapheresis. Patients with subacute thyroiditis are treated with beta-blockers, nonsteroidal anti-inflammatory drugs for pain, and if needed corticosteroids. Once Graves’ disease is con- firmed, treatment may include antithyroid drugs (ATDs), radio- active iodine, or surgery. Patient preference is an important factor in deciding on a treatment modality. However, patients with acute cardiopulmonary disease who are clinically unstable are usually treated with ATDs followed by radioactive iodine treatment, particularly if they are still at high surgical risk. Patients who are pregnant, lactating mothers, those with coexist- ing thyroid cancer, and those unable to comply with radiation safety guidelines or planning a pregnancy within 4–6 months should not receive radioactive iodine. On the other hand, definite contraindications to antithyroid medication usage and switching include major adverse reactions such as agranulocytosis and hepatotoxicity. Methimazole is the preferred ATD with the potential exception of thyroid storm, the first trimester of pregnancy, and minor reac- tions to methimazole when propylthiouracil (PTU) is preferred. Starting dose of methimazole is usually 10–20 mg once daily and is titrated based on the clinical and biochemical response. PTU is shorter acting and is administered multiple times a day with start- 9 Thyroid Problems Encountered Specifically in Inpatients… 107 ing dose from 50 to 150 mg three times daily. Patients are moni- tored for side effects including rash, agranulocytosis (fever, sore throat), and cholestasis (pale stools, jaundice, abdominal pain, nausea, vomiting). Thyrotoxicosis due to toxic multinodular goiter (TMNG) or toxic adenoma (TA) should be treated with radioactive iodine or surgery. Chronic low-dose methimazole can be considered for those with contraindications to definitive treatment. In patients with cardiovascular disease or elderly patients or in situations where there is high risk of worsening of hyperthyroidism post- radioactive iodine treatment, beta-blockers should be initiated prior to administering radioactive iodine treatment. |
Patients undergoing surgery for Graves’ disease should be treated with beta-blockers and rendered clinically and biochemi- cally euthyroid preoperatively with ATDs. Potassium iodide may be administered in the immediate preoperative period. If the patient needs urgent surgery, beta-blocker, ATDs, and potassium iodide should be used as long as possible to achieve or approach a euthyroid state prior to surgery. Subclinical Hyperthyroidism Patients with subclinical thyrotoxicosis may be asymptomatic or present with resting tachycardia or atrial fibrillation. The 10-year risk of developing atrial fibrillation in elderly patients with a TSH less than 0.1 mIU/L is three times higher compared to euthyroid patients. Elderly patients with subclinical thyrotoxicosis have an increased risk of all-cause and cardiovascular mortality, while young and middle-aged people manifest cardiac changes includ- ing increased ventricular mass and contractility and reduced dia- stolic function. The decision to treat subclinical hyperthyroidism is based on risk. If TSH is persistently less than 0.1 mIU/L, patients older than 65 years, patients with cardiac risk factors or disease, and those with osteoporosis should be treated. In addi- tion, patients with clinical symptoms of hyperthyroidism and postmenopausal women who are not treated with estrogens or bisphosphonates are treated if TSH is persistently lower than 108 J. Sandeep and J. V. Hennessey 0.1 mIU/L. When TSH is less than normal but above 0.1 mIU/L, treatment would be considered for patients over 65 years of age, patients who are symptomatic, and those with cardiac disease. Treatment with Amiodarone in Patients with Cardiac Arrhythmias Amiodarone is iodine rich (37% by weight) and concentrates in several tissues resulting in an effective half-life of more than 50 days. Amiodarone can cause both hypothyroidism and thyro- toxicosis. There are two types of amiodarone-induced thyrotoxico- sis (AIT). Type 1 AIT is a form of endogenous hyperthyroidism where there is overproduction of thyroid hormone and occurs in patients with underlying thyroid disease including Graves’ or mul- tinodular goiter. Type 1 AIT occurs more frequently in areas of iodine deficiency. Type 2 AIT is a form of thyroiditis where pre- formed thyroid hormone is released from the thyroid in an unregu- lated manner. Treatment for type 1 AIT includes antithyroidal drugs, potassium perchlorate (to block thyroidal iodine uptake), or surgery. Type 2 may be observed, and if mild, may be treated with glucocorticoids or if severe may be treated with surgery if not responsive to medical therapy. It may be difficult to differentiate type 1 from type 2 AIT, and a combination of antithyroidal drugs (MMI) and glucocorticoids is frequently used as the initial treat- ment. There is debate if amiodarone needs to be stopped when thyrotoxicosis occurs. As amiodarone is lipophilic and may not be cleared for 6 months or more after stopping the drug, discontinua- tion is not of short-term use. If treatment with amiodarone is criti- cal to controlling the arrhythmias, amiodarone should be continued. Hypothyroidism and Cardiac Disease Impact of Hypothyroidism on Cardiovascular Risk Factors Both overt and subclinical hypothyroidism (SCHypo) are asso- ciated with changes in lipid parameters and are considered risk 9 Thyroid Problems Encountered Specifically in Inpatients… 109 factors for cardiovascular disease. Total LDL cholesterol and apolipoprotein B levels are adversely affected by insufficient circulating thyroid hormone as decreased expression of the hepatic LDL receptor and reduced activity of cholesterol α-monooxygenase activity diminish cholesterol clearance. Other CV risk factors such as C-reactive protein and homocysteine are also elevated in the hypothyroid state. This risk profile may lead to the progression of undiagnosed coronary artery and vascular disease in patients with hypothyroidism. Additionally, the effec- tiveness and safety of treatment of dyslipidemia with statin med- ications, specifically myopathy, may be impacted by the presence of hypothyroidism. Cardiovascular Hemodynamics in Hypothyroidism Systemic vascular resistance (SVR) is increased and cardiac out- put declines. Thyroid hormone has a direct vasodilator effect on vascular smooth muscle and indirect effect by inducing endothelium- derived nitric oxide release. Both of these actions are impaired in mild and overt hypothyroidism which results in further increase in the systemic vascular resistance. Cardiac con- tractility is negatively affected leading to a reduction in stroke volume and decrease in heart rate which together lead to a reduc- tion in cardiac output. Additional changes include diminished stimulation of erythropoietin production decreasing plasma and circulating blood volume. Capillary permeability increases result- ing in gravity-d ependent edema and pericardial and pleural effu- sions which may further compromise both cardiac (tamponade physiology) and pulmonary function. Heart Failure and Arrhythmias in Hypothyroidism The impact of hypothyroidism on cardiac contractility may result in clinical cardiac failure, often characterized as diastolic dysfunc- tion that results in abnormal cardiac muscle relaxation. However, heart failure caused by hypothyroidism differs physiologically from heart failure caused by non-thyroidal causes. Despite reduc- 110 J. Sandeep and J. V. Hennessey tion in cardiac output, hypothyroid patients have normal arteriove- nous (AV) oxygen extraction as against patients with organic heart disease and heart failure who have increased AV oxygen extrac- tion. Patients with hypothyroidism are able to mount cardiac response to the exercise in terms of increasing the cardiac output and reduction in SVR as against patients with classic CHF. In addi- tion, signs of right heart failure are rare in hypothyroid patients, and they are able to excrete sodium load when compared with patients with CHF from organic heart disease. Exercise intolerance seen in hypothyroid patients is due to weakness of skeletal muscle and due to respiratory etiology rather than cardiac failure. As noted above, the presence of CAD risk factors potentially predispose these patients to atrial fibrillation (Afib) which further compromises optimal cardiac function. Recent data indicated that hypothyroidism may predict persistently symptomatic atrial fibril- lation impacting cardiovascular outcomes. A prolonged QT inter- val is commonly noted in hypothyroid subjects likely indicating a ventricular vulnerability to arrhythmia, while conduction defects across the AV node and through the ventricles are also reported. Amiodarone-Induced Hypothyroidism As a result of the substantial (37% by weight) iodine content of amiodarone, those with previously damaged thyroid glands due to autoimmune thyroid disease or 131-I ablation for Graves’ are especially susceptible to the Wolff-Chaikoff effect, thereby decreasing thyroid hormone production and lapse into hypothy- roidism after long-term treatment. Due to its prolonged half-life and the danger posed by the underlying arrhythmias that amiodarone so successfully treats, discontinuation of amiodarone is not usually undertaken as it is neither an effective solution to the hypothyroidism nor a prudent decision from a cardiac perspective. Diagnosis of Hypothyroidism Diagnosis requires measurement of TSH and free T4 (FT4) levels. There is no utility in measuring T3 or reverse T3 (rT3) if hypothyroidism is suspected. Caution should be exercised 9 Thyroid Problems Encountered Specifically in Inpatients… 111 in interpreting TSH levels (dopamine and glucocorticoids suppress TSH) and FT4 levels (change due to non-thyroidal illness [NTI]) in acutely ill patients. Overt primary hypothy- roidism is characterized as a clearly elevated TSH (greater than 10 uLU/L) and low FT4. Overt central hypothyroidism is recognized when TSH is suppressed or inappropriately nor- mal and FT4 is below the expected range. Subclinical hypo- thyroidism is defined as elevation of TSH with a normal FT4. TSH elevation should be reproducible to rule out the effect of non-thyroidal illness and greater than age-adjusted expected ranges. SCHypo is seldom definitively diagnosed in hospital- ized patients due to the impact of NTI on TSH levels. Antithyroid antibodies to thyroid peroxidase (TPO) or thyro- globulin (Tg-ab) are useful to document the presence of auto- immune thyroid disease, and TPO may predict an increased risk of progression to overt hypothyroidism in those with SCHypo. Treatment of Overt Hypothyroidism Treatment with levothyroxine (LT4) improves LDL cholesterol metabolism, diastolic hypertension, and cardiac dysfunction, accelerates heart rate, and delays the progression of atherosclero- sis. Additionally, prospective data clearly demonstrate that LT4 therapy will reverse the cardiac muscle lipid accumulation and reduction in cardiac output associated with short-term overt hypothyroidism. Due to the potential presence of underlying CAD in some subjects with prolonged duration of hypothyroid- ism, some caution in reestablishing the euthyroid state may be warranted. The full replacement dose of levothyroxine is generally 1.6–1.7 microgram/kg daily in patients with overt hypothy- roidism. However, this recommendation varies in those with SCHypo where residual endogenous thyroxine production is present. The cardiovascular system in patients with SCHypo clearly responds positively to LT4 when TSH is greater 10 mIU/L especially in those under 65 years of age. Out of an 112 J. Sandeep and J. V. Hennessey abundance of caution, lower initial replacement doses than those employed in young adults are advisable in the elderly and those with known CVD and titrated up slowly (start low and go slow). The recommended starting dose of levothyroxine in patients above 50–60 years of age is 50 microgram daily in the absence of known CAD and in those with known cardiac issues where initial doses of 12.5–25 microgram daily are rec- ommended. LT4 should be ingested fasting with water only 60 min before breakfast or other medications for optimal absorption. Following the institution of LT4 therapy, adequate time (4–8 weeks) should pass before reevaluation of thyroid function is carried out. Thyroid Hormone Treatment in Cardiac Failure and Patients Undergoing Cardiac Surgery It has long been felt that emergency coronary bypass surgery is considered safe in patients with hypothyroidism. Other reports raise concern about prolonged postoperative recovery from anes- thetics, ileus, and infections going undetected due to a lack of fever as well as atrial fibrillation of hypothyroid patients undergo- ing cardiac surgery. Preoperatively, a ll patients should be treated with adequate doses of thyroid hormone. Unless there are contra- indications such as bradycardia and advanced COPD, beta- blockers should also be given to reduce the risk of frequently encountered post-cardiac surgery atrial fibrillation. In patients with heart failure and normal TSH and T4, those with a low T3 concentration had more severe heart failure as assessed by New York Heart Association criteria. Short-term treatment with T3 in patients with cardiac failure has resulted in a predictable decrease in systemic vascular resistance and subse- quent improvement in cardiac output without adverse effects but is not generally suggested due to limited confirmatory data. There are no guidelines which recommend treatment with IV T3 in patients with cardiac disease undergoing bypass surgery with low T3 syndrome. Presently, we do not recommend treating patients with cardiac disease with IV T3. 9 Thyroid Problems Encountered Specifically in Inpatients… 113 Suggested Reading Alexander EK, Pearce EN, Brent GA, Brown RS, Chen H, Dosiou C, et al. 2017 Guidelines of the American Thyroid Association for the diagnosis and management of thyroid disease during pregnancy and the postpartum. Thyroid. 2017;27(3):315–89. Bogazzi F, Tomisti L, Bartalena L, Aghini-Lombardi F, Martino E. Amiodarone and the thyroid: a 2012 update. J Endocrinol Invest. 2012;11(5):340–8. Burch HB, Cooper DS. Management of Graves’ disease: a review. JAMA. 2015;314(23):2544–54. De Leo S, Lee SY, Braverman LE. Hyperthyroidism. Lancet. 2016;388(10047):906–18. Garber JR, Cobin RH, Gharib H, Hennessey JV, Klein I, Mechanick JI, American Thyroid Association Taskforce on Hypothyroidism in Adults, et al. Clinical practice guidelines for hypothyroidism in adults: cospon- sored by the American Association of Clinical Endocrinologists and the American Thyroid Association. Thyroid. 2012;22(12):1200–35. Martin SS, Daya N, Lutsey PL, Matsushita K, Fretz A, McEvoy JW, et al. Thyroid function, cardiovascular risk factors, and incident atherosclerotic cardiovascular disease: the atherosclerosis risk in communities (ARIC) study. J Clin Endocrinol Metab. 2017;102(9):3306–15. Ross DS, Burch HB, Cooper DS, Greenlee MC, Laurberg P, Maia AL, et al. ATA hyperthyroidism management guidelines. Thyroid. 2016;26(10):1343–421. Sun J, Yao L, Fang Y, Yang R, Chen Y, Yang K. Relationship between sub- clinical thyroid dysfunction and the risk of cardiovascular outcomes: a systematic review and meta-analysis of prospective cohort studies. Int J Endocrinol. 2017;2017:8130796. Teasdale SL, Inder WJ, Stowasser M, Stanton T. Hyperdynamic right heart function in Graves’ hyperthyroidism measured by echocardiography normalises on restoration of euthyroidism. Heart Lung Circ. 2017;26(6):580–5. Udovcic M, Pena RH, Patham B, Tabatabai L, Kansara A. Hypothyroidism and the heart. Methodist Debakey Cardiovasc J. 2017;13(2):55–9. houstonmethodist.org/debakey-journal. Severe Hypercalcemia 10 Antonia E. Stephen and Johanna A. Pallotta Contents Introduction 116 Etiology 116 Presentation 117 Diagnostic Approach 118 Treatment 119 Summary 121 Suggested Reading 122 A. E. Stephen Harvard Medical School, Massachusetts General Hospital, Department of Surgery, Boston, MA, USA e-mail: astephen@partners.org J. A. Pallotta (*) Harvard Medical School, Beth Israel Deaconess Medical Center, Department of |
Medicine, Endocrinology and Metabolism, Boston, MA, USA e-mail: jpallott@bidmc.harvard.edu © Springer Nature Switzerland AG 2020 115 R. K. Garg et al. (eds.), Handbook of Inpatient Endocrinology, https://doi.org/10.1007/978-3-030-38976-5_10 116 A. E. Stephen and J. A. Pallotta Introduction Hypercalcemia is a common clinical problem. The majority of patients with hypercalcemia are asymptomatic and are often diagnosed on routine laboratory studies. They do not typically require immediate treatment. In distinction to patients with mild hypercalcemia, patients with severe hypercalcemia are often symptomatic and usually require urgent admission and treat- ment. In addition to treating the acute hypercalcemia, the under- lying cause must be investigated and treated when possible, to avoid ongoing or repeated episodes of severe calcium elevation. In over 90% of patients, the cause of hypercalcemia is either pri- mary hyperparathyroidism or malignancy; other causes are far less common. The focus of this chapter is on the etiology of hypercalcemia and the presentation and treatment of severe hypercalcemia. Etiology The etiologies of hypercalcemia are primarily distinguished between those that are parathyroid (PTH)-dependent and those arising from non-PTH-dependent mechanisms (Table 10.1). Among all causes of hypercalcemia, hyperparathyroidism (excess PTH production) remains the most common. Included in this cat- egory are primary (adenoma, hyperplasia, or rarely carcinoma of the parathyroid glands) and tertiary hyperparathyroidism ( physiologic hypertrophy of the parathyroid glands). Among non- PTH- dependent etiologies, the most common cause is hyper- calcemia of malignancy. This can occur as a result of the excess production of PTH-related peptides (PTHrP), from osteolytic bone metastases, or from excess vitamin D production. Less com- mon causes of hypercalcemia include hypervitaminosis D, also known as vitamin D intoxication, where excessive vitamin D intake results in hypercalcemia, and granulomatous diseases ( sarcoidosis or tuberculosis). Other causes include thyrotoxicosis, pheochromocytoma, and medications such as thiazide diuretics 10 Severe Hypercalcemia 117 Table 10.1 Causes of hypercalcemia PTH dependent Primary hyperparathyroidism Adenoma Hyperplasia Inherited syndromes – MEN and hyperparathyroidism-jaw tumor syndrome Parathyroid carcinoma Familial hypocalciuric hypercalcemia (FHH) Non-PTH dependent Hypercalcemia of malignancy Paraneoplastic syndrome (PTHrP) Osteolytic metastases (IL-1) Excess 1,25 D production Milk-alkali (calcium-alkali) syndrome Vitamin D or A toxicity Granulomatous diseases (sarcoidosis, tuberculosis, fungal infections) Hormonal disorders (hyperthyroidism, acromegaly, pheochromocytoma, adrenal insufficiency) Medications (thiazide diuretics, lithium) Prolonged immobilization, parenteral nutrition and lithium. In general, severe hypercalcemia is almost always a result of hyperparathyroidism or malignancy. Presentation The majority of patients with hypercalcemia are asymptomatic. In general, symptoms of hypercalcemia usually present when the cal- cium level is >12 mg/dL. The presence and severity of symptoms may be related to the time course of the rise in calcium level. If the hypercalcemia is chronic, patients may have nonspecific and rela- tively well-tolerated symptoms such as fatigue, constipation, and depression. A more acute rise in the calcium level to the 12–14 mg/dL range will likely result in more noticeable symptoms such as muscle weakness, nausea, abdominal pain, polyuria/ 118 A. E. Stephen and J. A. Pallotta polydipsia, irritability, and changes in sensorium. Calcium levels of >13 mg/dL may result in cardiovascular complications noted on an electrocardiogram as a prolonged PR interval and a short- ened QT interval, a result of a shortened myocardial action poten- tial. Arrhythmias have been reported in patients with severe hypercalcemia. Diagnostic Approach The most important initial step in the evaluation of severe hyper- calcemia is repeating and confirming the laboratory test result and correcting the calcium level for the albumin to obtain an accurate calcium result (Table 10.2). This correction is done using the fol- lowing formula: corrected calcium (mg/dL) = measured total Ca (mg/dL) + 0.8 (4.0 − serum albumin [g/dL]), where 4.0 repre- sents the average albumin level. If the patient has prior calcium levels recorded, these should be reviewed to determine time course of the hypercalcemia. The level and chronicity of calcium elevation can be helpful in determining the cause of hypercalce- mia. Patients with primary hyperparathyroidism usually have milder and more chronic calcium elevations, compared with patients with hypercalcemia of malignancy. Once the level of hypercalcemia has been confirmed, an intact PTH level should be measured. This will then guide further workup and management. An elevated or high/normal PTH level is consistent with a diagnosis of primary hyperparathyroidism. Although the majority of patients with this diagnosis will have a PTH well above the upper limit of normal, some patients with primary hyperparathyroidism will have an intact PTH level in the normal range. If the level is in the high/normal range, then pri- mary hyperparathyroidism is still the most likely diagnosis, as the Table 10.2 Initial evaluation of patients with severe hypercalcemia 1. Repeat calcium level and correct for albumin 2. S erum PTH level to distinguish PTH-mediated versus non-PTH- mediated hypercalcemia 10 Severe Hypercalcemia 119 PTH should be suppressed in patients with an elevated calcium level for causes other than hyperparathyroidism. The PTH should be low in cases of non-PTH-dependent hypercalcemia. Most patients with PTH-dependent hypercalcemia have mild calcium elevations. There are circumstances, however, where PTH-dependent hypercalcemia can be more severe. If the patient has severe hypercalcemia and an elevated PTH, then the diagnosis of parathyroid carcinoma or a large parathyroid adenoma should be considered. These patients often have much higher PTH levels than most patients with primary hyperparathyroidism. The degree of hypercalcemia often, but not always, correlates with the PTH level. In turn, the size of the lesion can correlate with the PTH level. Patients with larger parathyroid tumors, benign or malig- nant, are more likely to have higher PTH levels and therefore be at higher risk for episodes of severe hypercalcemia. In patients with renal insufficiency, hypercalcemia can increase the severity because of decreased renal filtration of serum calcium. Severe hypercalcemia is most common among patients with a non-PTH-dependent mechanism, often malignancy. In these cases, the patient frequently has more advanced malignant dis- ease, and the diagnosis and cause of hypercalcemia may be quite obvious. Treatment The treatment of hypercalcemia depends primarily on the calcium level. Patients with mildly elevated levels (Ca < 12 mg/dL) often do not need treatment but should be instructed regarding factors that can exacerbate the hypercalcemia. These factors include dehydration/volume depletion, medications (thiazide diuretics and lithium therapy), prolonged bed rest or inactivity, and a high calcium diet (>1000 mg/day). It is important to instruct patients to maintain adequate hydration (at least six to eight glasses of water per day) and to consider contacting their physician if they are unable to maintain oral hydration due to illness. The treatment of moderate hypercalcemia (12–13 mg/dL) depends on the time course of the calcium elevation and if the 120 A. E. Stephen and J. A. Pallotta patient is experiencing symptoms. All patients who are acutely symptomatic should be admitted to the hospital and treated. If the calcium level is <13 mg/dL and the patient is not symptomatic, they do not necessarily require immediate treatment, but the cause of the hypercalcemia should be investigated and promptly treated to avoid further elevation in the calcium level. These patients should be instructed as outlined above regarding factors that could exacerbate the hypercalcemia and their calcium levels closely fol- lowed until the underlying cause is treated. Any patient who has symptomatic hypercalcemia or a calcium level of >13 mg/dL should be admitted to the hospital and treat- ment initiated to lower the calcium level. There are four available treatment approaches to lower the calcium levels: 1. Intravenous hydration to promote excretion of calcium 2. Calcitonin 3. Bisphosphonates 4. Denosumab The combination of intravenous hydration and calcitonin should lower calcium levels within hours, while the bisphospho- nates are effective within days. The intravenous hydration to expand intravascular volume and promote calcium excretion should be initiated first. The patient’s volume status should be closely assessed and monitored. The recommended infusion should start at 0.9% saline at twice the maintenance rate and the urine output monitored. The infusion rate can then be adjusted depending on the patient’s age, overall medical conditions, urine output, and calcium level. It is important to expand the intravascu- lar volume before a diuretic such as furosemide is given. Salmon calcitonin is used in the acute setting for the treatment of hypercalcemia. It is usually administered intramuscularly or subcutaneously. The recommended starting dose is 4 international units/kg every 12 h; this can be increased up to 6–8 international units/kg every 6 h as needed. Prior to giving calcitonin, a skin test should be done to rule out any allergy to the medication. Bisphosphonates are most effective in treating patients with malignancy-associated hypercalcemia. Bisphosphonates such as pamidronate and zoledronate inhibit osteoclast activity and t herefore decrease the release of calcium from the bone. These agents are 10 Severe Hypercalcemia 121 long-acting and should be used judiciously in patients with PTH- dependent hypercalcemia, as a curative operation may lead to hypo- calcemia if the source of excess PTH is successfully removed and the bisphosphonates are still active in the patient’s system. Bisphosphonates should never be given to patients with hypo- parathyroidism who develop iatrogenic hypercalcemia from over- treatment with calcium and vitamin D supplements. Since they lack parathyroid hormone, these patients are at risk for profound and persistent hypocalcemia with bisphosphonates. In addition, patients with renal failure should be given these agents cautiously and at a lower dose. Denosumab can be used when bisphosphonates are contraindi- cated (e.g. severe renal failure). As the serum calcium level is low- ered into the normal range, the cause of the hypercalcemia should be investigated and treated when possible. In the case of surgi- cally correctable primary hyperparathyroidism, surgery should be performed as soon as possible to avoid repeated episodes of severe hypercalcemia. An alternative for patients with hypercalcemia secondary to hyperparathyroidism is the relatively newer agent, cinacalcet. This is often an effective treatment in patients with an adenoma who are poor surgical candidates as well as for patients with inoperable parathyroid carcinoma. Once diagnosis is clarified, which will require further investigation, steroids are a therapeutic option for granulomatous disease and lymphoma mediated by 1,25-hydroxy-vitamin D production. It is also important to rule- out tuberculosis prior to administering steroids. Summary The most common causes of hypercalcemia in general are hyper- parathyroidism and malignancy. Severe hypercalcemia can result in either of these clinical circumstances, although the majority of patients with hyperparathyroidism have mild calcium elevations. Patients with calcium levels >13 mg/dL and any patient with symptomatic hypercalcemia should be admitted to the hospital and promptly treated, with the underlying cause addressed and corrected when possible to avoid future episodes of clinically significant hypercalcemia. 122 A. E. Stephen and J. A. Pallotta Suggested Reading Bilezikian JP, Cusano NE, Khan AA, Liu JM, Marcocci C, Bandeira F. Primary hyperparathyroidism. Nat Rev Dis Primers. 2016;2:16033. Mohammad KS, Guise TA. Hypercalcemia of malignancy: a new twist on an old problem. J Oncol Pract. 2016;12(5):435–6. Peacock M, Belzikian J. Cinacalcet HCL reduces hyperalcemia in primary hyperparathyroidism across a wide spectrum of disease severity. J Clin Endocrinol Metabol. 2011;96(1):E9–E18. Srividya N, Gossman WG. Hypercalcemia. StatPearls https://knowledge. statpearls.com/chapter/acls/23158/. Wisneski L. Salmon calcitonin in the acute management of hypercalcemia. Calcif Tissue Int. 1990;46(Suppl):S26–30. Hypocalcemia 11 Alan Ona Malabanan Contents Hypocalcemia Should Be Considered in Those with Muscle Cramping or Bone Pain, Cardiac Dysrhythmias, Seizure Disorders, and Perioral/Digital Paresthesias 124 A Total Serum Calcium Should Be Measured with a Concomitant Serum Albumin 125 A Free Ionized Serum Calcium from Venous Blood Gas Testing May Provide a Timelier Test Result than Total Serum Calcium 125 The Free Serum Calcium Decreases with Alkalemia and Increases with Acidemia 126 The Electrocardiographic QT Interval Is Prolonged in Those with Hypocalcemia 126 Post-parathyroidectomy and Post-t hyroidectomy Patients Should Be Monitored Postoperatively for Symptoms and Physical Signs of Hypocalcemia, as Well as an Estimate of Free Calcium 126 Hypocalcemia Should Be Evaluated with an Estimate of Free Serum Calcium (Free Ionized Calcium or Total Serum Calcium Corrected for Serum Albumin), Serum Phosphate, Serum Magnesium, Serum 25-Hydroxyvitamin D, and Serum Parathyroid Hormone (PTH) 127 A. O. Malabanan (*) Beth Israel Deaconess Medical Center, Harvard Medical School, Division of Endocrinology, Diabetes and Metabolism, Boston, MA, USA e-mail: amalaban@bidmc.harvard.edu © Springer Nature Switzerland AG 2020 123 R. K. Garg et al. (eds.), Handbook of Inpatient Endocrinology, https://doi.org/10.1007/978-3-030-38976-5_11 124 A. O. Malabanan Symptomatic Hypocalcemia Is a Medical Emergency, Particularly When Acute and Should Be Treated with Intravenous 10% Calcium Gluconate (with EKG Monitoring) Until the Symptoms Resolve |
127 After Emergent Treatment with Intravenous Calcium Gluconate, a Calcium Gluconate IV Drip Should Be Maintained (with EKG Monitoring) Titrating the Free Serum Calcium Estimate to the Lower Limit of Normal 128 Chronic Treatment of Hypocalcemia Includes Treating the Underlying Causes (Hypomagnesemia, Vitamin D Deficiency, Inadequate Calcium Intake, Hypoparathyroidism, Hypercalciuria) and, in Addition, May Include 500–1000 mg of Elemental Calcium (1250–2500 mg of Calcium Carbonate) tid Along with an Activated Vitamin D Analog Such as Calcitriol (0.25–0.50 mcg bid) 128 Serum Calcium, Albumin, Phosphate, Creatinine, and 24-h Urine Calcium and Creatinine Should Be Monitored Closely and Therapy Adjusted Accordingly 129 Thiazide Therapy Should Be Used with Extreme Caution in Those Also on Calcium and Calcitriol, Particularly if There Is Concomitant Chronic Kidney Disease 129 Potent Antiresorptive Therapy with Oral and Intravenous Bisphosphonates or Subcutaneous Denosumab Is Contraindicated in Those with Hypocalcemia 129 Long-Term Parathyroid Hormone (1–84 PTH Analog) Is Now Approved by the FDA for the Management of Chronic Hypoparathyroidism 132 Suggested Reading 132 Hypocalcemia Should Be Considered in Those with Muscle Cramping or Bone Pain, Cardiac Dysrhythmias, Seizure Disorders, and Perioral/ Digital Paresthesias Calcium is important for the proper functioning of several of the human body’s organ systems and cellular processes. As a divalent cation, it is important in maintaining an electrochemical gradient. 11 Hypocalcemia 125 Hypocalcemia is associated with tetany and muscle cramping. Latent tetany may be identified by eliciting Chvostek’s or Trousseau’s signs. Neurologic irritability, with hypocalcemia, is associated with oral and digital paresthesias as well as seizures. Hypocalcemia results in cardiovascular irritability with atrial and ventricular dysrhythmias and may also cause laryngospasm with respiratory arrest. Calcium is important, along with phosphate, for normal bone mineralization. Inadequate serum calcium will lead to osteomalacia and bone pain. A Total Serum Calcium Should Be Measured with a Concomitant Serum Albumin The most commonly measured serum calcium level is total serum calcium. About half of the total serum calcium is bound to albu- min or complexed with organic ions such as phosphate. The cal- cium unbound to albumin or complexed with organic ions is termed the free calcium, which is the physiologically important portion. Free calcium levels are therefore affected by albumin lev- els. Hypoalbuminemia will lead to a decrease in total serum cal- cium levels. If the albumin is less than 4.0 g/dl, the total serum calcium should be corrected by adding 0.8 mg/dl of calcium to every 1.0 g/dl of albumin below 4.0. A Free Ionized Serum Calcium from Venous Blood Gas Testing May Provide a Timelier Test Result than Total Serum Calcium A total serum calcium level may take hours to return, while a free ionized serum calcium from an arterial blood gas analyzer often takes minutes to return, related to the assay methodology used. For patients with rapidly declining calcium levels, a free ionized serum calcium from venous blood gas testing may have an advantage in being able to adjust therapy. Accurate ionized calcium results require proper specimen collection and timely processing. 126 A. O. Malabanan The Free Serum Calcium Decreases with Alkalemia and Increases with Acidemia Acid-base balance affects the negative charges on albumin. Acidemia (i.e., increased H+ ions) decreases them leading to decreased ionized calcium binding to albumin and increasing free calcium. Alkalemia (i.e., decreased H+ ions) increases them lead- ing to increased ionized calcium binding and decreasing free cal- cium. Respiratory alkalemia from hyperventilation will lower free calcium levels and may precipitate tetany or seizures. The Electrocardiographic QT Interval Is Prolonged in Those with Hypocalcemia The presence of QT prolongation confirms the risk of cardiovascu- lar sequelae of hypocalcemia and should prompt urgent evaluation and treatment. Since electrocardiographic assessment may produce a result even more quickly than a venous blood gas, this is the quickest way for assessing calcium status in a patient. Post-parathyroidectomy and Post- thyroidectomy Patients Should Be Monitored Postoperatively for Symptoms and Physical Signs of Hypocalcemia, as Well as an Estimate of Free Calcium The risk of hypocalcemia after thyroid or parathyroid surgery is dependent on the type of surgery performed as well as the skill and experience of the surgeon. Preoperative vitamin D deficiency may also increase the risk for postoperative hypocalcemia. Four gland exploration/subtotal parathyroidectomy and total thyroidectomy for thyroid cancer or Graves’ disease have an increased risk for hypocalcemia. Hungry bone syndrome post- parathyroidectomy is increased in those with severe primary or secondary hyperparathy- roidism associated with lower bone density and increased bone turnover. Prophylactic treatment with calcium and calcitriol, as well as correction of preexisting vitamin D deficiency, may reduce 11 Hypocalcemia 127 the risk for symptomatic hypocalcemia post-thyroidectomy. Postoperative calcium and parathyroid hormone may be helpful in guiding postoperative management. Assessment for a baseline Chvostek’s sign should be done before surgery as 10% of normal individuals may have a Chvostek’s sign. Hypocalcemia Should Be Evaluated with an Estimate of Free Serum Calcium (Free Ionized Calcium or Total Serum Calcium Corrected for Serum Albumin), Serum Phosphate, Serum Magnesium, Serum 25-Hydroxyvitamin D, and Serum Parathyroid Hormone (PTH) Once a low free calcium is confirmed, the laboratory evaluation of hypocalcemia can suggest its etiology and need for additional sup- portive treatment beyond calcium. PTH is responsible for increas- ing calcium release from bone to normalize serum calcium levels. At the same time, increased PTH causes phosphaturia and leads to hypophosphatemia. Ineffective PTH action may result from hypo- magnesemia, and hypomagnesemia may also impair PTH release. Severe vitamin D deficiency, especially if long- standing with depletion of bone calcium stores, may cause hypocalcemia. Hungry bone syndrome is characterized by low calcium, phos- phate, and magnesium resulting from the reincorporation of these bone mineral components after cure of the hyperparathyroidism. Symptomatic Hypocalcemia Is a Medical Emergency, Particularly When Acute and Should Be Treated with Intravenous 10% Calcium Gluconate (with EKG Monitoring) Until the Symptoms Resolve Seizures, tetany, cardiac dysrhythmias, paresthesias, laryngo- spasm/stridor, or prolonged QT interval should be treated urgently with intravenous calcium gluconate (with EKG monitoring). Calcium gluconate is used in preference to calcium chloride, due 128 A. O. Malabanan to calcium chloride’s vein irritation. One to two amps (10–20 mL) of 10% calcium gluconate may be infused over 10 min watching for bradycardia. Those with chronic kidney disease or on concom- itant digoxin therapy should be infused more cautiously. After Emergent Treatment with Intravenous Calcium Gluconate, a Calcium Gluconate IV Drip Should Be Maintained (with EKG Monitoring) Titrating the Free Serum Calcium Estimate to the Lower Limit of Normal Because free calcium is rapidly filtered into the glomerulus, serum calcium levels will drop without an ongoing source of calcium, and hypocalcemia will recur. With EKG monitoring, a calcium gluconate IV drip using 100 ml of 10% calcium gluconate in 1 L of D5W may be started at 30 ml/h titrating to symptoms, free cal- cium levels, or QT intervals. Free calcium levels should be moni- tored every 2–4 h. Chronic Treatment of Hypocalcemia Includes Treating the Underlying Causes (Hypomagnesemia, Vitamin D Deficiency, Inadequate Calcium Intake, Hypoparathyroidism, Hypercalciuria) and, in Addition, May Include 500–1000 mg of Elemental Calcium (1250–2500 mg of Calcium Carbonate) tid Along with an Activated Vitamin D Analog Such as Calcitriol (0.25–0.50 mcg bid) Underlying causes of hypocalcemia, such as hypomagnesemia, vitamin D deficiency, hypercalciuria due to loop diuretics, or use of potent antiresorptives such as bisphosphonates or denosumab, should be addressed. Hypomagnesemia may require intravenous treatment with magnesium sulfate (see Hypomagnesemia). Vitamin D deficiency can be treated with high-dose ergocalciferol (50,000 IU weekly × 8 weeks) followed by 2000 IU c holecalciferol 11 Hypocalcemia 129 daily, although those with gastric bypass surgery or intestinal malabsorption may require higher doses of 6000–10,000 IU daily. Bisphosphonates should be discontinued until the hypocalcemia is corrected, and dose reduction or cessation of loop diuretics should be considered (Table 11.1). Serum Calcium, Albumin, Phosphate, Creatinine, and 24-h Urine Calcium and Creatinine Should Be Monitored Closely and Therapy Adjusted Accordingly The target free calcium should be in the low normal range. The calcium-phosphate product should be maintained <55 mg2/dl2 to minimize the risk for soft tissue calcification. The 24-h urine cal- cium excretion should be maintained <250 mg/day to minimize the risk for nephrolithiasis. Thiazide Therapy Should Be Used with Extreme Caution in Those Also on Calcium and Calcitriol, Particularly if There Is Concomitant Chronic Kidney Disease Thiazides decrease urinary calcium excretion and together with calcium and calcitriol therapy may cause hypercalcemia. Because thiazides decrease urinary excretion of calcium, the hypercalcemia is more difficult to treat. Potent Antiresorptive Therapy with Oral and Intravenous Bisphosphonates or Subcutaneous Denosumab Is Contraindicated in Those with Hypocalcemia Bisphosphonates and denosumab inhibit osteoclast-mediated bone resorption and prevent calcium release from the bone, dis- rupting calcium homeostasis and causing hypocalcemia. As such, 130 A. O. Malabanan Table 11.1 Medications used for hypocalcemia Mechanism of Route of Medication action administration Dose (elemental calcium) Comments Calcium carbonate Source of calcium Oral 1250–2500 mg tid (500–1000 mg tid) Requires gastric acid to aid dissolution and absorption Calcium citrate Source of calcium Oral 2992–4488 mg tid (630–945 mg tid) Oral preparation of choice in those with achlorhydria Calcium acetate Source of calcium Oral 2001–4002 mg tid (507–1014 mg tid) Typically used as a phosphate binder Calcium gluconate Source of calcium Intravenous 1000–2000 mg for symptomatic (1000 mg/10 mL) hypocalcemia (93–186 mg) then 30 mL/h of 100 mL in 1 L D5W as infusion titrating to calcium. Calcium chloride Source of calcium Intravenous 500–1000 mg for symptomatic Give only as slow IV (1000 mg/10 mL) hypocalcemia (136–273 mg) injection due to vein sclerosis Ergocalciferol Vitamin D2 Oral 50,000–100,000 daily to weekly Fat soluble and long (50,000 IU) half-life, by prescription only Cholecalciferol Vitamin D3 Oral 50,000–100,000 daily to weekly Fat soluble and long half-life, OTC Calcitriol Activated Oral, IV 0.25–0.50 mcg twice daily Onset of action in 1–2 days vitamin D 11 Hypocalcemia 131 Hydrochlorothiazide Hypocalciuric Oral 25–50 mg twice daily Hyperuricemia, thiazide hypokalemia, and hyponatremia may result Chlorthalidone Hypocalciuric Oral 25–50 mg once daily Hyperuricemia, thiazide hypokalemia, and hyponatremia may result Amiloride Mild Oral 5–10 mg once daily Potassium-sparing diuretic; hypocalciuric may be used in diuretic combination with thiazides Parathyroid hormone PTH Subcutaneous 50–100 mcg once daily REMS necessary to (1–84) prescribe, osteosarcoma risk 132 A. O. Malabanan they are contraindicated in those patients with hypocalcemia or known hypoparathyroidism. Long-Term Parathyroid Hormone (1–84 PTH Analog) Is Now Approved by the FDA for the Management of Chronic Hypoparathyroidism Replacement therapy with once daily 80 mcg parathyroid hormone is now available and can decrease oral calcium and calcitriol requirements. However, its role in inpatient management of hypo- calcemia is not yet clear. Long-term safety is also unclear. Suggested Reading Cooper MS, Gittoes NJL. Diagnosis and management of hypocalcaemia. BMJ. 2008;336:1298–302. https://doi.org/10.1136/bmj.39582.589433.BE. Mannstadt M, Bilezikian JP, Thakker RV, Hannan FM, Clarke BL, Rejnmark L, et al. Hypoparathyroidism. Nat Rev Dis Primers. 2017;3:17055. https:// doi.org/10.1038/nrdp.2017.55. Mathur A, Nagarajan N, Kahan S, Schneider EB, Zeiger MA. Association of parathyroid hormone level with postthyroidectomy hypocalcemia: a sys- tematic review. JAMA Surg. 2018;153:69–76. https://doi.org/10.1001/ jamasurg.2017.3398. Ross DS, Burch HB, Cooper DS, Greenlee MC, Laurberg P, Maia AL, et al. 2016 American Thyroid Association guidelines for diagnosis and man- agement of hyperthyroidism and other causes of thyrotoxicosis. Thyroid. 2016;26:1343–421. https://doi.org/10.1089/thy.2016.0229. Witteveen JE, van Thiel S, Romijn JA, Hamdy NA. Therapy of endocrine disease: hungry bone syndrome: still a challenge in the post-operative management of primary hyperparathyroidism: a systematic review of the literature. Eur J Endocrinol. 2013;168:R45–53. https://doi.org/10.1530/ EJE-12-0528. Perioperative Evaluation 12 of Primary Hyperparathyroidism J. Carl Pallais Contents Confirm the Preoperative Diagnosis of Primary Hyperparathyroidism 134 Review the Indications for Parathyroidectomy 134 Review Preoperative Parathyroid Imaging Studies 135 Review the Surgical Approach 136 Determine Possible Association with Hereditary Syndromes 136 Obtain Biochemical Evidence of Surgical Cure 137 Monitor for Postoperative Hypocalcemia 138 Evaluate for Signs and Symptoms of Postsurgical Hypocalcemia 139 Evaluate for Biochemical Evidence of Hypoparathyroidism 139 Assess for Evidence of the Hungry Bone Syndrome 140 Prevent and Treat Hypocalcemia 141 Follow-Up After Discharge 142 Suggested Reading 143 J. C. Pallais (*) Brigham and Women’s Hospital, Division of Endocrinology, Department of Medicine, Boston, MA, USA e-mail: jpallais@bwh.harvard.edu © Springer Nature Switzerland AG 2020 133 R. K. Garg et al. (eds.), Handbook of Inpatient Endocrinology, https://doi.org/10.1007/978-3-030-38976-5_12 134 J. C. Pallais Confirm the Preoperative Diagnosis of Primary Hyperparathyroidism Primary hyperparathyroidism is confirmed by the findings of inappropriately elevated |
parathyroid hormone (PTH) levels in the setting of hypercalcemia without renal failure. PTH-dependent hypercalcemia in the setting of prolonged renal failure could indi- cate tertiary hyperparathyroidism. Calcium levels should be cor- rected for serum albumin. Occasionally the PTH levels will be within the normal range despite hypercalcemia. Because elevated calcium levels normally suppress PTH secretion, “normal” PTH levels in the setting of hypercalcemia indicate inappropriately increased PTH secretion. In patients in whom previously normal calcium levels cannot be confirmed, measurement of 24-hour urine calcium is important to differentiate primary hyperparathyroidism from familial hypocalciuric hypercalcemia (FHH). The latter condition is a contraindication for parathyroidectomy as it is associated with a high risk of surgical failure. In these patients, hypercalcemia typically recurs with subtotal parathyroidectomy. Review the Indications for Parathyroidectomy Parathyroidectomy is indicated for patients with primary hyper- parathyroidism and symptomatic kidney stones or fragility frac- tures. According to the recent guidelines, asymptomatic patients with primary hyperparathyroidism should be considered candi- dates for parathyroidectomy if they have any of the following indications: • Age <50 years old • Calcium levels >1 mg/dL above the upper limits of normal • Abnormal renal function • Osteoporosis at any site (spine, hip, or distal wrist) • Presence of vertebral fracture on dedicated imaging studies • Presence of kidney stones on abdominal imaging • High risk of developing kidney stones on 24-hour urine analysis 12 Perioperative Evaluation of Primary Hyperparathyroidism 135 Some patients may require urgent parathyroidectomy if they develop hypercalcemic crisis. This is characterized by the rapid onset of hypercalcemia, usually with calcium levels greater than 14 mg/dL, and evidence of multiorgan dysfunction. Aggressive fluid resuscitation and medical management are required prior to parathyroidectomy. Parathyroidectomy can also be considered in patients with pri- mary hyperparathyroidism without any of these indications if there are barriers to long-term follow-up. Surgical intervention is the only definitive treatment for primary hyperparathyroidism and could obviate the need for long-term monitoring. Finally, parathyroidectomy can be considered in patients with primary hyperparathyroidism and no other indication if they are undergoing neck surgery for other reasons. Frequently this involves surgical evaluation of concurrent thyroid nodules. It is important to evaluate thyroid nodules in patients with primary hyperparathyroidism as the FNA results can impact the decision to undergo surgery or modify the surgical approach to parathy- roidectomy. Review Preoperative Parathyroid Imaging Studies Imaging studies are not part of the diagnostic plan for primary hyperparathyroidism, but they help the surgeon define the surgical strategy. The most commonly utilized localizing studies are cervi- cal ultrasounds, sestamibi parathyroid scans, and four-d imensional computed tomography (4D CT) scan. Cervical ultrasounds are relatively inexpensive, do not involve radiation exposure, and have the added benefit of detecting concomitant thyroid nodules that may impact the surgical strategy for parathyroidectomy. In 4D CT, multiple scans are obtained after administration of IV contrast and provide good anatomic detail for planning the surgery. It is important to remember that patients with negative imaging studies remain candidates for parathyroidectomy, particularly as the sensitivity of these tests are significantly lower in patients with multigland involvement. 136 J. C. Pallais Review the Surgical Approach Parathyroidectomy is carried out via bilateral neck exploration or a minimally invasive approach. The choice between these two sur- gical strategies is determined in large part by the results of the imaging studies and the experience of the surgeon. Bilateral parathyroid exploration has been the standard surgi- cal approach for parathyroidectomy with a high surgical success rate of >95%. This is the preferred approach for patients with multigland disease and those with discordant or non-localizing imaging studies. Approximately 85% of cases of primary hyper- parathyroidism are caused by a single adenoma. If a single ade- noma is confirmed on localization studies, a focused minimally invasive operative strategy with measurement of intraoperative PTH could be attempted. PTH has a short half-life, and intraop- erative monitoring helps to confirm resection of the culprit ade- noma while limiting the scope of dissection. Elevated intraoperative PTH values help to identify persistent disease. If multigland disease is discovered during surgery or an abnor- mal gland is not identified through a minimally invasive approach, then the surgery should be converted to bilateral exploration. Likewise, if intraoperative PTH levels do not drop appropriately after resection of an abnormal gland, conversion to bilateral explo- ration is recommended to avoid persistence of hyperparathyroid- ism. Unilateral parathyroidectomy has been associated with similar success rates as bilateral exploration in properly selected patients. Autotransplantation of normal parathyroid glands is occasion- ally attempted to preserve the function of glands that appear devascularized after surgical manipulation or in subtotal parathy- roidectomy with multigland involvement. Determine Possible Association with Hereditary Syndromes Approximately 5–10% of patients with hyperparathyroidism have an underlying hereditary syndrome, some of which are caused by mutations in known genes. These genetic syndromes∗ and their 12 Perioperative Evaluation of Primary Hyperparathyroidism 137 associated genes are listed below: ∗MEN, multiple endocrine neoplasia syndrome; HPT-JT, hyperparathyroidism-jaw tumor syndrome; and FHH, familial hypocalciuric hypercalcemia. • MEN1 (MEN1) • MEN2A (RET) • MEN4 (CDKN1B) • HPT-JT (HRPT2/CDC73) • Familial isolated hyperparathyroidism • FHH1 (CASR) • FHH2 (GNA11) • FHH3 (AP2S1) Identification of these syndromes should ideally be done preop- eratively as the diagnosis may influence the surgical strategy and may prompt screening for other associated features. Patients with heredi- tary syndromes associated with hyperparathyroidism tend to be younger, have multiple gland involvement, and have a greater likeli- hood of negative localization studies and hyperparathyroidism per- sistence or recurrence. Thus, screening for these syndromes should be considered in young patients with hyperparathyroidism, those with an affected first-degree relative, or patients that have other asso- ciated syndromic features. In a ddition, patients of any age should be considered candidates for genetic screening if they present in with multigland parathyroid disease or persistent/recurrent hyperparathyroidism following parathyroidectomy. Although parathyroidectomy is generally contraindicated for patients with FHH, the diagnosis may have been missed prior to parathyroidectomy if hypocalciuria was not identified or tested. Hypercalcemia typically persists/recurs after subtotal parathyroidectomy. These patients should not undergo repeat parathyroid operations. Obtain Biochemical Evidence of Surgical Cure The immediate goal of parathyroidectomy in patients with pri- mary hyperparathyroidism is to reestablish normal calcium homeostasis. Persistent disease is manifested as a failure to 138 J. C. Pallais achieve normocalcemia within 6 months of surgery. Operative failure may be predicted by inadequate decrease in intraoperative PTH levels. If normocalcemia is achieved for at least 6 months following parathyroidectomy, patients are considered to have had a surgical cure. Primary hyperparathyroidism that recurs after 6 months of normocalcemia following parathyroidectomy is con- sidered recurrent disease. Monitor for Postoperative Hypocalcemia Postoperative hypocalcemia is the most common endocrine complication following parathyroidectomy, occurring in nearly 50% of cases in some case series. Injury to the parathyroid glands, inadvertent resection of parathyroid tissue, damaged blood supply to the remaining parathyroid glands, or failed auto- transplantation can cause transient or permanent hypoparathy- roidism. In addition to functional hypoparathyroidism, the reversal of bone resorption with increased bone formation after parathyroidectomy causes a net influx of calcium into bones contributing to the fall of serum calcium levels. Typically, the hypocalcemia is transient because the bone disease is mild and the remaining parathyroid tissue recovers function within 1 or 2 weeks. In the hands of high-v olume parathyroid surgeons, per- manent hypoparathyroidism is relatively uncommon after initial parathyroid surgery with an estimated frequency of <4%. Severe hypocalcemia caused by hungry bone is a rare complication of parathyroidectomy. Hypocalcemia may be symptomatic or asymptomatic and may be associated with variable PTH levels. The duration and severity of hypocalcemia vary and may depend on the routine use of calcium and vitamin D supplementation, the degree of injury to the remaining parathyroid glands, the severity of the underlying bone disease, and preoperative clinical features. Patients with impaired intestinal absorption such as those with prior gastric bypass surgery, vitamin D deficiency, renal dys- function, or hypomagnesemia are at higher risk of developing postoperative hypocalcemia. 12 Perioperative Evaluation of Primary Hyperparathyroidism 139 Evaluate for Signs and Symptoms of Postsurgical Hypocalcemia Acute hypocalcemia may be associated with a spectrum of clin- ical manifestations. At the mild end of the spectrum, asymptom- atic biochemical findings may be the only manifestations. Severe findings include laryngospasm, neurocognitive dysfunction, papilledema, seizures, and heart failure. Neuromuscular irrita- bility is the most common manifestation of acute hypocalcemia. This includes perioral numbness, acral paresthesias, muscle cramps, stiffness, or carpopedal spasms. On physical exam, patients may have Chvostek’s signs and/or Trousseau’s sign, which are markers of latent tetany. Chvostek’s sign is the con- traction of the facial muscles in response to tapping the facial nerve which causes twitching of the ipsilateral lip. Trousseau’s sign is the development of carpal spam characterized by adduc- tion of the thumb, extension of the interphalangeal joints, and flexion of the MCP joints and wrist elicited by the insufflation of a blood pressure cuff above the systolic blood pressure for 3 min. Trousseau’s sign is more specific for hypocalcemia as Chvostek’s sign may be present in up to 10% of normal subjects. Hypocalcemia may also cause QTc prolongation and may be associated with dysrhythmias. Evaluate for Biochemical Evidence of Hypoparathyroidism The biochemical signature of hypoparathyroidism involves hypo- calcemia with suppressed PTH levels. Approximately 40% of the total circulating calcium is bound to albumin, with the unbound or free portion referred to as ionized calcium. Total calcium measure- ment should be corrected for albumin levels according to the fol- lowing formula: corrected calcium (mg/dL) = measured calcium (mg/dL) + 0.8 (4.0 – measured albumin [g/dL]). If hypocalcemia is confirmed by either corrected calcium mea- surement or ionized calcium levels, hypoparathyroidism is diagnosed if the PTH levels are inappropriately suppressed. 140 J. C. Pallais As hypocalcemia normally elevates PTH levels, PTH values within the normal range are still considered inappropriately low in the setting of hypocalcemia. PTH increases circulating calcium levels by stimulating cal- cium efflux from the bone, promoting reabsorption of filtered cal- cium in the kidney, and indirectly increasing intestinal calcium absorption by promoting the activation of vitamin D through the expression of 1-alpha hydroxylase in the proximal tubule. Suppressed PTH release due to the resection or injury of parathy- roid glands lowers serum calcium levels by reversing these physi- ologic processes. In addition, PTH is one of the primary regulators of phosphorus in the body and promotes urinary phosphate excre- tion thorough its effects on the NaPi transporters in the proximal tubules. In hypoparathyroidism, the serum phosphorous concen- tration tends to be in the high-normal or frankly elevated range due to impaired phosphate excretion. As low magnesium levels can impair PTH secretion and action, it is important to exclude hypomagnesemia as the cause of hypo- parathyroidism or as a contributor to the hypocalcemia. Assess for Evidence of the Hungry Bone Syndrome Patients with severe preoperative bone disease caused by chronic bone resorption mediated by elevated PTH levels may have severe and prolonged hypocalcemia following parathyroidectomy. The reversal of advanced bone resorption from the acute withdrawal of PTH is coupled with accelerated bone formation and causes a strong influx of both calcium and phosphate into the bone in these patients. This lowers the calcium levels despite a compensatory increase in PTH production by the remaining parathyroid tissue. The clinical markers of the hungry bone syndrome include per- sistent hypocalcemia and hypophosphatemia on postoperative day 3 following parathyroidectomy. The hypocalcemia typically nadirs 2–4 days after parathyroidectomy but may last up to sev- eral months. In addition to low serum phosphorous concentra- tions, associated biochemical features frequently include 12 Perioperative Evaluation of Primary Hyperparathyroidism 141 hypomagnesemia and occasionally hyperkalemia. Risk factors for developing the hungry bone syndrome include large volume of the resected adenoma, elevated preoperative blood urea nitrogen level, elevated preoperative alkaline phosphatase activity, older age, and preoperative radiographic findings of osteitis fibrosa or bone erosions. Occasionally, patients with bone disease caused by hyperthyroidism may also develop the hungry bone syndrome fol- lowing thyroidectomy. This must be a consideration for patients undergoing combined thyroid and parathyroid surgeries. Prevent and Treat Hypocalcemia Regular monitoring of calcium, albumin, phosphorus, magne- sium, and vitamin D levels and occasional PTH measurements are required after parathyroidectomy to confirm surgical cure and detect development of hypocalcemia. Oral calcium and vitamin D supplementation are commonly started immediately following parathyroidectomy to prevent hypocalcemia. Between 1.5 and 3 |
g of elemental calcium is typically given orally in divided doses in the postoperative periods for several days to weeks depending on the serum calcium and PTH concentrations. Aggressive vitamin D repletion with high-dose ergocalciferol or cholecalciferol can be considered in patients with preoperative vitamin D deficiency. Most cases of hypocalcemia are mild and can be treated with oral calcium and vitamin D supplementation in the outpatient set- ting. As the hypocalcemia worsens, the dose of elemental calcium is increased. For patients with achlorhydria or on proton pump inhibitors, the use of the calcium citrate formulation is preferred over calcium carbonate for improved calcium absorption. For symptomatic patients or those who have developed hypoparathy- roidism, calcitriol may be added to their regimen. Calcitriol is the bioactive form of vitamin D, has a faster onset of action than ergo- calciferol or cholecalciferol, and is more effective in stimulating intestinal calcium absorption. However, because of its greater potency, it has a narrower therapeutic window, and careful moni- toring is required to ensure that serum or urinary calcium levels do not become excessively elevated. 142 J. C. Pallais Patients with more severe hypocalcemia may require longer hospital stays as their hypocalcemia may represent a medical emergency. Intravenous calcium administration should be consid- ered for patients with moderate to severe symptoms of hypocalce- mia or those with corrected calcium levels <7.5 mg/dL or ionized calcium concentrations <1.0 mmol/L. The typical starting dose is 1–2 g of IV calcium gluconate administered over 10–20 min. This bolus dose translates to approximately 90–180 mg of elemental calcium. Following the IV bolus, a continuous infusion of cal- cium gluconate of approximately 50–100 mg of elemental calcium/h can be initiated for several hours until symptoms resolve. Transition to oral calcium and calcitriol can then be initi- ated. In hypoparathyroidism or the hungry bone syndrome, large calcium doses may be required to facilitate enteral calcium absorption. Calcitriol doses can range from 0.25 to 4 mcg per day. As magnesium depletion may impair PTH release as well as its action, aggressive magnesium replacement is required. In con- trast, phosphate administration is typically avoided in patients with hypophosphatemia and hypocalcemia as it can bind to cal- cium and further lower ionized calcium concentrations. In severe cases of the hungry bone syndrome with extreme hypophosphate- mia, phosphate repletion may be considered but cautious admin- istration is advised. Follow-Up After Discharge The discharge plan should include a timely follow-up visit for continued evaluation of calcium concentrations. An appoint- ment should be made for the patient within 1–2 weeks following surgery to measure the calcium and PTH levels and adjust the calcium and vitamin D doses. It is important that the patient is educated about the signs and symptoms of hypercalcemia and hypocalcemia and that they are able to contact their providers if they experience suggestive symptoms in order to have labora- tory levels checked. For patients with persistent or permanent hypoparathyroidism, calcium and vitamin D/calcitriol dosing is adjusted to keep calcium levels in the lower limits of normal to 12 Perioperative Evaluation of Primary Hyperparathyroidism 143 prevent hypercalciuria. Thiazide diuretics may be added if hypercalciuria develops. Selected patients with hypoparathy- roidism may be candidates for treatment with parathyroid hor- mone injections. Suggested Reading Bilezikian JP, Brandi ML, Eastell R, Silverberg SJ, Udelsman R, Marcocci C, et al. Guidelines for the management of asymptomatic primary hyperpara- thyroidism: summary statement from the Fourth International Workshop. J Clin Endocrinol Metabol. 2014;99(10):3561–9. Jain N, Reilly RF. Hungry bone disease. Curr Opin Nephrol Hypertens. 2017;26(4):250–5. Stack BC Jr, Bimston DN, Bodenner DL, Brett EM, Dralle H, Orloff LA, et al. American association of clinical endocrinologists and American col- lege of endocrinology disease state clinical review: postoperative hypo- parathyroidism–definitions and management. Endocr Pract. 2015;21(6): 674–85. Udelsman R, Akerstrom G, Biagini C, Duh QY, Miccoli P, Niederle B, et al. The surgical management of asymptomatic primary hyperparathyroidism: proceedings of the Fourth International Workshop. J Clin Endocrinol Metabol. 2014;99(10):3595–606. Wilhelm SM, Wang TS, Ruan DT, Lee JA, Asa SL, Duh QY, et al. The American association of endocrine surgeons guidelines for definitive management of primary hyperparathyroidism. JAMA Surg. 2016;151(10): 959–68. Management 13 of Osteoporosis in the Inpatient Setting Marcy A. Cheifetz Contents Definition of Osteoporosis 146 Significance of Fragility Fractures 146 Fragility Fractures of the Hip 147 Fragility Fractures of the Vertebra 147 Inpatient Management of Fragility Fractures 148 Laboratory Evaluation 153 Continuing Pre-hospitalization Osteoporosis Medications as an Inpatient 154 Preventing Future Fractures 156 Follow-Up After Discharge 156 Suggested Reading 157 M. A. Cheifetz (*) Harvard Vanguard Medical Associates, Atrius Health, Department of Endocrinology, Chestnut Hill, MA, USA e-mail: marcy_cheifetz@atriushealth.org © Springer Nature Switzerland AG 2020 145 R. K. Garg et al. (eds.), Handbook of Inpatient Endocrinology, https://doi.org/10.1007/978-3-030-38976-5_13 146 M. A. Cheifetz Definition of Osteoporosis Osteoporosis is defined as a disease of low bone mass and abnor- mal bone microarchitecture that leads to decreased bone strength and increased risk of fragility fracture. The term “fragility frac- ture” indicates a fracture that would not occur when bone strength and quality are normal, such as after a fall from a standing height. Osteoporotic fractures are defined as fragility fractures that occur at the vertebrae, hip, wrist, humerus, or pelvis. Although it has been well established that osteoporosis can be diagnosed with a bone density test, it is not as well appreciated that osteoporosis can also be diagnosed clinically. A hip or vertebral fragility frac- ture is synonymous with a clinical diagnosis of osteoporosis. Fragility fractures become increasingly prevalent as people age. Worldwide, one in three women and one in five men over age 50 will experience a fragility fracture in their lifetime. Fragility frac- tures that are most commonly seen in the inpatient setting include fractures of the hip and vertebrae. Hip fractures are particularly prevalent among the elderly population, especially for those resid- ing in long-term care institutions who are most prone to imbal- ance and falls. Significance of Fragility Fractures Osteoporotic fragility fractures are associated with significant morbidity, as well as an increased risk of mortality. The osteopo- rotic fractures most associated with negative health outcomes are hip fractures and vertebral fractures. Hip fractures, in particular, are associated with significant morbidity and an increased risk of mortality. At 1-year post-hip fracture, mortality rates reach nearly 40% in men and 25% in women, and mortality rates have been shown to remain elevated for up to 5–15 years after the fracture. Increased mortality rates have also been seen after fragility frac- tures of the spine. A prior fragility fracture of the hip or vertebrae confers up to a fivefold increased risk of future fracture. For these reasons, prevention of future fracture is of the utmost importance. However less than 20% of patients admitted with 13 Management of Osteoporosis in the Inpatient Setting 147 fragility fractures of the hip or spine ultimately receive osteopo- rosis treatment. Fragility Fractures of the Hip The majority of patients who are admitted to the hospital with a hip fracture will require surgical intervention. Approximately 50% of hip fracture patients never regain their prior level of phys- ical function, and many do not return to independent living. A high percentage report chronic pain even after 1-year postfracture. Approximately half of all patients who present with a hip fracture have already had a previous fragility fracture. Fragility Fractures of the Vertebra Vertebral fragility fractures are a common occurrence in the older osteoporosis population. Vertebral fractures also can have signifi- cant adverse effects on quality of life, and mortality rates are also substantial, with some studies showing over 20% greater age- adjusted mortality rates in women with one or more vertebral fractures. Furthermore, vertebral fractures can cause or exacer- bate kyphosis, restrictive lung disease, and chronic pain. Although they may be triggered by a fall or trauma, fragility fractures of the spine can occur spontaneously without a known inciting event. Two-thirds of vertebral fragility fractures are asymptomatic. The third that are clinically symptomatic can present with severe pain and associated disability that may necessitate hospitalization. The majority of cases can be managed conservatively with institution of pain control measures and physical therapy, as tolerated. In cases where adequate pain control cannot be achieved, vertebral augmentation with either percutaneous vertebroplasty or balloon kyphoplasty may be considered. However, whether such proce- dures are truly effective remains controversial. Overall, manage- ment of the vertebral fracture patient often requires a multidisciplinary approach that may involve pain management, interventional radiology, neurosurgery, and physical therapy. 148 M. A. Cheifetz Inpatient Management of Fragility Fractures There are many interventions that can be instituted by the inpa- tient care team for patients with fragility fractures. Non- pharmacological interventions such as initiation of calcium and vitamin D for those not already taking supplementation should be standard of care to help ensure adequate mineral stores and reduce the risk of secondary hyperparathyroidism and osteomalacia. Additionally, ensuring adequate nutritional status is vital, particu- larly in the elderly population that may be more at risk for malnu- trition. It is also critical to identify an individual’s modifiable risk factors for falling to help potentially reduce the risk of recurrent falls and fractures in the future. Risk factors associated with fall- ing in the elderly population include arrhythmias, impaired gait and balance, impaired vision, and neurological or musculoskele- tal disorders. Interventions and treatments that address these com- mon comorbidities can have significant benefits on reducing future fracture risks. Similarly, close scrutiny of an individual’s medication list is critical to help identify and potentially discon- tinue or change medications that may alter mental status or bal- ance and contribute to fall risk. Involvement of physical therapy to help address a patient’s risk for falling and recommend fall- prevention measures that can be instituted as an outpatient is also an important aspect of the care of these patients. The initiation of pharmacologic treatment for osteoporosis should also be consid- ered in the inpatient setting after an acute fragility fracture (see Table 13.1). In the presence of a fragility fracture of the hip or spine, which is indicative of osteoporosis regardless of bone den- sity status, it is not necessary to obtain a bone density test before initiating osteoporosis treatment. Osteoporosis treatment can be instituted in the acute setting immediately after a fragility fracture and does not need to be delayed until the fracture heals. Bisphosphonates, such as alendronate, risedronate, and zole- dronic acid, are the most commonly utilized osteoporosis medica- tions for osteoporosis. Studies have shown that bisphosphonates significantly reduce the risk of future fracture by 50–70% at the spine and 40–50% at the hip over 3–5 years of treatment in patients with or without prevalent vertebral fracture. The Horizon 13 Management of Osteoporosis in the Inpatient Setting 149 Table 13.1 Acute fragility fracture pharmacologic therapy Continue When to resume if after acute stopped after acute Drug Start after fracture and when fracture fracture Comment Bisphosphonate Yes. Can be initiated within Yes – Discontinue in setting of atypical femur Alendronate 2 weeks of fracture fracture (AFF) Risedronate Zoledronic acid Anabolic Yes. Can be initiated within Yes – Avoid in setting of preexisting therapy 1 week of fracture, although hyperparathyroidism, hypercalcemia, Teriparatide data limited to case reports and nephrolithiasis, Paget’s disease of the bone, Abaloparatide small clinical trials history of skeletal malignancy, or history of radiation to skeleton SERM Not first line. Can be initiated No Only if and when Associated with increased DVT risk, which Raloxifene immediately after fracture in back to baseline may be exacerbated by immobility, and the absence of DVT but limited ambulatory status with small increased stroke risk. by lack of efficacy in as an outpatient Discontinue in setting of DVT, MI, stroke preventing non-vertebral or immobility. fractures (continued) 150 M. A. Cheifetz Table 13.1 (continued) Continue When to resume if after acute stopped after acute Drug Start after fracture and when fracture fracture Comment Anti-rank ligand Can be initiated immediately Yes – Should be discontinued in setting of AFF. Denosumab after fracture Should not be abruptly discontinued without transition to bisphosphonate due to risk of rebound vertebral fracture. Romosozumab Likely can be initiated Yes – Given association with increased CV risks, immediately after fracture but should be discontinued in setting of MI or data re: effects on fracture stroke. healing not yet available HRT Not first line No Only if |
and when In oral forms, estrogen is associated with back to baseline increased DVT risk, which may be ambulatory status exacerbated by immobility. Discontinue in as an outpatient the setting of DVT, MI, stroke, or immobility 13 Management of Osteoporosis in the Inpatient Setting 151 Recurrent Fracture Trial, a randomized, controlled trial of yearly zoledronic acid administered to hip fracture patients within 90 days after surgical repair, showed a 35% relative risk reduction in rates of any new clinical fracture over the ensuing 2 years com- pared to placebo. Furthermore, in this same study, the group that received zoledronic acid experienced an almost 30% reduction in mortality from any cause, a particularly important finding given the known association of hip fracture with increased mortality. Additionally, there was no difference seen in the incidence of delayed union between the zoledronic acid group and the placebo group, suggesting that there is no evidence of impaired fracture healing when bisphosphonate therapy is initiated within 90 days of hip fracture repair. In a separate analysis, there was similarly no effect on healing seen with different timing intervals even when zoledronic acid was administered within 2 weeks of hip fracture repair. Other studies examining oral bisphosphonates such as alendronate and risedronate demonstrated similar findings, with no relationship seen between the use or timing of bisphosphonates on healing of femoral, humeral, or distal radius fractures even when administered within 2 weeks of the fracture event. Prior to administration of bisphosphonate treatment, particu- larly intravenous zoledronic acid, vitamin D deficiency must be corrected in order to avoid development of hypocalcemia. In the aforementioned Horizon Recurrent Fracture Trial, vitamin D lev- els were measured prior to zoledronic acid infusion, with levels below 15 ng/mL treated with a loading dose of vitamin D 50,000– 120,000 units orally or intramuscularly 2 weeks prior to the first infusion of IV zoledronic acid, followed by daily calcium 1000– 1500 mg and daily vitamin D 800–1200 IU thereafter. Due to the high incidence of vitamin D deficiency found in this population, the study protocol was ultimately changed so that all enrolled patients received a loading dose of vitamin D 2 weeks prior to the initial zoledronic acid infusion regardless of baseline vitamin D levels. In addition to vitamin D deficiency, renal dysfunction may also prove to be a limiting factor with the use of bisphosphonates, particularly in the hospital setting. Oral bisphosphonates should not be administered below an estimated creatinine clearance of 152 M. A. Cheifetz 30–35 ml/min, and intravenous zoledronic acid should not be administered below an estimated creatinine clearance of 35 ml/min. The anabolic agents teriparatide and abaloparatide have also been shown to be efficacious for the treatment of osteoporosis and osteoporotic fractures. Teriparatide, which is a recombinant form of PTH (1–34), and abaloparatide, which is an analog of PTH-r elated peptide (PTH-rp), both exert their anabolic effects through stimulation of the PTH receptor. The net effect of this stimulation is increased recruitment and activation of osteoblasts and enhancement of bone formation. In addition to their proven role in reducing the risk of vertebral and non-vertebral fracture, there has been growing evidence that these anabolic agents may also have beneficial effects on fracture healing. Several small studies and case reports of teriparatide have demonstrated effi- cacy in promoting more rapid callus formation and radiographic healing time in the acute fracture setting. Anecdotal reports have also shown positive effects of teriparatide in promoting healing in circumstances of delayed or nonunion fractures and in peri- prosthetic fractures. Furthermore, small studies have shown a possible role for teriparatide in promoting the healing of atypi- cal femur fractures. At the present time, data for the beneficial use of abaloparatide for promoting fracture healing is limited to animal studies. Because of reports of osteosarcoma development in rats given teriparatide and abaloparatide, anabolic agents are contraindicated in individuals with a history of radiation to the skeleton, Paget’s disease of the bone, bone metastases, or skeletal malignancies. Anabolic agents should also be avoided in patients with underlying hyperparathyroidism, hypercalcemia, and active nephrolithiasis. At the present time, all of the data supporting the utility of anabolic agents in the acute fracture setting come from small clinical trials or case reports, and neither of the currently available anabolic therapies have been officially approved for use in fracture repair. Larger prospective trials are needed to confirm the efficacy of anabolic therapies for the promotion of fracture healing. 13 Management of Osteoporosis in the Inpatient Setting 153 Other osteoporosis agents, such as denosumab, a human mono- clonal antibody against RANK-ligand, and romosozumab, a humanized monoclonal antibody to sclerostin, are not easily initiated in the inpatient setting but are similarly effective medica- tions that could be considered as alternative choices for treatment as an outpatient. Laboratory Evaluation All patients with fragility fracture should undergo a comprehen- sive laboratory evaluation to exclude secondary causes of osteo- porosis. General recommendations for screening labs include 25-hydroxyvitamin D, PTH, serum calcium, phosphate, creati- nine, eGFR, and TSH. Interpretation of vitamin D levels in the inpatient setting may be confounded by the severity of the under- lying illness. In the setting of critical illness, vitamin D defi- ciency has been found to be highly prevalent, and several meta-analyses have demonstrated an association between vita- min D deficiency and poorer outcomes. Vitamin D deficiency in the ICU population may relate to preexisting nutritional deficits or disease, but studies have shown that critical illness can also lead to dysregulation of vitamin D metabolism, further exacer- bating the deficiency. In the ICU settings, this is often further compounded by fluid resuscitation, interstitial extravasation, liver dysfunction, and renal insufficiency. In men, hypogonadism is also associated with development of osteoporosis, but testosterone should not be measured in the acute hospital setting due to an increased likelihood of falsely low lev- els. In cases of vertebral fracture, evaluation for multiple myeloma with measurement of serum and/or urine protein electrophoresis is also recommended. More extensive laboratory testing can be undertaken in the outpatient setting, including 24-h urine calcium measurement, to ensure calcium intake and absorption and to exclude hypercalciuria. 154 M. A. Cheifetz Continuing Pre-hospitalization Osteoporosis Medications as an Inpatient Patients who are admitted with an acute fragility fracture and are already taking osteoporosis medication can, in most cases, continue their medication as an inpatient. As previously discussed, bisphosphonates do not significantly interfere with fracture healing and therefore can typically be continued during hospitalization for an acute fracture. However, given their long-term retention in the bone, short-term discontinuation of bisphosphonate therapy, if necessary, is unlikely to have a significant negative impact on bone health. Furthermore, bisphosphonates should not be administered in the setting of creatinine clearance below 30–35 ml/min and should be discontinued in the setting of acute renal failure. Like bisphosphonates, denosumab does not impair fracture healing or increase the risk of nonunion when administered within 6 weeks before or after a fracture, according to results from the Freedom trial. Furthermore, discontinuation of denosumab without transition to a bisphosphonate leads to significant rebound bone loss that can be associated with spontaneous vertebral fracture and therefore should be avoided in the inpatient setting. Anabolic agents such as teriparatide or abaloparatide can typically be continued in the hospitalized patient after a fragility fracture unless significant hypercalcemia is noted. In that case, the medication should be held until the hypercalcemia resolves and then can be restarted on an every other day schedule as long as there is close follow-up of calcium levels post-discharge. Raloxifene is an oral selective estrogen receptor modulator that is given daily to some postmenopausal women with osteoporosis, although it is less commonly used than other osteoporosis medications, particularly in elderly individuals, due to associated increased risk of DVT and possibly stroke. In the acute setting after hip fracture and possibly after vertebral fracture, when patients are often immobile, raloxifene should be discontinued to minimize the risk of DVT. In the absence of other contraindications, it can be restarted as an outpatient, although switching to a more potent osteoporosis agent post-discharge would be advisable, particularly since raloxifene has not been shown to reduce the risk of hip fracture. Romosozumab, a humanized monoclonal antibody to sclerostin that has been recently approved for treatment of osteoporosis for those at high 13 Management of Osteoporosis in the Inpatient Setting 155 risk for fracture, is administered as a subcutaneous injection once a month for up to 12 months. There is currently no data available regarding its effect on fracture healing, but given its anabolic effects it is unlikely to interfere. Since it is given monthly, administration of romosozumab in the inpatient setting would only be required during prolonged hospital stays. Romosozumab has been associated with an increased risk of cardiovascular disease, and currently the labeling includes a black box warning stating that it may increase the risk of heart attack, stroke, and cardiovascular death. If a patient experiences a heart attack or stroke during treatment, romosozumab should be discontinued. Although osteoporosis medications can typically be continued after hospitalization for an acute fracture, one notable exception is in the case of a proven atypical femur fracture (AFF). Atypical femur fracture is a fracture of the femoral shaft that occurs after minimal or no trauma and is an extremely rare occurrence in patients receiving antiresorptive therapies, such as bisphosphonates or denosumab. The rates of AFF associated with the use of bisphosphonates in doses administered for osteoporosis treatment have been estimated at approximately 2 per 100,000 person-years after 2 years of bisphosphonate use. However, the incidence of AFF appears to increase with long-term use, with reports of 78 cases per 100,000 patient-years after 8 years of bisphosphonate exposure, most of these occurring after 5 years of use. In cases of suspected or proven AFF in a patient currently taking an oral bisphosphonate, such as alendronate, risedronate, or ibandronate, the medication should be immediately discontinued. AFFs have also been associated with denosumab use, although in the Freedom Extension Study, only one AFF was noted after 10 years of denosumab use. Similarly rare rates of AFF have been noted with romosozumab, although a causal link has not yet been definitively established. Since medications such as intravenous zoledronic acid or subcutaneous denosumab are given on a biannual or annual basis, cessation of therapy is not typically feasible in the inpatient setting, but future administration should be avoided if AFF occurs during treatment. In the case of denosumab, discontinuation leads to significant rebound bone loss and has been associated with an increased risk for spontaneous vertebral fracture; for this reason, discontinuation should be undertaken with caution and preferably with the involvement of an endocrinologist. 156 M. A. Cheifetz Preventing Future Fractures Despite the high prevalence of osteoporotic fractures in the elderly population and the high risk of future fracture in those who have already suffered a fragility fracture, the vast majority of patients who experience such a fracture are never identified as having osteoporosis or having started on osteoporosis medication. The inpatient setting represents a unique opportunity to identify indi- viduals as having osteoporosis and initiate interventions and anti- fracture treatment to help minimize future fracture risks. Many hospitals worldwide have instituted fracture liaison services (FLS) led by hospital-based coordinators to identify patients with fragility fracture and, using a multidisciplinary approach, facili- tate bone density testing, laboratory evaluations, initiation of osteoporosis therapy, and follow-up osteoporosis care as an out- patient. Studies of FLS programs have shown significantly higher rates of treatment initiation and significantly lower rates of recur- rent fracture and mortality in patients compared to patients receiv- ing usual care. Follow-Up After Discharge Many patients who have suffered a fragility fracture, particularly of the hip or spine, will require physical rehabilitation after discharge, and in some cases transfer to an inpatient rehabilitation facility may be necessary. Such decisions should be made on an individualized basis. All patients who have been admitted with a fragility fracture of the hip or spine should be set up for a follow- up visit with their primary care team for further evaluation and management of their osteoporosis after discharge. A bone density test should be arranged post-discharge. If osteoporosis treatment has not been initiated during the hospitalization, patients should be discharged with instructions to follow up with their primary care doctors to initiate osteoporosis treatment as an |
outpatient. 13 Management of Osteoporosis in the Inpatient Setting 157 Suggested Reading Bone HG, Wagman RB, Brandi ML, Brown JP, Chapurlat R, Cummings SR, C et al. 10 years of denosumab treatment in postmenopausal women with osteoporosis: results from the phase 3 randomised FREEDOM trial and open-label extension. Lancet Diabetes Endocrinol. 2017;5(7):513–23. Camacho PM, Petak SM, Binkley N, Clarke BL, Harris ST, Hurley DL, et al. American Association of Clinical Endocrinologists and American College of Endocrinology Clinical Practice guidelines for the diagnosis and treatment of postmenopasual osteoporosis–2016. Endocr Pract. 2016;22(9):1111–8. Colón-Emeric C, Nordsletten L, Olson S, Major N, Boonen S, Haentjens P, HORIZON Recurrent Fracture Trial, et al. Association between timing of zoledronic acid infusion and hip fracture healing. Osteoporos Int. 2011;22(8):2329–36. Cosman F, de Beur SJ, LeBoff MS, Lewiecki EM, Tanner B, Randall S, et al. Clinician’s guide to prevention and treatment of osteoporosis. Osteoporos Int. 2014;25(10):2359–81. Ip TP, Leung J, Kung AW. Management of osteoporosis in patients hospitalized for hip fractures. Osteoporos Int. 2010;21(Suppl 4):S605–14. Lamy O, Gonzalez-Rodriguez E, Stoll D, Hans D, Aubry-Rozier B. Severe rebound-associated vertebral fractures after denosumab discontinuation: 9 clinical cases report. J Clin Endocrinol Metab. 2017;102(2):354–8. Lyles KW, Colón-Emeric CS, Magaziner JS, Adachi JD, Pieper CF, Mautalen C, HORIZON Recurrent Fracture Trial, et al. Zoledronic acid and clinical fractures and mortality after hip fracture. N Engl J Med. 2007;357(18):1799–809. Molvik H, Khan W. Bisphosphonates and their influence on fracture healing; a systematic review. Osteoporos Int. 2015;25:1251–60. Ong T, Kantachuvesiri P, Sahota O, Gladman JRF. Characteristics and out- comes of hospitalised patients with vertebral fragility fractures: a system- atic review. Age Ageing. 2018;47:17–25. Roberts SJ, Ke HZ. Anabolic strategies to augment bone fracture healing. Curr Osteoporos Rep. 2018;16:289–98. Sànchez-Riera L, Wilson N. Fragility fractures & their impact on older peo- ple. Best Pract Res Clin Rheumatol. 2017;31:169–91. Wu CH, Tu ST, Chang YF, Chan DC, Chien JT, Lin CH, et al. Fracture liaison services improve outcomes of patients with osteoporosis-related fractures: a systemic literature review and meta-analysis. Bone. 2018;111: 92–100. Calcium Disorders 14 in End- Stage Renal Failure Including Those on Dialysis Alan Ona Malabanan Contents Calcium Metabolism in Chronic Kidney Disease (CKD) Is Characterized by Aberrations in Calcium and Phosphate Clearance, Decreases in 1-α-Hydroxylase Activity with Decreased Calcium Absorption, and Parathyroid Hormone Resistance . . . . . . . . . 160 Calcium Status in CKD Stages 3–5 Should Be Assessed with an Estimate of Ionized Calcium (i.e., Total Serum Calcium Corrected for Serum Albumin), Serum Phosphate, Serum Parathyroid Hormone, and Serum Bone-Specific Alkaline Phosphatase . . . . . . . . . 161 Calcium Disorders in CKD Should Be Managed in Close Coordination with the Patient’s Primary Nephrologist, Carefully Reconciling the Medications Being Taken as an Outpatient and Being Given in Dialysis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 162 Hypocalcemia Should Be Managed as Previously Described for Chronic Hypocalcemia but Being Particularly Cautious About Avoiding Hypercalcemia, an Elevated Calcium-Phosphate Product, and Parathyroid Hormone/Bone Alkaline Phosphatase Suppression . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 162 A. O. Malabanan (*) Beth Israel Deaconess Medical Center, Harvard Medical School, Division of Endocrinology, Diabetes and Metabolism, Boston, MA, USA e-mail: amalaban@bidmc.harvard.edu © Springer Nature Switzerland AG 2020 159 R. K. Garg et al. (eds.), Handbook of Inpatient Endocrinology, https://doi.org/10.1007/978-3-030-38976-5_14 160 A. O. Malabanan Secondary Hyperparathyroidism May Be Managed with Dietary Phosphate Restriction or Phosphate Binding, Adequate Calcium Intake, Activated Vitamin D, or Cinacalcet Use . . . . . . . . . . . . . . . . . . 163 Tertiary Hyperparathyroidism May Be Managed with Adequate Fluid Intake, Reducing Calcium and Activated Vitamin D Intake, Cinacalcet Use, or Parathyroid Surgery . . . . . . . . . . . . . . . . . . . . . . . . 164 Suggested Reading . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 164 Calcium Metabolism in Chronic Kidney Disease (CKD) Is Characterized by Aberrations in Calcium and Phosphate Clearance, Decreases in 1-α-Hydroxylase Activity with Decreased Calcium Absorption, and Parathyroid Hormone Resistance Serum calcium is controlled by the interaction between the bone, the kidney, and the gut through the actions of dietary calcium, vitamin D, and parathyroid hormone. With the loss of kidney function, there is ultimately the loss of the 1-alpha-hydroxylase, lowering the production of 1,25-dihydroxyvitamin D and impair- ing gastrointestinal calcium absorption. However, aberrations in calcium metabolism occur before this critical loss of renal mass and 1-alpha-hydroxylase activity. The kidneys are also responsi- ble for phosphate clearance, important because of the marked effi- ciency of gastrointestinal phosphate absorption and the omnipresence of phosphate in our diet. With increased phosphate levels, fibroblast growth factor 23 (FGF-23) increases due to its role as a phosphaturic factor. FGF-23 inhibits the renal 1-alpha- hydroxylase (since 1,25-dihydroxyvitamin D increases phosphate absorption) and lowers 1,25-dihydroxyvitamin D levels. Parathyroid hormone (PTH) rises, as compensation, increasing bone turnover and release of calcium from the bone, to maintain calcium homeostasis. In addition, hyperphosphatemia may directly stimulate PTH secretion, since PTH is also a phosphaturic 14 Calcium Disorders in End-Stage Renal Failure Including Those… 161 factor. Worsening azotemia also results in PTH resistance, further requiring higher PTH levels to maintain calcium homeostasis. Calcium Status in CKD Stages 3–5 Should Be Assessed with an Estimate of Ionized Calcium (i.e., Total Serum Calcium Corrected for Serum Albumin), Serum Phosphate, Serum Parathyroid Hormone, and Serum Bone-Specific Alkaline Phosphatase Hypoalbuminemia in nephrotic syndrome may lower total serum calcium levels, so serum calcium levels should always be assessed with a concomitant serum albumin. The total serum calcium should be corrected for hypoalbuminemia (corrected serum calcium = total serum calcium + ((4.0 − Albumin) × 0.8)). Aberrations in acid-base status may necessitate a direct mea- surement of ionized calcium, since acidemia increases ionized calcium levels. Hyperparathyroidism is associated with bone and vascular disease and should be monitored. Appropriate ranges for PTH are typically above the normal reference range due to PTH resistance and a risk for adynamic bone disease with lower than optimal PTH levels. Bone-specific alkaline phospha- tase reflects PTH action on the bone and may help in individual- izing PTH targets. Optimal PTH ranges for those not on dialysis with CKD 3a to 5 are unknown. PTH has poor sensitivity and specificity in identifying high and low turnover. In addition, PTH has marked variability with regard to diet and diurnal changes. The Kidney Disease Improving Global Outcomes (KDIGO) guidelines have focused on following PTH trends rather than individual values and correcting vitamin D defi- ciency, hyperphosphatemia, high phosphate diet, and hypocalce- mia. For those with CKD 5D, PTH target range has been recommended at 2× to 9× the upper limit of normal since high or rising PTH levels are associated with increased metabolic bone disease, morbidity, and mortality. 162 A. O. Malabanan Calcium Disorders in CKD Should Be Managed in Close Coordination with the Patient’s Primary Nephrologist, Carefully Reconciling the Medications Being Taken as an Outpatient and Being Given in Dialysis Often patients receiving hemodialysis are followed in outpatient dialysis centers, and they have frequent lab testing as well as long- acting medications given in dialysis. It is critical to obtain these records and reconcile medication lists to plan appropriate man- agement. Direct communication with the patient’s outpatient pri- mary nephrologist is paramount both on admission and on discharge. Hypocalcemia Should Be Managed as Previously Described for Chronic Hypocalcemia but Being Particularly Cautious About Avoiding Hypercalcemia, an Elevated Calcium-Phosphate Product, and Parathyroid Hormone/Bone Alkaline Phosphatase Suppression Hypocalcemia is managed by ruling out pseudo-hypocalcemia related to hypoalbuminemia and ruling out vitamin D deficiency or hypomagnesemia as a cause. Treatment is focused on correct- ing vitamin D deficiency, assuring adequate calcium intake and then considering activated vitamin D analogues. Because the impaired kidneys may not be able to clear excess calcium or phos- phate, attention and care should be paid to avoiding hypercalce- mia and an elevated calcium-phosphate product. An elevated calcium-phosphate product increases the risk for metastatic calci- fication of soft tissues and, as mentioned in the chapter on hypo- calcemia, should be maintained <55 mg2/dl2. 14 Calcium Disorders in End-Stage Renal Failure Including Those… 163 Secondary Hyperparathyroidism May Be Managed with Dietary Phosphate Restriction or Phosphate Binding, Adequate Calcium Intake, Activated Vitamin D, or Cinacalcet Use Hypocalcemia and hyperphosphatemia are associated with increased mortality and vascular disease, as is secondary hyper- parathyroidism. The KDIGO guidelines suggest dietary phosphate restriction in the setting of hyperphosphatemia, making sure that other nutrient intake isn’t compromised. Guidance and teaching from a dietitian would be helpful. It is unclear what PTH target should be considered for patients with CKD not on dialysis. KDIGO recommends PTH targets from two times upper limit of normal to nine times upper limit for those on dialysis. For those with CKD G3a-G5 and rising PTH levels, addressing modifiable etiologies such as vitamin D deficiency, hypocalcemia, and hyper- phosphatemia is warranted. With hypocalcemia, calcium supple- ments and calcitriol, as outlined in the hypocalcemia chapter, would be indicated. If dietary phosphate restriction is insufficient to control phosphate levels, nonaluminum phosphate binders are recommended, with non-calcium phosphate binders such as sevelamer having some advantage over calcium-containing phos- phate binders. Activated vitamin D therapy and calcium-based phosphate binders should not be used in patients with hypercalce- mia. If serum calcium levels are high normal, paricalcitol and dox- ercalciferol may be preferred to calcitriol due to a lower tendency to raise serum calcium levels. Cinacalcet, a calcium sensing recep- tor agonist, may be helpful in lowering PTH if the above measures are unsuccessful. GI upset is a side effect. Cinacalcet should not be used in patients with hypocalcemia. Cinacalcet use might lower the incidence of mortality and cardiovascular events in older dialy- sis patients by lowering FGF-23 levels. Normalization of PTH and suppressing bone-specific alkaline phosphatase should be avoided to minimize the risk for adynamic bone disease. 164 A. O. Malabanan Tertiary Hyperparathyroidism May Be Managed with Adequate Fluid Intake, Reducing Calcium and Activated Vitamin D Intake, Cinacalcet Use, or Parathyroid Surgery Occasionally secondary hyperparathyroidism leads to worsening parathyroid hyperplasia and autonomy, eventually causing hyper- calcemia, most often after renal transplantation. Maintaining ade- quate fluid intake and lowering or stopping the calcium and activated vitamin D may control the hypercalcemia. Cinacalcet is often started at 30 mg p.o. daily with lab testing at least 12 h after dosing. If medical therapy is insufficient to control serum calcium levels or there is significant bone involvement, surgical therapy is indicated for parathyroid debulking. Suggested Reading Kidney Disease: Improving Global Outcomes (KDIGO) CKD-MBD Update Work Group. KDIGO 2017 clinical practice guideline update for the diag- nosis, evaluation, prevention, and treatment of chronic kidney disease– mineral and bone disorder (CKD-MBD). Kidney Int Suppl. 2017;7:1–59. Moe SM, Chertow GM, Parfrey PS, Kubo Y, Block GA, Correa-Rotter R, et al. Cinacalcet, fibroblast growth factor-23, and cardiovascular disease in hemodialysis: the evaluation of cinacalcet HCl therapy to lower cardio- vascular events (EVOLVE) trial. Circulation. 2015;132:27–39. Parfrey PS, Drüeke TB, Block GA, Correa-Rotter R, Floege J, Herzog CA, et al. The effects of cinacalcet in older and younger patients on hemodi- alysis: the evaluation of cinacalcet HCl therapy to lower cardiovascular events (EVOLVE) trial. Clin J Am Soc Nephrol. 2015;10:791–9. Disorders of the Serum 15 Sodium Concentration Julian L. Seifter and Hsin-Yun Chang Contents Basic Physiology of Sodium and Water Balance 166 Osmoregulation of ADH 168 Relation Between Plasma Osmolality and Sodium Concentration 169 Relation Between Osmolality and Tonicity 170 Initial Approach to Dysnatremia 171 Clinical Features of Dysnatremia and Cell Adaptation 172 Diagnostic Approach to Hyponatremia 173 Is the Hyponatremia “True or Fictitious”? 173 Is the Hyponatremia Associated with H ypo-osmolairty 174 Is the ADH Activity Appropriately Suppressed? 175 |
Diagnostic Categories of Hyponatermia Based on the Extracellular Volume 175 Hypervolemic Hyponatremia 177 Hypovolemic Hyponatremia 178 Euvolemic Hyponatremia 180 J. L. Seifter (*) Brigham and Women’s Hospital, Department of Medicine, Boston, MA, USA e-mail: jseifter@bwh.harvard.edu H.-Y. Chang National Cheng Kung University Hospital, Department of Family Medicine, Tainan City, Taiwan © Springer Nature Switzerland AG 2020 165 R. K. Garg et al. (eds.), Handbook of Inpatient Endocrinology, https://doi.org/10.1007/978-3-030-38976-5_15 166 J. L. Seifter and H.-Y. Chang Management of Hyponatremia 182 Diagnostic Approach to Hypernatremia 184 Hypervolemic Hypernatremia 184 Hypovolemic/Euvolemic Hypernatremia 185 Management of Hypernatremia 186 Suggested Reading 187 Abbreviations ACE Angiotensin-converting enzyme ADH Antidiuretic hormone ANP Atrial natriuretic peptide AQP2 Aquaporin type 2 AVP Arginine vasopressin CHF Congestive heart failure CRH Corticotropin-releasing hormone ECF Extracellular fluid FES Flame emission spectrophotometer ICF Intracellular fluid ODS Osmotic demyelination syndrome RAAS Renin-angiotensin-aldosterone system SIADH Syndrome of inappropriate antidiuresis hormone (SIADH) SNS Sympathetic nervous system Basic Physiology of Sodium and Water Balance The concentrations of Na+, the most abundant extracellular fluid (ECF) cation, and K+, the major intracellular cation, determine the osmolality of total body water. More than 90% of the total osmotic content of the ECF is accounted for by Na+ and its accompanying anions, principally Cl− and HCO − 3 . 15 Disorders of the Serum Sodium Concentration 167 Plasma osmolality can be seen as that of total body water since osmolality of almost all body compartments is the same; we then have the equation shown below: Extracellular Intracellular solutes Plasma osmolality Total body water 2 Na K 2 Na Total body water Therefore, plasma [Na+] ≃ (Na+ + K+)/total body water. Na+ content is determined by dietary intake and regulated excretion independent of water regulatory mechanisms in order to maintain an adequate blood pressure and plasma volume required for perfusion of tissues. The state of total body potassium is also a reflection of diet and regulated excretion that determines cellular volume. Since most cell membranes are highly permeable to water, the regulation of osmolality usually depends on water balance. Plasma [Na+] is kept within a narrow range of 135–145 mmol/ kg (~mEq/L); an even narrower range of ~2% difference in an individual is often observed. Despite constantly changing dietary intake of salt and water, this finely regulated homeostatic control is due to an important thirst mechanism and renal regulation by means of the rapid stimulated release of the posterior pituitary peptide hormone, arginine vasopressin (AVP) , when conserving water is required and the rapid degradation of AVP in states of water excess. In turn, adequate ability to concentrate urine to maximal levels in humans (~1200 mOsm/kg) requires intact tubu- lar functions of the kidney, adequate salt and protein diets to allow for urinary concentrating ability, and a complex system of countercurrent exchange and multiplication. The systems of regulating osmolality and extracellular volume (and therefore blood pressure) are mostly different, but they inter- sect in the setting of changes in volume expansion or depletion (Fig. 15.1). 168 J. L. Seifter and H.-Y. Chang Na+ Excretion Volume H2O Excretion & Reabsorption & Retention Osmolality R-A-S ANP ADH SNS >10% Thirst Volume depletion Fig. 15.1 The systems regulating osmolality and volume are mostly differ- ent but interact in the setting of changes in volume. ADH secretion is stimu- lated as systemic osmolality is raised above a threshold level of 285 mOsm/ kg. Over the physiologic range of effective circulating volume, ADH levels are determined almost entirely by plasma osmolality. However, extracellular volume depletion of 10% or greater also significantly influences ADH levels. Both increase in plasma osmolality and decrease in extracellular volume stimulate the “thirst center.” The sympathetic nerve system (SNS) and renin- angiotensin system (RAS) , on the other hand, respond to smaller decrements of extracellular volume changes. In excessive fluid loss, baroreceptors stimu- late sympathetic activity to the kidneys, triggering vasoconstriction mainly in efferent arterioles to maintain GFR as well as renin secretion and Na+ reab- sorption along nephron. In renin-angiotensin system (RAS), angiotensin II also causes vasoconstriction in efferent arteriole to maintain GFR and pro- motes aldosterone secretion so as to stimulate increased Na+ reabsorption. Atrial natriuretic peptide (ANP) can be seen as the counter regulatory system for the RAS, causing systemic vasodilation and increased Na+ and water excretion in response to extracellular volume expansion Osmoregulation of ADH The absence or presence of ADH is the major physiologic deter- minant of urinary water excretion or retention. ADH secretion is stimulated as systemic osmolality is raised above a threshold level of 285 mOsm/kg. Decreases in blood pressure and intravascular fluid volume also stimulate ADH release and thirst but in a less sensitive manner. In addition, there are other non-osmotic stimuli that activate ADH release, including hypoxemia, nausea, stress (pain, emotion, exercise), alcohol, serotonin, and multiple drugs. 15 Disorders of the Serum Sodium Concentration 169 ADH acts on renal V2 receptors to increase permeability to water in the collecting ducts, permeability to urea in the inner medullary collecting ducts, and reabsorption of NaCl by the thick ascending limb, distal tubule, and collecting duct. Increases in plasma osmolality or decrease in volume stimu- lates the “thirst centers,” which is located in the same regions of hypothalamus as involved with ADH secretion. Other thirst recep- tors are located in the oropharynx. Osmotic threshold for trigger- ing thirst is higher than that for ADH secretion (295 vs. 285 mOsm/ kg). ADH will be suppressed by hypotonicity once ADH thresh- old is reached. The secretion of ADH reduces water loss in urine in the setting of water deprivation, and the ADH threshold being lower than that of thirst prevents an otherwise continuous cycle of polyuria and polydipsia. In diabetes insipidus, ADH is either inadequate in concentration or absent. The major sign is potentially massive dilute urine production, which becomes serious if water consumption is not available. On the other hand, in the syndrome of inappropriate antidiuretic hormone secretion (SIADH) , inges- tion of water does not adequately suppress ADH, and the urine remains more concentrated than expected. Relation Between Plasma Osmolality and Sodium Concentration Osmolality is a measure of the number of particles present in solution and is independent of the size or weight of the particles. Plasma osmolality (Posm) can be estimated as the calculated osmolarity (Posm): Posm 2 Na glucosemg / dL /18 blood urea nitrogen mg / dL / 2.8 The multiple of 2 for the plasma sodium concentration accounts for the osmotic contribution of its accompanying anions in the extracellular fluid. The concentrations of glucose and blood urea nitrogen (BUN) being divided by 18 and 2.8 are to convert the frequently measured units of mg/dL into mmol/L. 170 J. L. Seifter and H.-Y. Chang In healthy subjects, glucose and urea are both present in low concentrations and are ineffective osmoles because they can cross cell membranes. Therefore, sodium acts as the main effective osmole in plasma, and the equation can be simplified as Posm ≃ 2 × [Na+]. Hyponatremia can result from either loss of Na+ and K+ or increase in total body water due to retention of ingested or infused water. Solute losses from vomiting or diarrhea typically occur in fluids that are iso-osmotic to plasma, which do not lead to changes in plasma [Na+]. Only if the fluids are replaced with ingested water will hyponatremia occur because ECF depletion leads to non-osmotic ADH release. Therefore, the cause for nearly all cases of hyponatremia is abnormal water retention leading to excess water in relation to solute. On the other hand, continuous water loss, and sometimes sodium overload, accounts for the occurrence of hypernatremia. Relation Between Osmolality and Tonicity Plasma tonicity, also called the effective plasma osmolality, equals the sum of the concentrations of the solutes which have the capac- ity to exert an osmotic force across the membrane. It reflects the concentration of solutes that do not easily cross cell membranes and therefore determines the transcellular distribution of water between the cells and the ECF. Fluid expansion and depletion contributing to disorders of serum [Na+] are summarized in Table 15.1. Hyponatremia occurs when a defect in urinary dilution is combined with water intake that exceeds the ability to quantitatively excrete enough water, while hypernatremia develops when there is loss of water in excess of sodium without appropriate water intake or by expansion with hypertonic fluids. Note that both hyponatremia and hypernatremia can be associated with increased, decreased, or normal ECF vol- ume. This is because ECF depletion, which always accompanies Na+ loss, may be due to losses of Na+ as hypertonic fluid (hypona- tremia), isotonic fluid (normonatremia), or hypotonic fluid (hyper- natremia). The expansion syndromes similarly accompany gains 15 Disorders of the Serum Sodium Concentration 171 Table 15.1 Syndromes of fluid expansion and depletion ECF ICF Hematocrit [Protein] [Na+] volume volume Examples Expansion Na > H2O ↓ ↓ ↑ ↑ ↓ Hypertonic expansion (hypertonic NaHCO3 or NaCl infusion) Na = H2O ↓ ↓ – ↑ – Isotonic expansion (saline infusion) Na < H2O ↓ ↓ ↓ ↑ ↑ Hypotonic expansion (1/2 NS infusion) Depletion Na > H2O ↑ ↑ ↑ ↓ ↑ Hypertonic depletion (diabetes insipidus) Na = H2O ↑ ↑ – ↓ – Isotonic depletion (sweating, vomiting) Na < H2O ↑ ↑ ↓ ↓ ↓ Hypotonic depletion (salt- wasting) of hypotonic fluids (hyponatremia), isotonic fluids (normonatre- mia), or hypertonic fluids (hypenatremia). Initial Approach to Dysnatremia Direct history and initial physical examination often provide use- ful information and guide the subsequent diagnostic approach. For example, a history of fluid loss from vomiting, diarrhea, and 172 J. L. Seifter and H.-Y. Chang diuretic therapy, or signs of extracellular fluid volume depletion such as decreased skin turgor and orthostatic or persistent hypo- tension, may suggest hypovolemic state. Inadequate fluid intake or poor diet, presence or absence of thirst and polyuria, medical history consistent with malignancy, heart failure, recent surgery, and certain medication use including antiepileptics and antipsy- chotics may all direct toward determining the causes of dysnatre- mias and further management. Routine laboratory chemistries may provide certain information, e.g., renal dysfunction and hyperkalemia suggesting hypoaldosteronism. Further investiga- tion should include urine chemistries. Imaging may be necessary to detect or confirm associated etiology. Note that dysnatremias are often multifactorial and clinical evaluation should consider all possible causes. Clinical Features of Dysnatremia and Cell Adaptation The symptoms of dysnatremia are mainly neurological due to the effects on the central nervous system. In hyponatremia, a fall in plasma tonicity results in osmotic water movement from the ECF into the cells, including brain cells, and leads to neurologic dys- function. In hypernatremia, there is an osmotic water movement out of the brain cells due to increased plasma tonicity. Symptoms of dysnatremia are associated with the rapidity of the changes in the plasma sodium concentration. Nausea and malaise are com- mon in early stage, while severe symptoms including seizures, brainstem herniation, and coma may develop when dysnatremia is acute or if a chronic condition is corrected too rapidly. When encountering changes in plasma tonicity, the brain attempts to adapt to hyponatremia by losing intracellular solutes (potassium and organics, e.g., amines, polyols, amino acids, glyc- erophosphocholine) and to hypernatremia by increasing intracel- lular solutes. The process of cell adaptation may be completed in 1–2 days with major implications for therapy. Brain cell volume may normalize within 1–2 days despite the continued change in 15 Disorders of the Serum Sodium Concentration 173 osmolality and may change abruptly if osmolality is corrected instantly. This can explain why patients with chronic dysnatremia are less likely to develop severe neurological deficits upon presenta- tion but are predisposed to cerebral edema and seizures if encoun- tering overcorrection of plasma sodium concentration (> 8–10 mM/d). Diagnostic Approach to Hyponatremia Is the Hyponatremia “True or Fictitious”? Hyponatremia is defined as a serum sodium level of less than 135 mmol/L. Decreased serum sodium often reflects a hypotonic state; however, hyponatremia may also occur with iso-osmotic or hyperosmotic plasma. It is prerequisite to confirm hypotonic and exclude non-hypotonic hyponatremia (Fig. 15.2). Plasma osmolality Hypertonic Isotonic Hypotonic Acute or severe >290 mOsm/kg 275~290 mOsm/kg <275 mOsm/kg symptoms? • Hyperglycemia • Hyperproteinemia Consider Urine • Mannitol • Hyperlipidemia immediate Osmolality • Glycine treatment with • Maltose hypertonic saline < 100 mOsm/L > 100 mOsm/L • Primary polydipsia See Figure 3. • Beer potomania |
• Low solute intake Fig. 15.2 Establish the type of hyponatremia by first measuring plasma osmolality, and obtain urine osmolality to assess ADH activity in the hypo- tonic hyponatremic patients. Note that a rapid decline in plasma sodium over 24–48 h is a medical emergency and requires acute intervention 174 J. L. Seifter and H.-Y. Chang • Iso-osmotic hyponatremia is caused factitiously by hyperpro- teinemia and hyperlipidemia, as solids that may contribute to more than the normal volume of plasma (>10%) and if the measurement is made by indirect potentiometry, a method of diluting of serum. The laboratory artifact is known as pseudohyponatremia. Excluding factitious hyponatremia requires a measure of serum osmolality or the Na+ concentration by direct potentiometry (undiluted sample) usually on a blood gas analyzer. Is the Hyponatremia Associated with Hypo-osmolairty The presence of solutes which do not penetrate cell membranes such as glucose (in the absence of insulin) and mannitol decreases plasma sodium by shifting water from intracellular to extracellu- lar space. A decrease in serum [Na+] of 2.4 mmol/L occurs for every 100 mg/dL increase in plasma glucose particularly when glucose is greater than 400 mg/dL. Estimates of the serum sodium concentration corrected for the presence of hyperglycemia can be obtained from the equations: Corrected serum Na measured Na 2.4 mg m glucose 100 g dL dL 100 mg dL Plasma osmolality can alsobe increased by certain solutes including urea, ethanol, methanol, and ethylene glycol. These sol- utes are cell membrane permeable and do not translocate water into the intra- or extracellular space. Their presence does not cause hyponatremia but can lead to a normal or high measured plasma osmolality in a hyponatremic patient from other cause. These patients should be approached as having a hypotonic disor- der given their decreased effective plasma tonicity. 15 Disorders of the Serum Sodium Concentration 175 Is the ADH Activity Appropriately Suppressed? • Obtain urine osmolality to assess ADH activity in the hypo- tonic hyponatremic patient. To evaluate hyponatremia, urine osmolality is used to assess ADH activity. The development of hyponatremia along with hypo-osmolality is often caused by underlying disorders affecting the renal diluting mechanism. Such patients have a greater than maximally dilute urine, which is 50–100 mOsm/kg, unless hypo- osmolality fails to fully suppress ADH release (the reset osmo- stat). When the urine osmolality is < 100 mOsm/kg, indicating maximally dilute urine, the hyponatremia is primarily caused by excess water intake or low solute intake. Psychogenic polydipsia and beer potomania are classic examples. This example demon- strates the difference between urinary dilution, a measure of con- centration, and excretion of quantitatively enough dilute urine, measured by free water clearance rate, in ml/min. Diagnostic Categories of Hyponatermia Based on the Extracellular Volume Ingestion of a normal diet in a healthy subject results in the excre- tion of approximately 600 mOsm of solute per day, which includes primarily sodium, potassium salts, and urea. If the minimum urine osmolality is 50 mOsmol/kg, the maximum urine output will be 12 L/day. In beer drinkers (beer potomania) or those on a very poor diet, there is little solute (low sodium, potassium, or protein) in the diet. Also the carbohydrate load in beer may further sup- press endogenous protein breakdown. Therefore, daily solute excretion may be less than 150 mOsm, and hyponatremia occurs if daily fluid intake exceeds 3 L/day. Patients with hyponatremia due to beer potomania and low solute intake respond rapidly to intravenous saline and a resumption of a normal diet. However, patients with beer potomania are at high risk of developing osmotic demyelinating syndrome (ODS) due to the associated hypokalemia, alcoholism, malnutrition, and potentially overcor- rected plasma sodium concentration. 176 J. L. Seifter and H.-Y. Chang Primary polydipsia occurs when more hypotonic fluid is con- sumed than excreted in a maximally dilute urine. It is characterized by increase in thirst and is most often seen in patients with psychi- atric illnesses. Changes in plasma osmolality play the most impor- tant role in regulating ADH secretion. Osmolality is sensed by osmoreceptors in the anterior hypothalamus, which shrink or swell in response to changes in osmolality. Decrease in plasma osmolal- ity will cause osmoreceptors to swell and thereby decrease ADH secretion. In primary polydipsia, the patients continue to drink until the thirst threshold, causing fall in plasma osmolality sup- pressing ADH secretion with diuresis and subsequently continued stimulation of thirst. An acute water load of 3–4 L may cause fatal hyponatremia even though the urine is maximally dilute. • Determine the patient’s volume status and obtain urine sodium concentration. In the patient with hypotonic hyponatremia whose urine is not dilute (>100 mOsm/L), an assessment of the ECF volume has been proposed to help further differentiate the underlying causes (Fig. 15.3). However, in clinical practice, a mixed process may occur, or a hypovolemic state often presents as clinical euvolemia, making such classification debatable. Measuring urine Na+ and K+ concentrations is therefore always essential. Calculations of electrolyte- free water clearance are recommended (CH2O = V – (UNa + UK)V/PNa). Note that since water is coming from TBW, both Na and K are required. This equation enables independent calculations of isotonic and free water excretion. It is helpful in diagnosis and treatment. For example, a positive CH2O and hypernatremia suggests diabetes insipidus. CH2O also improves management as it informs about ongoing urinary losses. While deficits are calculated based on an abnormal serum [Na+] and must be corrected at a safe rate, ongoing losses will lead to a defi- cit if not replaced quantitatively. Another advantage of calculating CH2O is in the choice of management strategy. Thus, if the urine was hypertonic in a hyponatremic patient, giving saline may make a patient with SIADH more hyponatremic. Also, in the same patient, a large negative value for CH2O predicts that fluid restric- 15 Disorders of the Serum Sodium Concentration 177 True hyponatremia with urine osmolality >100 mOsm/L ECF volume Hypervolemia Euvolemia Hypovolemia UNa <20 UNa >20 UNa <20 UNa >20 • Heart failure • Renal • Diarrhea • Renal losses • Cirrhosis insufficiency UNa >20 • Vomiting • Salt-losing deficiency • Nephrotic • Adrenal insufficiency • Nasogastric • Recent diuretics syndrome • Hypothyroidism suction • Hypoaldosteronism • SIADH • Extrarenal • Reset osmostat losses • Other causes of increased ADH secretion (drugs, pain, stress) Fig. 15.3 Determine the patient’s volume status and obtain urine sodium concentration for further diagnosis tion may be inadequate. In that case, treatment with a loop diuretic may be helpful to diminish the maximal urine osmolality, or cau- tious use of hypertonic saline may be required. When using a loop diuretic in a patient with hypertonic urine, it is necessary to recal- culate CH2O to assure success in creating hypotonic urine. Hypervolemic Hyponatremia When hyponatremia occurs with excess ECF volume, both total body sodium and total body water are increased, with total body water being increased to a greater extent. In this setting, the edem- atous state may be due to congestive heart failure (CHF), cirrho- sis, nephrotic syndrome, or advanced kidney disease. In CHF, cirrhosis, and nephrotic syndrome, a decreased effec- tive circulating arterial volume leads to increased ADH secretion. Aquaporin 2 (AQP2) water channels may also be increased, resulting in decreased water clearance. Urinary sodium level is often very low (may be < 10 mmol/L) in these cases, as renin- angiotensin- aldosterone system (RAAS) increases sodium reten- 178 J. L. Seifter and H.-Y. Chang tion. However, sodium retention can be obscured by diuretics, which are often used concomitantly to treat such patients. In advanced renal insufficiency, hyponatremia is associated with water intakes exceeding the ability to excrete equivalent vol- umes, and the minimum urine osmolality can rise to as high as 200–250 mOsmol/L. A decrement in GFR and the impairment of free water excretion with increase in thirst contribute to the reten- tion of ingested water and the development of a hypervolemic hyponatremic state. Hypervolemic hyponatremia due to CHF will often respond to improved therapy of the underlying cardiomy- opathy, e.g., following the institution or intensification of angiotensin- converting enzyme (ACE) inhibition. Hypovolemic Hyponatremia As noted earlier, plasma sodium concentration can be determined by: 2 Na K / Total body water The loss of sodium and possibly potassium may contribute to hyponatremia, if these losses are not accompanied by parallel decrements in total body water. When there are substantial fluid losses, from either renal or extrarenal sources, volume contraction stimulates secretion of ADH. If these losses are replenished with water or hypotonic fluids, hyponatremia will result. We know that over the physiologic range of effective circulating volume, ADH levels are determined almost entirely by plasma osmolality. However, volume depletion of 10% or greater will significantly influence ADH levels. Therefore, in the presence of hypovolemia, ADH is secreted with subsequent water retention even in the pres- ence of hypotonicity. On examination, a low jugular venous pres- sure, decreased skin turgor, orthostatic hypotension, and tachycardia may be noticed. A urinary sodium concentration of less than 20 mEq/L indicates a normal renal response to volume depletion by conserving sodium, and an extrarenal loss is sug- gested. Vomiting or diarrhea, or fluid losses into third spaces such 15 Disorders of the Serum Sodium Concentration 179 as burns or pancreatitis, can all lead to hypovolemia. The urinary sodium concentration can be as low as <10 mEq/L. However, in patients with vomiting and metabolic alkalosis presenting bicar- bonaturia, urinary sodium concentration can be greater than 20 mEq/L, while urinary chloride concentration will be low since bicarbonate anion dominates. Both the sodium and chloride con- centrations can be as high as 40 meq/L in hypovolemic hypona- tremic patients with renal salt losses, which is most commonly seen with diuretic therapy if the urine electrolytes are measured while the effect of the diuretic is still present. The variation in the hyponatremia risk relates to the site of action in different diuret- ics. Loop diuretics interfere with sodium chloride (NaCl) reab- sorption in the thick ascending limb of the loop of Henle by impairing the accumulation of NaCl in the medulla. Although the loop diuretic can increase ADH levels by inducing volume deple- tion, responsiveness to ADH is diminished because of the impair- ment in the medullary gradient. As a result, water retention and the development of hyponatremia will be limited. The thiazides, in comparison, act in the cortex of distal tubule and do not inter- fere with medullary function or with ADH-induced urinary con- centration in volume depletion. In addition to water retention, increased sodium and potassium excretion due to the diuretic as well as enhanced water retention can result in the excretion of electrolyte-rich urine with a sodium plus potassium concentration higher than that of the plasma and directly promote the develop- ment of hyponatremia regardless of water intake. Hyponatremia related to use of thiazides begins soon after initiation and is often evident within 14 days. Furosemide-related hyponatremia tends to occur after many months of therapy, often when an intercurrent illness develops in polydipsic patients. If urinary sodium concentration higher than 20 mEq/L accom- panies hyperkalemia and elevated plasma urea and creatinine, hypoaldosteronism should be suspected. Hypovolemic hyponatremia responds to volume restoration with isotonic normal saline – most importantly, the recognition of underlying etiology needs to be identified. It should be obvious that the urinary chemistries in hypovolemic hyponatremia and hypervolemic hyponatremia, as in CHF, are similar. The one hor- 180 J. L. Seifter and H.-Y. Chang monal difference in the plasma may be a high BNP (B-type natri- uretic peptide) in CHF, whereas it will be low in hypovolemia. Euvolemic Hyponatremia Euvolemic hyponatremia is the most heterogeneous and com- monly encountered hyponatremia in hospitalized patients. Patients may have slightly excessive volume in the absence of edema, and it may be hard to distinguish from hypovolemia. Urine chemistry again is vital to differentiation, and sodium is expected to be >20 mEq/L. Euvolemic hyponatremia can occur in any of the set- tings mentioned above and is seen in other scenarios. The ques- tion often arises as to why patients with water overload but not salt and water overload do not get edema. One reason is that only 6% of a water load expands the plasma volume as most water goes |
into cells. By the time water was expanded enough to cause edema, life-threatening hyponatremia would develop. A second reason is that an acute water load expands the plasma volume enough to cause a mild, acute natriuresis. But distinctively the cause of edema in ECF expansion is raised intravascular volume and pressure due to the gravitational effect on the veins. The result is an increased intracapillary hydrostatic pressure gradient in dependent areas such as lower extremities. In contrast, hypo- osmotic expansion with water will affect oncotic forces through- out the body, and there will be no effect of gravity to increase Starling forces in dependent areas. Secondary adrenal insufficiency due to pituitary disease may lead to euvolemic hyponatremia, while decreased aldosterone in primary adrenal insufficiency causes hypovolemic hyponatremia. In either primary or secondary adrenal insufficiency, glucocorti- coid deficiency leads to co-secretion of corticotropin-releasing hormone (CRH) and ADH by the paraventricular nuclei in the hypothalamus. Impaired water excretion with reduced water delivery to the collecting ducts is also associated with glucocorticoid deficiency. Hydrocortisone replacement in these patients will reduce ADH secretion and therefore normalize its response to osmolality. 15 Disorders of the Serum Sodium Concentration 181 In patients with hypothyroidism, the cardiac output is often reduced and may be the non-osmotic stimuli to ADH release, while the concomitant reduction in GFR leads to diminished free water excretion. Hyponatremia in this case can be reversed by treatment with levothyroxine. The syndrome of inappropriate antidiuretic hormone (SIADH) is a common cause of euvolemic hyponatremia in hospitalized patients. The diagnosis is made mainly by excluding other causes and can be summarized in Table 15.2. In normal individuals, plasma ADH levels are very low when the plasma osmolality is below 280 mOsmo/kg, permitting the excretion of ingested water. ADH levels increase progressively as the plasma osmolality rises above 280 mOsm/kg, and the higher the plasma ADH, the more concentrated the urine. In most patients with SIADH, ingestion of water does not adequately suppress ADH, and the urine remains concentrated. Sustained increases in ADH limit distal renal tubular transport, thereby preserving a relatively hypervolemic state with hyponatremia. Such patients are not euvolemic but rather subclinically volume-expanded. Serum uric acid is often low (<4 mg/dL) in patients with SIADH, while hyperuricemia is often seen in patients with hypovolemic hyponatremia. Common causes of SIADH include pulmonary disease, central nervous sys- tem disorders, and malignancies, most commonly in small-cell lung carcinoma. Patients with euvolemic hyponatremia due to SIADH may respond to successful treatment of the underlying cause. However, not all causes of SIADH are immediately revers- ible, and pharmacologic therapy may be necessary at certain point. Oral tolvaptan, the ADH V2 antagonist, may be considered Table 15.2 Diagnostic criteria for SIADH Decreased serum osmolality (<275 mOsm/kg) Increased urine osmolality (>100 mOsm/kg) Clinical euvolemia Increased urinary sodium concentration (>40 mmol/L) under normal salt and water intake Absence of adrenal, thyroid, pituitary, or renal insufficiency or recent diuretic use 182 J. L. Seifter and H.-Y. Chang in significant and uncontrolled SIADH which is not responsive to the treatment with water restriction, oral furosemide, and salt tablets. The “reset osmostat” is sometimes considered a variant of SIADH, in which the threshold for ADH secretion is reset down- ward so that ADH is secreted at a lower value instead of beyond 280–285 mOsm/kg as in most individuals. Diagnosing reset osmostat is a diagnosis of exclusion. Individuals with reset osmo- stat should be able to concentrate and dilute the urine appropri- ately, and a water challenge should result in a dilute urine (<100 mOsm/kg), while a water deprivation test results in a con- centrated urine. Reset osmostat often occurs in pregnancy, malnu- trition, and neurologic conditions such as epilepsy and paraplegia. A patient initially diagnosed with SIADH will sometimes be proven with virtually reset osmostat when it becomes apparent that fluid restriction does not successfully raise the serum sodium level. Management of Hyponatremia The major considerations in managing hyponatremia are: 1. The presence or absence, as well as severity, of symptoms 2. The duration of the disorder 3. Recognizing the underlying cause Patients with acute hyponatremia (with hyponatremia developing within 48 h) may present with symptoms ranging from headache, nausea, or vomiting to lethargy, seizures, or even coma and are also at greater risk of developing permanent neuro- logic sequelae. Patients with chronic hyponatremia (present for >48 h) are less likely to have severe symptoms. The risk of sei- zures remains low until the serum sodium concentration falls below 115 meq/L, and rarely patients may even be awake and talking with a serum sodium of <100 meq/L. However, patients with chronic hyponatremia are at greater risk for osmotic demy- elinating syndrome (ODS) if plasma sodium concentration is 15 Disorders of the Serum Sodium Concentration 183 corrected by >8–10 mM within the first 24 h or by >18 mM within the first 48 h. In contrast, in acute hyponatremia, overly rapid correction is less of a concern since the brain has not yet adapted completely to the hypotonic environment. Clinically, it may be unclear which treatments should be applied or what increases in plasma sodium concentration we should pursue. While treatment can be diagnosis specific, a single infusion of 150 mL 3% hypertonic saline may be suggested to avoid further drop in plasma sodium concentration. Nevertheless, frequent monitoring of plasma sodium concentration during corrective therapy is always crucial because a variation in the volume and electrolyte content of the urine produced concomitantly may also have an impact. Aggressive therapy to rapidly raise the serum sodium with hypertonic saline is indicated when patients present with severe symptoms such as seizures or obtundation or acute hyponatremia even with mild symptoms. The goal of such therapy is to rapidly increase the serum sodium by 4–6 mEq/L over a period of several hours. Note that the increase in serum sodium should not exceed 8 mEq/L in any given 24-h period. Patients who are asymptomatic or have mild to moderate symptoms with even acute or severe hyponatremia (i.e., serum sodium ≤ 120 mEq/L) do not require emergent therapy, and the goal is to slowly raise the serum sodium and alleviate symptoms. In general, raising the serum sodium by 4–6 mEq/L should improve a patient’s symptoms. Calculating a proper dose of 3% saline can be reasoned as follows: 3% saline has 513 meq/L NaCl (~0.5 meq/ml). Total body water is ~50% body weight in kilogram. Therefore, giving 1 ml/kg body weight will raise the [Na+] by 1 meq/L. Thus, to raise the serum [Na+] by 1 meq/L over 4 h in a 70 kg man, one would give 3% saline at a rate of 70 ml/hr for 4 h. Once the corrective therapy has been established and initiated, treatment should be directed at the underlying disease. In the case of overcorrection of hyponatremia (raising the Na+ greater than 8 mEq/L/day), water can be given as D5W with an amount to lower the Na+ to a value appropriate for the time elapsed. In cases where large elecrolyte free water clearance may correct hyponatremia too rapidly (as after saline given to a patient with 184 J. L. Seifter and H.-Y. Chang hypovolemic hyponatremia) SC or IV DDAVP may be adminis- tered to clamp the urine output to low levels. Then the adminis- tration of 3% saline allows correction at an appropriate rate. Since 3% saline is ~0.5 meq Na+/ml and total body water is ~0.5 times the body weight, it follows that administering 3% saline at 1 ml/kg body weight will raise the serum Na+ by 1 meq/L. Diagnostic Approach to Hypernatremia Hypernatremia is defined as an increase in the plasma Na+ con- centration to >145 mmol/L, reflecting losses of water via both renal and nonrenal routes in excess of sodium and potassium. Net water loss accounts for the majority. In order for hypernatremia to occur, either ADH function or thirst mechanism must be impaired, and limited access to water is often involved. In those who are alert and have an intact thirst mechanism and adequate access to water, persistent hypernatremia should rarely occur. The higher the GFR, or proximal tubule sodium, glucose, or urea delivery, the higher the urine volume. A detailed history and physical examination often reveal the underlying causes of hypernatremia. In the elderly, it is often due to water losses without adequate replacement due to altered men- tal status or limited access. Still, further investigation may be nec- essary when etiology is unclear (Table 15.3). As in hyponatremia, hypernatremia must be considered along with ECF status. Hypervolemic Hypernatremia If hypervolemia is present, sodium gains from hypertonic fluid administration or mineralocorticoid excess must be considered. Urine sodium concentration, if obtained, is often >20 mmol/L. The urine may in fact be hypertonic, though rarely maximally concen- trated due to washout of the medullary solute gradient. However, the net hypertonic salt intake must exceed the net hypertonic salt output. It is often asked whether someone can survive by drinking 15 Disorders of the Serum Sodium Concentration 185 Table 15.3 Common causes of hypernatremia Dehydration (nonrenal loss) Insensible losses Gastrointestinal losses Primary hypodipsia Sodium gains Hypertonic sodium load Hyperaldosteronism Cushing’s syndrome Osmotic diuresis Glucosuria High urea in high-protein tube feedings Mannitol Water diuresis Central diabetes insipidus Nephrogenic diabetes insipidus ocean water. Sea water is about 1000 meq Na+ and Cl−. The bowel can only absorb isosmotically. Thus, drinking seawater will increase isotonic salt water reabsorption, but the remaining hyper- tonic salt will induce severe isotonic diarrhea. The total body water will decrease. But the serum Na+ will rise, dehydrating cells while expanding the ECF. The result is hypertonic expansion. Urine osm and tonicity will rise (high ADH) and polyuria will result. Hypovolemic/Euvolemic Hypernatremia There may be evident history of extrarenal losses, e.g., increased. insensible loss, gastrointestinal loss, or burn. Minimum volume of maximally concentrated urine with urine osmolality >700 mOsm/kg and urinary sodium concentration <10 mmol/L may further support the diagnosis. If the urine osmolality appears less than 300 mOsm/ kg, the patient is suspected with either central or nephrogenic diabe- tes insipidus, which can be distinguished by the administration of exogenous ADH (dDAVP), followed by monitoring of the urine osmolality and volume every 30 min over the next 2 h. 186 J. L. Seifter and H.-Y. Chang If the urine osmolality is intermediate (between 300 and 800 mOsmol/kg), the hypernatremia may be due to diabetes insip- idus or an osmotic diuresis. Such patients can be differentiated by measuring the total solute excretion. As mentioned earlier, inges- tion of a normal diet in a healthy subject results in the excretion of approximately 600 mOsm (600–900 mOsm) of solute per day. A value above 900 mOsm/day suggests a significant contribution from increased solute excretion, indicating osmotic diuresis resulting from possibly glucosuria, mannitol, or high solute loads. If an osmotic diuresis is not present, a workup to rule out diabetes insipidus should be performed. Management of Hypernatremia The water deficit in the hypernatremic patient can be estimated from the following formula: Serum Na Free water deficit Current total body water 1 140 Total body water is estimated by multiplying weight in kilo- grams by 0.6 for men and by 0.5 for women. The formulas estimate the amount of water required to have been lost to raise the serum sodium from a relatively normal level of 140 to the hypernatremic value. To correct the [Na+] would require replacing that amount of water. Chronic hypernatremia (>48 h) or hypernatremia of unknown duration should be corrected at a safe rate at which the serum sodium concentration should be lowered no more than 10 meq/L per day to avoid cerebral edema caused by excess fall in serum [Na+]. As for acute hypernatremia, serum sodium level should be corrected over the next 24 h. Concurrent electrolyte disturbances should not be ignored and must be replenished accordingly. Meanwhile, ongoing free water losses, including losses in sweat, stool, dilute urinary, or gastrointestinal tract, must be replaced as well. In addition, this formula does not include com- bined sodium and water loss, as in diarrhea or an osmotic diuresis. 15 Disorders of the Serum Sodium Concentration 187 Suggested Reading Adrogue HJ, Madias NE. Hypernatremia. N Engl J Med. 2000;342(20):1493–9. Ashraf N, Locksley R, Arieff AI. Thiazide-induced hyponatremia associated with death or neurologic damage |
in outpatients. Am J Med. 1981;70(6):1163–8. Ayus JC, Caputo D, Bazerque F, Heguilen R, Gonzalez CD, Moritz ML. Treatment of hyponatremic encephalopathy with a 3% sodium chlo- ride protocol: a case series. Am J Kidney Dis. 2015;65(3):435–42. Chung HM, Kluge R, Schrier RW, Anderson RJ. Clinical assessment of extra- cellular fluid volume in hyponatremia. Am J Med. 1987;83(5):905–8. Hillier TA, Abbott RD, Barrett EJ. Hyponatremia: evaluating the correction factor for hyperglycemia. Am J Med. 1999;106(4):399–403. Hoorn EJ, Zietse R. Hyponatremia revisited: translating physiology to prac- tice. Nephron Physiol. 2008;108(3):p46–59. List AF, Hainsworth JD, Davis BW, Hande KR, Greco FA, Johnson DH. The syndrome of inappropriate secretion of antidiuretic hormone (SIADH) in small-cell lung cancer. J Clin Oncol. 1986;4(8):1191–8. Sahay M, Sahay R. Hyponatremia: a practical approach. Indian J Endocrinol Metab. 2014;18(6):760–71. Sanghvi SR, Kellerman PS, Nanovic L. Beer potomania: an unusual cause of hyponatremia at high risk of complications from rapid correction. Am J Kidney Dis. 2007;50(4):673–80. Sterns RH. Formulas for fixing serum sodium: curb your enthusiasm. Clin Kidney J. 2016;9(4):527–9. Sterns RH, Cappuccio JD, Silver SM, Cohen EP. Neurologic sequelae after treatment of severe hyponatremia: a multicenter perspective. J Am Soc Nephrol. 1994;4(8):1522–30. Sterns RH, Hix JK, Silver S. Treatment of hyponatremia. Curr Opin Nephrol Hypertens. 2010;19(5):493–8. Szatalowicz VL, Miller PD, Lacher JW, Gordon JA, Schrier RW. Comparative effect of diuretics on renal water excretion in hyponatraemic oedematous disorders. Clin Sci (Lond, England: 1979). 1982;62(2):235–8. Verbalis JG, Adler S, Schrier RW, Berl T, Zhao Q, Czerwiec FS. Efficacy and safety of oral tolvaptan therapy in patients with the syndrome of inappro- priate antidiuretic hormone secretion. Eur J Endocrinol. 2011;164(5): 725–32. Weisberg LS. Pseudohyponatremia: a reappraisal. Am J Med. 1989;86(3): 315–8. Inpatient Management 16 of Hyperkalemia Erika R. Drury and Bradley M. Denker Contents Obtain Whole Blood Potassium in the Setting of Hemolysis, Thrombocytosis, or Marked Leukocytosis 190 Evaluate Symptoms and EKG to Exclude Life-T hreatening Hyperkalemia 191 Order Calcium Gluconate (1–2 g IV) to Treat Severe Hyperkalemia 191 Order Insulin 10 Units Plus Glucose 40–60 g as IV Bolus or Albuterol Nebulizer 10–20 mg to Shift Potassium Intracellularly 192 Assess History, Physical Exam, and Other Laboratory Data to Determine the Source of Potassium Load and Defect in Renal Excretion 192 Order Intravenous Loop Diuretic (e.g., Furosemide 20–40 mg) in Patients with Normal or Mild Renal Impairment 195 E. R. Drury Division of Nephrology, Department of Medicine, University of Rochester School of Medicine, Rochester, NY, USA e-mail: erika_drury@urmc.rochester.edu B. M. Denker (*) Beth Israel Deaconess Medical Center, Department of Medicine, Nephrology Division and Harvard Medical School, Boston, MA, USA e-mail: bdenker@bidmc.harvard.edu © Springer Nature Switzerland AG 2020 189 R. K. Garg et al. (eds.), Handbook of Inpatient Endocrinology, https://doi.org/10.1007/978-3-030-38976-5_16 190 E. R. Drury and B. M. Denker Order a Low Potassium Diet 195 Discontinue Any Medications That Impair Renal Potassium Excretion 195 Order Oral Sodium Polystyrene Sulfonate (Kayexalate) 15–30 g One to Four Times per Day in Non-postoperative Patients 196 Obtain Nephrology Consultation for Hemodialysis in the Setting of ESRD, Advanced Renal Failure, or Patients with Rising Potassium Levels Not Responsive to Medical Therapy 196 Fludrocortisone May Be Used in Patients With Aldosterone Deficiency 197 Suggested Reading 197 Obtain Whole Blood Potassium in the Setting of Hemolysis, Thrombocytosis, or Marked Leukocytosis Pseudohyperkalemia refers to an elevation in potassium that occurs after the blood specimen has been drawn and does not represent true hyperkalemia. This should be suspected when there are no electrocardiographic changes such as peaked T waves a ssociated with elevated potassium levels (>6 mEq/L), when the laboratory measurements of potassium levels are widely varying, or when there is no apparent cause for the hyperkalemia. The most common cause of pseudohyperkalemia is hemolysis from the trauma of venipuncture, which leads to the release of potassium from hemolyzed cells. If the blood specimen has been hemolyzed, repeat the measurement. Patients with thrombocytosis (platelet count >500,000/mm3) may exhibit pseudohyperkalemia. A small amount of potassium moves out of cells when blood clots, but more potassium may be released in the presence of thrombocytosis. Ask for a measurement of the plasma (whole blood) potassium (from a heparinized blood sample) which will reveal the true in vivo potassium levels in these patients. Patients with marked leukocytosis (white cell count >100/mm3) may also exhibit hyperkalemia. Leukemic lymphocytes are fragile and may release potassium when exposed to heparin or shaken. To exclude these 16 Inpatient Management of Hyperkalemia 191 scenarios, whole blood potassium from a sample in a blood gas tube should be taken, or samples should be walked to the lab, respectively. If pseudohyperkalemia can be excluded, then further workup and management is indicated. Evaluate Symptoms and EKG to Exclude Life- Threatening Hyperkalemia The most dangerous effects of hyperkalemia are cardiac arrhyth- mias and ascending muscle weakness and paralysis. These usu- ally occur when the plasma potassium concentration is >7 mEq/L but can occur at lower concentrations if the hyperkalemia is acute or in the presence of hypocalcemia or acidemia. When plasma potassium levels are >6 mEq/L, order an electrocardiogram and place the patient on continuous telemetry monitoring. ECG changes associated with hyperkalemia begin with peaking of the T waves and shortening of the QT interval followed by widening of the QRS complex and the P wave and finally the appearance of the sine wave pattern followed by ventricular fibrillation or asys- tole. Rapid increases in serum potassium cause more pronounced cardiac toxicity (e.g., in acute renal failure). Ascending muscle weakness and flaccid paralysis usually occur only when the plasma potassium concentration is > 8 mEq/L but can occur at lower levels in patients with the genetic disorder hyperkalemic periodic paralysis. Order Calcium Gluconate (1–2 g IV) to Treat Severe Hyperkalemia Patients with a serum potassium concentration > 6.5 mEq/L and those with ECG changes or with muscle weakness require imme- diate treatment with measures aimed at reversing the effects of hyperkalemia followed by therapies to remove potassium from the body. Rapidly acting therapies include calcium, insulin, and β-agonists. Calcium does not lower serum potassium levels but lowers the myocyte membrane threshold potential and protects 192 E. R. Drury and B. M. Denker against the toxic effects of hyperkalemia. Give 1–2 g IV calcium gluconate (90–180 mg of elemental calcium) over 2–3 min. This acts within minutes but lasts only about 30–60 min, so repeated doses may be needed while potassium-l owering therapy is being administered. Order Insulin 10 Units Plus Glucose 40–60 g as IV Bolus or Albuterol Nebulizer 10–20 mg to Shift Potassium Intracellularly Insulin administration lowers the serum potassium concentration by driving it intracellularly. The usual regimen is 10 units of regu- lar insulin given with 25 g of glucose (i.e., one “amp” of D50). This will lower the potassium concentration by 1–2 mEq/L within 60 min and lasts up to 4 h. If needed, insulin and dextrose can be repeated every 2–4 h. Nebulized beta agonists (i.e., albuterol) also lead to redistribution of potassium intracellularly. Up to 10–20 mg of nebulized albuterol is needed to lower the serum potassium level, which is in contrast to the 2.5 mg albuterol dose that is used for bronchospasm. If albuterol is used, give at least five standard dose nebulizers. This acts within 30 min and lasts 2–4 h. While these rapidly acting therapies are given, measures aimed at removal of potassium from the body should be instituted. In patients with severely impaired renal function such as advanced chronic kidney disease or acute renal failure, dialysis is often needed. In patients with normal or only mildly impaired renal function, other methods of removing potassium may be employed which include loop diuretics and gastrointestinal cation exchangers. Assess History, Physical Exam, and Other Laboratory Data to Determine the Source of Potassium Load and Defect in Renal Excretion Once life-threatening hyperkalemia has been excluded or is being managed, a thoughtful approach to determining the etiology of the hyperkalemia will help guide the best treatment. Take a thor- 16 Inpatient Management of Hyperkalemia 193 ough history and review the patient’s laboratory values and medi- cations. In most cases, the etiology of the hyperkalemia is multifactorial, but an impairment in renal excretion is required for the development of hyperkalemia. First, assess for increased potassium release from cells. There are many factors that can contribute to hyperkalemia as a result of increased release from cells. In patients with metabolic acidosis, buffering of excess hydrogen ions leads to potassium shift out of the cell. Check an arterial or venous blood gas and measure the serum bicarbonate concentration. States of hyperglycemia and insulin deficiency lead to hyperkalemia, such as occurs in diabetic ketoacidosis (although often these patients are total body potas- sium depleted and will develop hypokalemia after treatment). Increased tissue catabolism as occurs with tumor lysis can lead to massive release of potassium into the extracellular space. Obtain laboratory tests that can suggest tumor lysis including uric acid, phosphorus, lactate dehydrogenase (LDH), and calcium. Evaluate for a history of fall or traumatic injury which leads to muscle cell necrosis and the development of rhabdomyolysis and elevated creatine phosphokinase (CPK) levels. Digitalis overdose can cause hyperkalemia as a result of inhibition of the Na-K-ATPase pump. For some of these conditions, measures aimed at correcting the abnormalities can help reduce the hyperkalemia. If a meta- bolic acidosis is present, treat the underlying cause (lactic acido- sis, diabetic ketoacidosis), and sodium bicarbonate may be used if the serum pH is <7.1. If hyperglycemia is present, correct this with appropriate insulin therapy. Second, assess for decreased urinary excretion of potassium. Reduced urinary excretion of potassium is the predominant driver for sustained hyperkalemia. Potassium excretion requires an adequate number of nephrons (GFR) and urine flow with dis- tal sodium delivery to promote urinary potassium excretion. Finally, aldosterone is required for potassium excretion. Estimation of the potassium concentration in the tubular fluid of the collecting duct, which reflects tubular potassium s ecretion, may be possible by calculating the trans-tubular potassium gra- dient (TTKG) ([urine potassium (mEq/L) × serum osm (mOsm/ kg)]/[serum potassium (mEq/L) × urine osm (mOsm/kg)]). 194 E. R. Drury and B. M. Denker Values of <7 may suggest inappropriate renal response to hyper- kalemia and aldosterone deficiency. However, many argue that the TTKG is not valid because the underlying assumption that osmoles are not reabsorbed in the medullary collecting duct is incorrect. Therefore, calculation of the TTKG should be used with caution and in combination with the entirety of a patient’s clinical picture. There are three major causes of reduced urinary potassium excretion: renal failure, effective arterial volume depletion, and hypoaldosteronism. To assess for acute or chronic renal failure, check for elevations in the serum urea nitrogen and creatinine. Hyperkalemia can occur in states of effective arterial volume depletion as potassium excretion requires deliv- ery of water and sodium to the distal tubule, which is impaired in these states. Look for physical examination findings of true volume depletion such as orthostatic vital sign changes, hypo- tension, tachycardia, and diminished skin turgor. Patients with hypervolemia secondary to heart failure or cirrhosis often exhibit effective arterial volume depletion, so exam findings of pulmonary edema and peripheral edema are helpful. In both of these states, urine sodium levels will be <20 mEq/L, unless a loop diuretic has been recently used. Finally, hypoaldosteron- ism is the result of either reduced aldosterone production or aldosterone resistance. Reduced aldosterone secretion can be caused by drugs such as angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers (ARB), nonsteroidal anti-inflammatory drugs (NSAID(s)), calcineurin inhibitors, and heparin. Aldosterone antagonists such as spironolactone and eplerenone directly inhibit potassium excretion, while potassium-sparing diuretics such as amiloride and triamterene block the aldosterone-responsive epithelial sodium channel that is necessary for creating the lumen-negative potential necessary for potassium secretion. If these drugs are not present and a diagnosis of hypoaldosteronism is suspected, check morning plasma renin activity and aldosterone concentrations. Hyporeninemic hypoaldosteronism is characterized by low renin activity, whereas in primary adrenal insufficiency and in enzyme deficiencies, the plasma renin activity is elevated. Hyporeninemic hypoaldosteronism is also known as type IV 16 Inpatient Management of Hyperkalemia 195 renal tubular acidosis and can be seen in patients with diabetes and tubular disorders. Order Intravenous Loop Diuretic (e.g., Furosemide 20–40 mg) in Patients with Normal or Mild Renal Impairment Diuretics are used to increase potassium excretion in states of volume |
expansion such as heart failure. Furosemide can be started at a dose of 40–80 mg IV twice a day, but higher doses may be needed in renal impairment. For patients who are not hypervolemic, loop diuretics can be given with an infusion of IV saline to maintain euvolemia and urine flow with distal sodium delivery. Oral loop diuretics can be effective at lowering potas- sium levels in chronic renal failure. Order a Low Potassium Diet In patients with normal renal function, increased intake of potas- sium is generally well tolerated and is not a cause of hyperkalemia unless potassium is ingested in large quantities (>160 mEq) and is given as an IV bolus or if excretion of potassium is impaired. Still, it is important to take a dietary history to assess for high p otassium intake that may be contributing to the persistence of hyperkale- mia. Dietary sources of high potassium include tomatoes, white potatoes, sweet potatoes, bananas, oranges/orange juice, raisins, and salt substitutes. Restrict potassium in the diet to no more than 2 g per day. Discontinue Any Medications That Impair Renal Potassium Excretion Regardless of the urgency of potassium-lowering therapy, any medications that can cause hyperkalemia should be stopped or at least held temporarily. Angiotensin-converting enzyme inhibitors, 196 E. R. Drury and B. M. Denker angiotensin II receptor blockers, and aldosterone receptor blockers should be stopped. Other medications that can cause hyperkalemia include potassium-sparing diuretics, heparin, NSAIDs, calcineurin inhibitors, sulfamethoxazole/trimethoprim (Bactrim), and beta receptor antagonists. Depending on the severity and etiology of hyperkalemia, consider holding these medications as well. Order Oral Sodium Polystyrene Sulfonate (Kayexalate) 15–30 g One to Four Times per Day in Non-postoperative Patients Gastrointestinal cation exchangers remove potassium via exchange with other cations. Sodium polystyrene sulfonate removes potassium via exchange with sodium. It can be given as a single 15–30 g dose and repeated up to four times per day. The onset of action is at least 2 h and the maximum effect may take 6 or more hours. There is a small risk of intestinal necrosis with sodium polystyrene sulfonate, particularly in patients with under- lying bowel disease and a bowel obstruction or who are postop- erative, and therefore the safety of sodium polystyrene sulfonate has been widely debated. Many advocate for its use only with life-threatening hyperkalemia when dialysis is not readily avail- able, while others use it routinely for control of hyperkalemia in CKD in the outpatient setting. With the development of newer cation exchangers including patiromer and zirconium cyclosili- cate, sodium polystyrene sulfonate use is decreasing. Obtain Nephrology Consultation for Hemodialysis in the Setting of ESRD, Advanced Renal Failure, or Patients with Rising Potassium Levels Not Responsive to Medical Therapy End-stage renal disease patients presenting with hyperkalemia usually need urgent hemodialysis. These patients often tolerate higher serum levels of potassium, but renal consultation should be 16 Inpatient Management of Hyperkalemia 197 ordered immediately to assist with the timing of dialysis. Gastrointestinal cation exchangers are often recommended if hemodialysis cannot be performed immediately. Patients with oli- guric or anuric acute renal failure will also need hemodialysis as loop diuretics are often not effective at promoting urinary potas- sium excretion. Temporizing measures described previously should be given while awaiting recommendations. Fludrocortisone May Be Used in Patients With Aldosterone Deficiency With demonstrated deficient aldosterone production, fludrocorti- sone can be used to correct the hyperkalemia. Start with an oral dose of 0.1 mg per day. Monitor for sodium retention, edema, and hypertension. Doses of up to 0.4 mg per day may be needed, par- ticularly in cases of hyporeninemic hypoaldosteronism. Suggested Reading Kovesdy CP. Management of hyperkalemia: an update for the internist. Am J Med. 2015;128(12):1281–7. Rose DB, Post DW. Hyperkalemia. In: Wonsciewicz M, McCullough K, Davis K, editors. Clinical physiology of acid-base and electrolyte disor- ders. 5th ed. New York: Mc-Graw Hill; 2001. Sterns RH, Grieff M, Bernstein PL. Treatment of hyperkalemia: something old, something new. Kidney Int. 2016;89(3):546–54. Weir MR, Rolfe M. Potassium homeostasis and renin-angiotensin-a ldosterone system inhibitors. Treatment of hyperkalemia: something old, something new. Clin J Am Soc Nephrol. 2010;5(3):531–48. Suspected Adrenocortical 17 Deficiency Anand Vaidya Contents Physiological Considerations 200 What Is a Normal Cortisol Level? 202 Primary and Secondary Adrenal Insufficiencies 203 Primary Adrenal Insufficiency 203 Secondary Adrenal Insufficiency 203 Clinical Presentation and Diagnosis 203 Primary Adrenal Insufficiency 203 Secondary Adrenal Insufficiency 205 Adrenal Insufficiency in Critically Ill Patients 206 Etiology 207 Treatment 208 Primary Adrenal Insufficiency 208 Secondary Adrenal Insufficiency 210 Stress Dosing 213 Suggested Reading 214 A. Vaidya (*) Harvard Medical School, Center for Adrenal Disorders, Division of Endocrinology, Diabetes, and Hypertension, Brigham and Women’s Hospital, Boston, MA, USA e-mail: anandvaidya@bwh.harvard.edu © Springer Nature Switzerland AG 2020 199 R. K. Garg et al. (eds.), Handbook of Inpatient Endocrinology, https://doi.org/10.1007/978-3-030-38976-5_17 200 A. Vaidya Physiological Considerations The adrenal cortex synthesizes glucocorticoids and mineralocor- ticoids that physiologically regulate the acute response to stress, glycemic homeostasis, hemodynamic homeostasis, potassium and acid balance, immune function, organogenesis, parturition, and many other functions. Adult adrenal glands are approximately 4 g in weight and usu- ally 4 cm long and 2 cm wide and 1 cm thick lying on top of the superior pole of each kidney. On cross-sectional imaging (such as CT or MRI), they appear as thin and wispy structures that resem- ble a Mercedes-Benz symbol. The adrenal gland is divided into the cortex and the medulla: Cortex stems from mesenchymal tissue and synthesizes ste- roids. There are three histologic layers: zona glomerulosa (ZG) produces aldosterone, zona fasciculata (ZF) produces cortisol, and zona reticularis (ZR) produces DHEA and androstenedione. Medulla, which is the core of the adrenal, arises from neural crest cells and functions primarily to synthesize catecholamines. The regulation of cortisol and androgen synthesis is entirely dependent on ACTH. Aldosterone synthesis is also stimulated by ACTH; however, the synthesis of aldosterone is also potently stimulated by angiotensin II (thus activation of the renin- angiotensin system stimulates adrenal aldosterone) and by high extracellular potassium. Therefore, in contrast to cortisol syn- thesis, aldosterone synthesis is not dependent on ACTH. Adrenal androgens play a minor role in adult human physiology but are important for adrenarche, including the development of axillary and pubic hair. Cortisol is a glucocorticoid that binds to and acti- vates the glucocorticoid receptor (GR), but it is also a mineralo- corticoid that can potently activate the mineralocorticoid receptor (MR). Cortisol is the main glucocorticoid in human physiology and therefore is the dominant ligand for the GR. Activation of the GR raises blood glucose, increases blood pressure, suppresses immune activity/inflammation, increases 17 Suspected Adrenocortical Deficiency 201 appetite, and depresses mood. These physiologic actions explain the pathophysiologic manifestations of diseases with cortisol deficiency (adrenal insufficiency) and cortisol excess (Cushing syndrome). Aldosterone is a pure mineralocorticoid and only activates the MR, principally in the distal nephron but also in other tis- sues such as the colon, heart, and vasculature. Activation of the renal MR increases renal sodium reabsorption, which facilitates the retention of water and results in intravascular volume expan- sion. Activation of the renal MR also increases renal potassium and hydrogen ion excretion. Therefore, another key role of aldosterone is to ensure normal potassium homeostasis and acid-base status by regulating urinary potassium and proton excretion. Notably, cortisol is also a potent mineralocorticoid and can activate the MR. Although cortisol circulates in the blood in 100- to 1000-fold higher concentrations than aldoste- rone, MR over-a ctivation (such as in primary aldosteronism) resulting in sodium retention, volume expansion, high blood pressure, and hypokalemia is prevented by 11β-hydroxysteroid dehydrogenase type 2 (11βHSD2), which is co-expressed with the MR in the kidney, and functions to convert cortisol to the inactive cortisone. In this manner, 11βHSD2 inactivates the majority of cortisol before it can bind to and activate the renal MR. The classical control of the adrenal cortex involves commu- nications between the hypothalamus, pituitary, and adrenal. The hypothalamus secretes corticotropin-releasing hormone (CRH), which stimulates the secretion of ACTH from the corti- cotrophs of the anterior pituitary. Cortisol binds to peripheral GR but also the centrally expressed GR in the hypothalamus and pituitary. Therefore, cortisol negatively regulates CRH and ACTH. ACTH also stimulates aldosterone secretion from the adrenal cortex; however, the dominant secretagogues of aldosterone are angiotensin II and potassium. Therefore, the predominant axis that regulates aldosterone is the renin-angiotensin system. 202 A. Vaidya Aldosterone acts on the MR expressed in the distal nephron to increase sodium retention and thereby expand the intravascular volume to counter the initial insult of renal hypoperfusion. This closes the renin-angiotensin-aldosterone feedback loop. High extracellular potassium also stimulates adrenal aldosterone pro- duction, and in turn activation of the MR by aldosterone increases urinary potassium excretion in the distal nephron to close this feedback loop. One of the major roles of cortisol is to help the body defend against stress. Stress can be defined as any physical or emotional stress or any condition that is perceived to be a threat or fear. In this regard, the stress response is designed to permit physiologic changes that defend against stress. The perception of stress stim- ulates CRH via central nervous system inputs. Other stressors such as hypoglycemia, hypotension, pain, and fever all stimulate the hypothalamic release of CRH to activate the axis and result in increases in cortisol proportional to the degree of stress to counter these stimuli. Vasopressin (also called antidiuretic hor- mone [ADH]), can stimulate pituitary ACTH secretion, as can cytokines that are increased during infections or inflammatory conditions. Another major regulator of the hypothalamic-pituitary-adrenal axis is light, thus creating a circadian rhythm. From a diagnostic standpoint, this diurnal secretion of cortisol is one of the main reasons why the diagnosis of adrenal insufficiency can be challenging. What Is a Normal Cortisol Level? A robust and elevated peak morning cortisol suggests a normal functioning hypothalamic-pituitary-adrenal axis; however, deter- mining when that peak arises and should be measured is often the challenge, particularly in the inpatient setting. Specific thresholds will be discussed below in Diagnosis. 17 Suspected Adrenocortical Deficiency 203 Primary and Secondary Adrenal Insufficiencies The term adrenal insufficiency refers to an absolute or relative deficiency of adrenal cortical hormones (cortisol and/or aldoste- rone) with respect to the current needs of the body. Primary Adrenal Insufficiency Primary adrenal insufficiency (Addison’s disease) refers to the destruction or inhibition of the entire adrenal cortex, resulting in an inability to synthesize and secrete cortisol and aldosterone (as well as androgens). The main signs and symptoms of this condi- tion are due to the lack of cortisol and aldosterone. In the absence of negative feedback from cortisol, the hypothalamus and pitu- itary augment secretion of CRH, POMC, and as a result ACTH and melanocyte-stimulating hormone (MSH). Secondary Adrenal Insufficiency Secondary adrenal insufficiency refers to the destruction or inhi- bition of the corticotroph cells in the anterior pituitary. Secretion of ACTH will be relatively insufficient or completely deficient. In the absence of ACTH, the adrenal cortex is not stimulated, and adrenal steroidogenesis is inhibited. This is particularly evident for cortisol and androgens. Since aldosterone synthesis and secre- tion can continue to be stimulated by angiotensin II and potassium, secondary adrenal insufficiency is mainly a syndrome of cortisol insufficiency; aldosterone regulation continues unabated. Clinical Presentation and Diagnosis Primary Adrenal Insufficiency Primary adrenal insufficiency typically presents with marked or critical illness. General malaise and feelings of being unwell, 204 A. Vaidya gastrointestinal symptoms (nausea, vomiting, diarrhea, abdomi- nal pain), and, in severe circumstances, hypoglycemia and hypo- tension are hallmarks of the illness and may be ongoing and progressively worsening for months to years before the diagnosis is made. Aldosterone insufficiency makes these patients espe- cially vulnerable. In the absence of aldosterone, renal sodium reabsorption is not maximal, resulting in renal sodium wasting and progressive intravascular volume depletion. This can mani- fest as symptoms of lightheadedness and orthostasis (dizziness and lightheadedness upon standing from a seated position) and frankly low blood pressure (hypotension and circulatory col- lapse) and salt cravings. Diffuse hyperpigmentation of the skin, particularly marked surrounding scar tissue and on mucosal membranes (such as the buccal mucosa and vaginal mucosa), is attributed to the high circulating levels of MSH- and ACTH- stimulating melanocytes. Primary adrenal insufficiency can be diagnosed by simultaneously evaluating a cortisol and ACTH – a relatively low or frankly low cortisol levels and concomitantly marked elevations in ACTH. |
Morning cortisol levels less than 5 mcg/dL confirm the diagnosis of adrenal insufficiency, along with a concomitant ACTH level that is at least twofold greater than the upper range of normal (but usually several hundred or even greater than a thousand, pg/mL). Further, the deficiency of aldosterone may result in hyponatremia, hyperkalemia, and a markedly elevated renin. Measuring a renin and aldosterone is recommended to assess the degree of mineralocorticoid defi- ciency in primary adrenal insufficiency. Patients with primary adrenal insufficiency will exhibit low serum aldosterone levels, despite low blood pressure and high potassium balance, and markedly elevated plasma renin activity. Performing a cosyntro- pin stimulation (measuring a morning cortisol level, then inject- ing 250 mcg of synthetic ACTH-like p eptide, followed by repeat cortisol measure at 30 and 60 min) can further confirm the diag- nosis. Because the pathophysiology involves destruction of the adrenal cortex, patients with primary adrenal insufficiency dis- ease exhibit markedly diminished cortisol stimulation when cosyntropin is injected. A failure to achieve a peak stimulated 17 Suspected Adrenocortical Deficiency 205 cortisol following cosyntropin of > 18 mcg/dL indicates adrenal insufficiency. Secondary Adrenal Insufficiency Secondary adrenal insufficiency can present with a wide variety of signs and symptoms. This is in part because aldosterone regu- lation is intact and therefore hemodynamic homeostasis may be intact. The clinical syndrome experienced by these patients reflects the degree of stress (physical or emotional) they are under and the disparity between how much cortisol they are able to produce and how much cortisol is needed at any given time. For example, a healthy patient with secondary adrenal insuffi- ciency and a relatively low cortisol may experience no symptoms or perhaps only mild weakness and fatigue. However, as the degree of stress the patient experiences increases (e.g., the devel- opment of a febrile illness like influenza or sustaining severe trauma and pain), the gap between the patient’s need for cortisol and ability to produce cortisol increases, and the clinical mani- festations become more severe. Ultimately, in the setting of severe stress or critical illness, these patients may develop a clin- ical syndrome that includes intravascular volume depletion and hypotension, resembling that of primary adrenal insufficiency. Secondary adrenal insufficiency is diagnosed by confirming an inappropriately low morning cortisol level (ideally < 5 mcg/dL) in combination with an inappropriately low ACTH. A suboptimal cosyntropin stimulation test (peak cortisol < 18 mcg/dL) can pro- vide further confirmation of the diagnosis of adrenal insuffi- ciency and insight into the chronicity of the problem. A robust and normal peak cortisol following cosyntropin indicates that the lack of ACTH is acute or subacute (hours, days, or a few weeks). A suboptimal response to cosyntropin suggests that the defi- ciency of ACTH is chronic (weeks to months); since ACTH is trophic to the adrenal cortex, prolonged deficiency results in atro- phy of the zona fasciculata and progressively diminished responses to cosyntropin. 206 A. Vaidya Adrenal Insufficiency in Critically Ill Patients Adrenal insufficiency in critically ill patients is often more chal- lenging to diagnose than in noncritically ill patients because critically ill patients (1) may not have normal circadian rhythms, (2) may have decreased metabolism and clearance of cortisol, and (3) may have reduced circulating binding globulins, thus lowering total cortisol but not necessarily free and bioavailable cortisol. An important response to critical illness is a rise in ACTH. Whereas some hypothalamic and pituitary hormones may exhibit a physiological suppression during critical illness, critical illness should result in a robust rise in ACTH and increased adrenal cortical stimulation. Therefore, theoretically, patients with critical illness should have appropriately elevated cortisol levels, in part because ACTH is elevated and also because cortisol metabolism is decreased. In patients who have markedly reduced concentrations of albumin, cortisol-binding globulin may also be decreased and, therefore, total cortisol levels may decline and correlation with presumed free cortisol levels may become more challenging. Measuring cortisol-binding globulin or free cortisol levels may be useful. However, because these assays are not routinely performed and may take days to weeks to return, they are not commonly used in the practical diagnosis and management of adrenal insufficiency. Rather, it is generally suggested that a critically ill patient with a relatively normal albumin of >2.5 g/dL and cortisol of <15 mcg/dL is indicative of adrenal insufficiency that may require glucocorticoid replace- ment therapy. In contrast, in a critically ill patient with more marked hypoalbuminemia (albumin <2.5 g/dL), a random corti- sol of <10 mcg/dL may indicate adrenal insufficiency. When a critically ill patient is hypotensive due to septic shock and resis- tant to vasopressor therapy, empiric treatment with glucocorti- coids without diagnostic testing may be considered as an emergency measure. 17 Suspected Adrenocortical Deficiency 207 Etiology Primary adrenal insufficiency, particularly in developed parts of the world, is most commonly autoimmune adrenalitis. It may occur in isolation, or as a part of a larger autoimmune polyglandu- lar syndrome. Other causes of primary adrenal insufficiency include bilateral infiltrative infections (such as tuberculosis and fungi), bilateral adrenal hemorrhage, infiltrative malignancies, bilateral adrenalectomy, congenital adrenal hyperplasia, adreno- leukodystrophy, and rarer genetic syndromes. Establishing the cause of primary adrenal insufficiency is important. A positive 21-hydroxylase antibody can provide reassurance for autoim- mune adrenalitis, whereas when the titer is negative, evaluation for other causes using serologic testing and/or imaging should be considered. The evaluation of other non-autoimmune causes should be considered on a case-b y- case basis depending on the practice location and pretest probability. Imaging of the adrenals can help identify hemorrhage, infiltrative infections, and malig- nancy. Suspicion for adrenoleukodystrophy can be confirmed with imaging and assessment of very long chain fatty acids. Evaluation for congenital adrenal hyper- or hypoplasia is best per- formed by measuring intermediate adrenal steroids. Certain med- ications can inhibit adrenal steroidogenesis transiently and result in a functional primary adrenal insufficiency: antifungal medica- tions, etomidate, and, rarely, heparin. Secondary adrenal insufficiency can be the result of any con- dition that interrupts or damages the hypothalamus and pitu- itary. These include principally benign pituitary or parasellar tumors and rarely primary or metastatic brain malignancy, infec- tion, hemorrhage, infiltrative diseases, and radiation that involved the hypothalamus or pituitary. The most common cause of sec- ondary adrenal insufficiency, however, is iatrogenic secondary adrenal insufficiency due to the frequent use of exogenous glucocorticoids (most often oral or intravenous but in some instances inhaled and topical as well). Opioid medications are also frequently used and in some instances can cause a transient suppression of ACTH. 208 A. Vaidya Treatment Primary Adrenal Insufficiency The treatment of primary adrenal insufficiency is focused on replacing the missing vital adrenal steroids: cortisol and aldoste- rone. Patients are typically treated with a glucocorticoid (such as hydrocortisone or prednisone) and in addition with a mineralocor- ticoid (such as fludrocortisone) to replace their deficiencies (Table 17.1). The choice of glucocorticoid can vary, but the most preferred option in adults is hydrocortisone (15–25 mg daily) in two divided doses, often the larger dose first thing in the morning and the smaller dose in the early afternoon. Hydrocortisone peaks within 1–3 h and nadirs within 5–7 h, thus providing an opportu- nity to give a physiologic regimen of glucocorticoid. A common glucocorticoid regimen is hydrocortisone 15–20 mg upon awak- ening and 10 mg between 12 and 2 pm. Some patients require a third smaller dose in the early evening. Prednisolone (3–5 mg daily) and prednisone (5–7.5 mg daily) are alternatives that can be given once or twice daily but have longer half-lives and therefore less physiologic profiles. Dexamethasone is not ideal since it has a very long half-life and the greatest risk for inducing Cushingoid effects. Efficacy of glucocorticoid dosing is determined by patient well-being, energy level, normal blood pressure, and electrolytes. Toxicity or signs of excessive glucocorticoid dosing are deter- mined by evidence of weight gain and other Cushingoid signs. All patients with mineralocorticoid deficiency should be treated with fludrocortisone, typically 0.05–0.15 mg once daily. The efficacy of fludrocortisone dosing can be monitored by observing normal blood pressure (without postural hypotension), normal sodium and potassium balance, and the lowering of the previously ele- vated renin levels. Patients should be instructed on how to remain well hydrated and consume sufficient dietary sodium, especially on warmer days when insensible loses of water and salt can be greater. 17 Suspected Adrenocortical Deficiency 209 Table 17.1 Treatment of primary adrenal insufficiency Minor-moderate Moderate-severe Maintenance illness illness or surgery Formulation/ Glucocorticoid: Double (fever If emesis and dose/action hydrocortisone >38 °C) or triple inability to take 15–25 mg in two (fever >39 °C) oral medications divided doses; glucocorticoid or fluids: alternatively dose for intramuscular or prednisolone 3–5 mg 2–3 days, intravenous daily or prednisone increase hydrocortisone 5–7.5 mg daily hydration with 50–100 mg and Mineralocorticoid: water and intravenous fluids fludrocortisone electrolyte-rich If major surgery 0.05–0.15 mg in a fluids with general single dose anesthesia, intensive care hospitalization, or delivery: 50–100 mg of intravenous hydrocortisone every 6–8 h and intravenous fluids If adrenal crisis: aggressive hydration with isotonic fluids, hydrocortisone 100 mg intravenous every 4–6 h Typical Hydrocortisone Double Intravenous example 15–20 mg in the hydrocortisone hydrocortisone morning and dose for 50–100 mg 5–10 mg in the early 2–3 days until Intramuscular afternoon and mild febrile hydrocortisone fludrocortisone illness abates 100 mg 0.10 mg in the morning (continued) 210 A. Vaidya Table 17.1 (continued) Minor-moderate Moderate-severe Maintenance illness illness or surgery Comment The dose of If symptoms do In addition to glucocorticoid and not abate or higher mineralocorticoid worsen, glucocorticoid can vary depending in-person dosing, hydration on the size of the evaluation with isotonic patient, daily activity should be fluids is a critical and workload conducted management (physical or other), element. For and other symptoms. patients unable to During exercise, maintain oral additional or higher hydration, doses may be intravenous required. A general hydration with rule of thumb to isotonic fluids minimize should be initiated supraphysiologic glucocorticoid effects is to establish the lowest dose of glucocorticoid that enables a good quality of life Secondary Adrenal Insufficiency The treatment of secondary adrenal insufficiency is focused on replacing glucocorticoids. Patients are typically treated with hydrocortisone or prednisone (Table 17.2). If the cause of second- ary adrenal insufficiency was iatrogenic glucocorticoid adminis- tration, then the goal of therapy should be to gradually taper the glucocorticoid down in hopes that the endogenous hypothalamic- pituitary- adrenal axis will revive and resume normal function. The precise tapering schedule can vary and should be created on a case-by-case basis and customized for the specific patient. The longer the exposure to supraphysiologic glucocorticoids, the more profound the inhibition of endogenous ACTH production and the longer the time to recovery. Symptoms of fatigue, orthostasis, and/or depression may be signs that they are experiencing relative 17 Suspected Adrenocortical Deficiency 211 Table 17.2 Treatment of secondary adrenal insufficiencies Minor- moderate Moderate- severe illness or Maintenance illness surgery Formulation/ Glucocorticoid: Double (fever If emesis and inability to take dose/action hydrocortisone 10–25 mg in two divided doses; >38 °C) or triple oral medications or fluids: alternatively prednisolone 1–5 mg daily or prednisone (fever >39 °C) intramuscular or intravenous 3–7.5 mg daily glucocorticoid dose hydrocortisone 50–100 mg and Mineralocorticoid: none for 2–3 days, intravenous fluids increase hydration If major surgery with general with water and anesthesia, intensive care electrolyte-rich fluids hospitalization, or delivery: 50–100 mg of intravenous hydrocortisone every 6–8 h and intravenous fluids If adrenal crisis: aggressive hydration with isotonic fluids, hydrocortisone 100 mg intravenous every 4–6 h Typical example Hydrocortisone 10–20 mg in the morning and Double Intravenous hydrocortisone 5–10 mg in the early afternoon or prednisone hydrocortisone or 50–100 mg 3–7.5 mg in the morning prednisone dose for Intramuscular hydrocortisone 2–3 days until mild 100 mg febrile illness abates (continued) 212 A. Vaidya Table 17.2 (continued) Minor- moderate Moderate- severe illness or Maintenance illness surgery Comment The dose of glucocorticoid can vary depending on the If symptoms do not In addition to higher size of the patient, daily activity and workload abate or worsen, glucocorticoid dosing, hydration (physical or other), and other symptoms. During in-person evaluation with isotonic fluids is a critical exercise, additional or higher doses may be required. should be conducted management element. For A general rule of thumb to minimize supraphysiologic patients unable to maintain oral glucocorticoid effects is to establish the lowest dose hydration, intravenous hydration of glucocorticoid that |
enables a good quality of life. with isotonic fluids should be If the cause of secondary adrenal insufficiency was initiated iatrogenic glucocorticoid administration, then the goal of therapy should be to gradually taper the glucocorticoid doses to permit normalization of the hypothalamic- pituitary- adrenal axis. The precise tapering schedule can vary and should be created on a case-by-case basis and customized for the specific patient. The longer the exposure to supraphysiologic glucocorticoids, the more profound the inhibition of endogenous ACTH production and the longer the time to recovery 17 Suspected Adrenocortical Deficiency 213 adrenal insufficiency and should prompt consideration to slow the pace of the taper. Measuring a morning cortisol and ACTH, 24 h after the last dose of glucocorticoid, can provide insight into the status of the hypothalamic-pituitary-adrenal axis. Low levels of each suggest a profound suppression of the axis. A rise in ACTH with a low cortisol suggests an awakening of the pituitary cortico- trophs and stimulation of the zona fasciculata by supraphysiologic ACTH, following which a gradual rise in cortisol should follow- ing the subsequent weeks to months. A morning cortisol greater than 10 mcg/dL, but ideally >15–18 mcg/dL, indicates restoration of normal endogenous HPA axis function and a concomitant com- pletion of the glucocorticoid taper. In addition, serial cosyntropin stimulation tests can be performed during the taper to evaluate not only basal ACTH and cortisol levels but also the magnitude of the stimulated value, to either assess normalization of adrenal func- tion or provide data to estimate the progress and duration of the glucocorticoid taper. Most patients with secondary adrenal insuf- ficiency do not need mineralocorticoid replacement. Stress Dosing Stress dosing of glucocorticoids is important counseling that should be provided to all patients with adrenal insufficiency. During critical illness, febrile illness, trauma, and/or other physi- cal stressors, the glucocorticoid needs of the body may increase. Patients reliant on exogenous glucocorticoids must therefore anticipate this by increasing their oral glucocorticoid dosing. Patients should typically be advised to double or triple their glu- cocorticoid doses during these situations, for a duration of a few days. If the illness and increased glucocorticoid dosing extends beyond 2–3 days, patients should seek counsel from their physi- cians to determine the necessity of glucocorticoid increases and search for potential causes of the illness. Gastrointestinal illnesses are notoriously the most concerning. Viral gastroenteritis induc- ing vomiting or diarrhea can result in volume depletion and lack of absorption (or intake) of steroids. Patients with adrenal insuf- ficiency can quickly spiral into a hemodynamic crisis in these 214 A. Vaidya situations and should be instructed to either go to an emergency room for intravenous hydration and steroid injections or be capa- ble of self-injecting intramuscular hydrocortisone or dexametha- sone. Patients with primary adrenal insufficiency are more susceptible to adrenal crisis with gastrointestinal illness given their mineralocorticoid deficiency. Patients should all be advised to wear a medic-alert bracelet or necklace that indicates that they have adrenal insufficiency for emergency providers. It is generally advisable to prescribe for them intramuscular hydrocortisone (100 mg) or dexamethasone in case they are not in proximity of an emergency room during an adrenal crisis. Suggested Reading Boonen E, Vervenne H, Meersseman P, Andrew R, Mortier L, Declercq PE, et al. Reduced cortisol metabolism during critical illness. N Engl J Med. 2013;368(16):1477–88. Bornstein SR, Allolio B, Arlt W, Barthel A, Don-Wauchope A, Hammer GD, et al. Diagnosis and treatment of primary adrenal insufficiency: an endo- crine society clinical practice guideline. J Clin Endocrinol Metab. 2016;101(2):364–89. Gomez-Sanchez CE. Adrenal dysfunction in critically ill patients. N Engl J Med. 2013;368(16):1547–9. Guran T, Buonocore F, Saka N, Ozbek MN, Aycan Z, Bereket A, et al. Rare causes of primary adrenal insufficiency: genetic and clinical characteriza- tion of a large nationwide cohort. J Clin Endocrinol Metab. 2016;101(1):284–92. Hamrahian AH, Fleseriu M, AACE Adrenal Scientific Committee. Evaluation and management of adrenal insufficiency in critically ill patients: disease state review. Endocr Pract. 2017;23(6):716–25. Cushing’s Syndrome 18 Brandon P. Galm and Nicholas A. Tritos Contents Consider Testing for Cushing’s Syndrome if the Patient Has a Cluster of Suggestive Signs and Symptoms, Unusual Symptoms or Features for Age (e.g., Hypertension or Osteoporosis in a Younger Patient), a Pituitary Gland Mass, or an Adrenal Adenoma 217 Use of Exogenous Glucocorticoids Is the Most Common Cause of Cushing’s Syndrome in the General Population and Should Always Be Considered First in the Evaluation of Patients with Suspected Hypercortisolism 218 Endogenous Cushing’s Syndrome Can Be Caused by Lesions of the Pituitary Gland (“Cushing’s Disease”), Adrenal Glands, or Other Organs (Ectopic ACTH-Secreting Tumors) 219 Diagnostic Testing Should Be Optimally Deferred to the Outpatient Setting Unless the Patient Has Acute Manifestations or Severe Comorbidities Potentially Related to Hypercortisolism 220 B. P. Galm (*) Neuroendocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA N. A. Tritos Harvard Medical School, Massachusetts General Hospital, Neuroendocrine Unit and Neuroendocrine & Pituitary Tumor Clinical Center, Boston, MA, USA e-mail: ntritos@mgh.harvard.edu © Springer Nature Switzerland AG 2020 215 R. K. Garg et al. (eds.), Handbook of Inpatient Endocrinology, https://doi.org/10.1007/978-3-030-38976-5_18 216 B. P. Galm and N. A. Tritos Confirm Pathologic, Autonomous Hypercortisolism as the First Step 220 Measure Plasma ACTH to Direct Further Investigations 221 Order a Pituitary-Directed MRI in ACTH- Dependent Cushing’s Syndrome 222 Order Adrenal Imaging in ACTH-Independent Cushing’s Syndrome 222 Assess and Manage Hypercortisolism-Related Consequences and Comorbidities 222 Refer for Tumor-Directed Surgery as First-Line Therapy for Cushing’s Syndrome 223 Consider Pharmacotherapy Prior to Surgery, if Surgery Is Contraindicated or Tumor Location Is Unknown, if the Patient Is Medically Unstable, or for Persistent or Recurrent Cushing’s Syndrome After Surgery 223 Consider Pituitary Radiotherapy in Persistent or Recurrent Cushing’s Disease or if Surgery Is Contraindicated 225 Consider Bilateral Adrenalectomy in Patients Who Have Refractory Cushing’s Syndrome 225 Minimize Glucocorticoid Exposure in Patients with Iatrogenic Cushing’s Syndrome 226 The Diagnosis and Management of Cushing’s Syndrome in Pregnancy Are Challenging but Tumor-Directed Surgery Remains First-Line Therapy and Can Be Life-Saving 226 Suggested Reading 227 18 Cushing’s Syndrome 217 Consider Testing for Cushing’s Syndrome if the Patient Has a Cluster of Suggestive Signs and Symptoms, Unusual Symptoms or Features for Age (e.g., Hypertension or Osteoporosis in a Younger Patient), a Pituitary Gland Mass, or an Adrenal Adenoma Consider testing for Cushing’s syndrome (CS) in the setting of a cluster of suggestive signs or symptoms (Table 18.1), although many are nonspecific when present in isolation, and in the setting of unusual symptoms or features for the patient’s age, such as unexplained hypertension or osteoporosis in a younger patient. The most discriminative (specific but not sensitive) features are reddish/purple striae > 1 cm wide, proximal Table 18.1 Features of Cushing’s syndrome Metabolic Cardiovascular Catabolic Central adiposity Hypertension Proximal Hyperglycemia/diabetes Myocardial infarction myopathy Hypertension Cardiomyopathy Bone loss Hypertriglyceridemia Stroke Striae Facial plethora Venous Ecchymoses Fat redistribution (dorsal fat thromboembolism Skin thinning pad, supraclavicular fullness, Weight loss facial fullness) Hypogonadal Mineralocorticoid Hyperandrogenic (women) Reduced fertility Hypokalemia Acne Low libido Metabolic alkalosis Hirsutism Irregular menses Hypertension Oligomenorrhea Edema Neuropsychiatric Others Pediatric Depression, anxiety Nephrolithiasis Decreased growth Emotional lability Infections velocity Mania Exophthalmos Altered timing of Changes in cognition Avascular necrosis puberty Lethargy Skin Insomnia hyperpigmentation Psychosis (ACTH-dependent) 218 B. P. Galm and N. A. Tritos myopathy, facial plethora, spontaneous ecchymoses, and dis- proportionate, central adiposity. Some patients, especially those with biochemically severe ectopic CS, may present in a cata- bolic state, with weight loss, muscle wasting, edema, and severe hypokalemia. In addition, consider testing for CS if the patient has an incidental pituitary gland lesion suggestive of an ade- noma. Most guidelines recommend that patients with an inci- dental adrenal lesion consistent with an adenoma should undergo testing for CS, usually with the low- dose 1-mg dexa- methasone suppression test (DST). Use of Exogenous Glucocorticoids Is the Most Common Cause of Cushing’s Syndrome in the General Population and Should Always Be Considered First in the Evaluation of Patients with Suspected Hypercortisolism The use of exogenous glucocorticoids is the most common cause of CS. This includes any route of administration, such as topical, inhaled, intra-articular, and rectal. Make sure to ask about joint injections (including the spine) over the last few months. Make sure to ask about strong cytochrome P450 (CYP450) inhibitors, especially ritonavir or cobicistat (antiretroviral therapy), as these increase the risk of CS with exogenous steroid use. Also ask about naturopathic or herbal supplements. Megestrol acetate (Megace®), an appetite stimulant, has glucocorticoid activity and can cause CS. Patients on exogenous steroids may appear Cushingoid with biochemical evidence of hypoadrenalism as a result of suppression of the pituitary-adrenal axis, including a low or undetectable serum cortisol level (if the exogenous gluco- corticoid has limited cross-reactivity with cortisol in the assay) and low plasma ACTH. Exogenous glucocorticoids may be detectable in urine specimens assayed by liquid chromatography tandem mass spectrometry, though this test is rarely needed in clinical practice. 18 Cushing’s Syndrome 219 Endogenous Cushing’s Syndrome Can Be Caused by Lesions of the Pituitary Gland (“Cushing’s Disease”), Adrenal Glands, or Other Organs (Ectopic ACTH-Secreting Tumors) Causes of endogenous CS are shown in Table 18.2. Table 18.2 Causes of endogenous Cushing’s syndrome ACTH- Pituitary Pituitary Females 3–5 times more, dependent (70%) adenoma peak 20–30s, 95% are (Cushing’s microadenomas disease; CD) Ectopic Small cell lung Peak 40–50s, especially ACTHa cancer smokers (10%) Carcinoids Peak 20–30s (bronchial, thymic) Othersb Rare, may have other paraneoplastic syndromes ACTH- Adrenal Adrenal adenoma Females 4–8 times more, independent (20%) (60%) peak 30–40s Adrenal Females 1–3 times more, carcinoma (40%) peak 40–50s, often large mass, may co-secrete androgens Bilateral nodular May be familial or adrenal associated with Carney hyperplasiac complex (<1%) aMay rarely be caused by ectopic CRH secretion (<1% of ACTH-dependent CS) bIncludes pancreatic neuroendocrine tumors, pheochromocytoma, medullary thyroid carcinoma, and others cIncludes bilateral macronodular adrenal hyperplasia and primary pigmented nodular adrenocortical disease 220 B. P. Galm and N. A. Tritos Diagnostic Testing Should Be Optimally Deferred to the Outpatient Setting Unless the Patient Has Acute Manifestations or Severe Comorbidities Potentially Related to Hypercortisolism Defer testing for CS to the outpatient setting, if possible (e.g., incidental adrenal or pituitary adenoma), as many tests may be difficult to interpret in the hospitalized patient and may not have been adequately validated in this population. Physiologic hyper- cortisolism (pseudo-Cushing’s syndrome) can be seen in severe obesity and in acute stress and illness, including depression, poorly controlled diabetes mellitus, and malnutrition, and 50–80% will have abnormal testing for CS. However, it is important to remember that patients with acute manifestations or severe comorbidities (such as sepsis, psychosis, or severe, unexplained hypokalemia with cachexia) that are suspected of being hypercor- tisolemic require urgent evaluation and management in the inpa- tient setting. Confirm Pathologic, Autonomous Hypercortisolism as the First Step Order the 24-h urinary free cortisol (UFC) (at least two collec- tions), late-night salivary cortisol (LNSC) (at least two samples), and/or the low-dose 1-mg DST. Urine creatinine and volume should be measured with UFC tests to ensure adequate collection and exclude high urinary volumes as an explanation for falsely elevated UFC. Consider measuring a plasma dexamethasone level during the DST to ensure adequate exposure during the test. The 2-day DST is usually deferred to the outpatient setting. At least two different tests should be positive before pathologic hypercor- tisolism is confirmed. Significant fluctuations of cortisol secretion can be seen, especially in the setting of cyclic CS. LNSC is rarely done in hospital due to the delayed turnaround time. Test charac- teristics are shown in Table 18.3. 18 Cushing’s Syndrome 221 Table 18.3 Initial tests used to evaluate for pathologic hypercortisolism (Cushing’s syndrome) False Test Cutoff Sensitivity Specificity False positives negatives 1 mg >1.8 μg/ 97–100% 80–90% Estrogens (OCP), CYP DST dL CYP inducersa, inhibitorsb rapid metabolizers UFC >ULNc 80–95% 90–95% Fluid intake >5 L/ Reduced day, some drugsd GFR LNSC >ULNc 90–95% 95–100% Tobacco or licorice use, altered sleep- wakefulness cycle Abbreviations: CYP cytochrome P450, DST dexamethasone suppression test, GFR glomerular filtration rate, LNSC late-night salivary cortisol, OCP oral contraceptive pill, UFC 24-h urinary free cortisol, ULN upper limit of normal aStrong CYP450 inducers include phenytoin, carbamazepine, rifampin, phe- nobarbital, ethosuximide, and pioglitazone bStrong CYP450 inhibitors include azole antifungals, ritonavir, fluoxetine, diltiazem, and cimetidine cUse the reference range provided by the laboratory, as assay types and cut- offs vary. Specificity for CS rises with greater UFC or LNSC elevations; |
how- ever, the effects of acute illness on cortisol levels should also be considered when interpreting test results dCarbamazepine, fenofibrate (in some assays), licorice, and carbenoxolone Measure Plasma ACTH to Direct Further Investigations Once CS is confirmed, measure plasma ACTH to determine whether CS is ACTH-dependent or ACTH-independent. ACTH is optimally assayed in morning specimens. Ensure that ACTH is collected properly, as it is degraded quickly and needs to be placed on ice immediately after collection. CS is ACTH- dependent if ACTH is inappropriately normal or high (>20 pg/ mL), while it is ACTH-independent if ACTH is suppressed (<5 pg/mL) in a patient with active hypercortisolism. Intermediate levels (5–20 pg/mL) may represent either possibility but are more often ACTH- dependent. 222 B. P. Galm and N. A. Tritos Order a Pituitary-Directed MRI in ACTH- Dependent Cushing’s Syndrome Order a pituitary-directed MRI to investigate for a pituitary ade- noma, although this may miss 40–50% of small adenomas caus- ing CS. Recall that pituitary incidentalomas occur in ~10% of the general population. Unless there is an adenoma >6–10 mm, pro- ceed with inferior petrosal sinus sampling (IPSS) to distinguish pituitary from ectopic CS. The high-dose DST is also sometimes used but has low specificity (~67%), and results should generally be confirmed on IPSS. For ectopic CS, order CT of the chest, abdomen, and pelvis. If this does not identify a source, functional nuclear imaging (octreotide scan, FDG PET, F-DOPA PET, or gallium DOTATATE PET) may be required. Order Adrenal Imaging in ACTH-Independent Cushing’s Syndrome Order adrenal imaging (CT or MRI) to investigate for an adrenal mass. Recognize that adrenal incidentalomas occur in ~10% of the population but are more likely to be the source of CS when hypercortisolism is present and ACTH is suppressed. Patients with ACTH-independent CS and bilateral adrenal adenomatous lesions may require adrenal vein sampling to determine which lesion is the culprit. Also order adrenal androgens to assess for co-secretion, which is common in adrenal carcinomas; in con- trast, serum DHEA-S is typically below normal in adrenal CS due to adrenal adenomas. Assess and Manage Hypercortisolism-Related Consequences and Comorbidities Assess for the presence of hyperglycemia, hypertension, dyslipid- emia, and osteoporosis, and manage these as per usual. Assess for psychiatric disorders and consider referral to psychiatry if 18 Cushing’s Syndrome 223 appropriate. Offer appropriate vaccinations, especially for pneumococcus, influenza, and (preferably not during active hypercortisolism) herpes zoster. Hypokalemia from overstimulation of the mineralocorticoid receptor by excess cortisol (especially in ectopic CS) should be monitored and treated with potassium supplements and spironolactone or eplerenone. Consider prophylaxis for venous thromboembolism, especially perioperatively and in those at high risk. Consider prophylaxis for opportunistic infections, especially Pneumocystis, in severe CS (UFC > 5 × ULN). Refer for Tumor-Directed Surgery as First-Line Therapy for Cushing’s Syndrome When localization has been successful, surgery (transsphenoidal pituitary surgery, unilateral adrenalectomy, or resection of ectopic tumor) performed by an experienced surgeon is first-line therapy for those who are appropriate candidates. Control of hypercorti- solism and its associated comorbidities, especially when severe, should be considered prior to surgery. If the source of CS cannot be identified (especially in ectopic CS), bilateral adrenalectomy may be an option, especially in life-threatening severe CS or in those who have contraindications or are refractory to medical therapy. Consider Pharmacotherapy Prior to Surgery, if Surgery Is Contraindicated or Tumor Location Is Unknown, if the Patient Is Medically Unstable, or for Persistent or Recurrent Cushing’s Syndrome After Surgery Options for pharmacotherapy are shown in Table 18.4. For rapid control, patients are usually started on ketoconazole and/or metyr- apone (mifepristone may also be considered, if available). For very rapid control in life-threatening CS in the critical care set- ting, etomidate may be useful but requires close monitoring for sedation. Cabergoline or pasireotide may be more useful in 224 B. P. Galm and N. A. Tritos Table 18.4 Pharmacotherapy for Cushing’s syndrome Approximate Medication Mechanism of action efficacya Dosing Adverse effects Cabergoline Dopamine receptor 2 30–40% 1–7 mg/wk GI upset, orthostatic hypotension, potentially agonist cardiac valvulopathy in high doses Pasireotide Somatostatin receptor 20–40% 600–1200 μg sc GI upset, cholelithiasis, transaminitis, ligand bidc hyperglycemia/diabetes, prolonged QT Ketoconazole Inhibits several adrenal 50–75% 400–1600 mg/d, Transaminitis, hepatitis, drug interactions, enzymes divided bid–tid gynecomastia, hypogonadism (men) Metyrapone Inhibits 11β-hydroxylase 50–75% 500–6000 mg/d, GI upset, hirsutism, acne, hypokalemia, edema, divided tid–qid hypertension Etomidate Inhibits several adrenal 100% 3–5 mg load then Sedation; requires monitoring in intensive care, enzymes (dose- 0.03–0.1 mg/kg/h given via central line dependent) Mitotane Adrenolytic, inhibits 75–85% 250–8000 mg/d, GI upset, CNS effects, transaminitis, alters several adrenal enzymes divided tid–qid binding proteins, inhibits CYP 3A4, drug interactions, hypothyroidism, teratogenic Mifepristone Glucocorticoid receptor 40–60%b 300–1200 mg GI upset, abortifacient, hypokalemia, antagonist once daily hypertension, edema, endometrial thickening Abbreviations: CNS central nervous system, CYP cytochrome P450, GI gastrointestinal aAll estimates are approximate, as various studies used different outcomes for efficacy. Treatment escape may develop in some patients (~25% on cabergoline, ~10% on ketoconazole, ~5% on metyrapone) bAs cortisol and UFC are not meaningful while on mifepristone, efficacy is reported as improvement in diabetes or hypertension cA long-acting formulation of pasireotide (10–40 mg intramuscularly every 4 weeks) has also been tested and FDA-approved for the treatment of CS 18 Cushing’s Syndrome 225 less- severe pituitary CS but take longer to control hypercorti- solism than adrenally acting agents. Combination therapy can also be useful (efficacious in 70–90%), especially in severe or refractory CS. Monitoring while hospitalized is generally per- formed with serum cortisol (although UFC can be used), with a target of ~10–15 μg/dL (exact targets vary depending on assay). Do not monitor cortisol levels in patients on mifepristone. All agents can cause hypoadrenalism as an extension of their pharma- cologic effects. Only pasireotide and mifepristone are FDA- approved for treatment of CS. Consider Pituitary Radiotherapy in Persistent or Recurrent Cushing’s Disease or if Surgery Is Contraindicated Consider pituitary-directed radiotherapy (RT) for refractory, per- sistent, or recurrent CD, for patients with contraindications to sur- gery, or for large adenomas with residual tumor after surgical debulking. As RT may take months to years to become effective, other medical therapies may need to be used in the interim. Consider Bilateral Adrenalectomy in Patients Who Have Refractory Cushing’s Syndrome Consider bilateral adrenalectomy in patients who have refractory CS despite medical therapy, tumor-directed surgery, and/or RT. Bilateral adrenalectomy may also be helpful in severe, life- threatening CS and in patients where the primary tumor (includ- ing ectopic CS) cannot be found. Bilateral adrenalectomy is generally advisable in patients with bilateral ACTH-independent (macro- or micronodular) adrenal hyperplasia. Patients require lifelong glucocorticoid and mineralocorticoid replacement after bilateral adrenalectomy. Monitor for Nelson’s syndrome (cortico- troph tumor progression) with regular ACTH levels and pituitary MRI examinations in patients with CD who undergo bilateral adrenalectomy. 226 B. P. Galm and N. A. Tritos Minimize Glucocorticoid Exposure in Patients with Iatrogenic Cushing’s Syndrome In patients with iatrogenic CS, minimize the glucocorticoid doses as needed to treat the underlying illness. If possible, avoid ritona- vir or cobicistat in patients on long-term glucocorticoids. For those patients on long-term steroids who no longer require phar- macologic doses, prescribe replacement doses (equivalent of prednisone 3–5 mg/day), with appropriate stress-dose coverage at the time of surgery or acute illness, until recovery of the hypothalamic- pituitary-adrenal (HPA) axis occurs. Although practice varies, clinicians will often monitor morning plasma cor- tisol (prior to steroid dose) or perform ACTH stimulation testing to document recovery of the HPA axis. The Diagnosis and Management of Cushing’s Syndrome in Pregnancy Are Challenging but Tumor-Directed Surgery Remains First-Line Therapy and Can Be Life-Saving Making the diagnosis is critical as CS in pregnancy is associated with significant morbidity and mortality for the fetus and mother. Do not use the DST. Use the UFC with a higher cutoff of 2–3 × prepregnancy ULN, since cortisol secretion rates rise during healthy pregnancies above pregestational levels. The LNSC may be useful, but more data are needed on reference ranges. Adrenal causes are proportionately more common during pregnancy (~50% of CS), but ACTH may not be fully suppressed. Order an abdominal ultrasound as the initial imaging modality; unen- hanced MRI of the adrenals or pituitary may be performed in consultation with radiology. Tumor-directed surgery, preferably during the second trimester, should be undertaken if a source is identified. No pharmacotherapy is approved for use in preg- nancy; metyrapone has been used the most, but cabergoline may also be useful. Mifepristone is absolutely contraindicated as it is an abortifacient. 18 Cushing’s Syndrome 227 Suggested Reading Elamin MB, Murad MH, Mullan R, Erickson D, Harris K, Nadeem S, et al. Accuracy of diagnostic tests for Cushing’s syndrome: a systematic review and metaanalyses. J Clin Endocrinol Metabol. 2008;93(5):1553–62. Lacroix A, Feelders RA, Stratakis CA, Nieman LK. Cushing’s syndrome. Lancet (Lond, Engl). 2015;386(9996):913–27. Nieman LK, Biller BMK, Findling JW, Murad MH, Newell-Price J, Savage MO, et al. Treatment of Cushing’s syndrome: an endocrine society clini- cal practice guideline. J Clin Endocrinol Metabol. 2015;100(8):2807–31. Nieman LK, Biller BMK, Findling JW, Newell-Price J, Savage MO, Stewart PM, et al. The diagnosis of Cushing’s syndrome: an endocrine society clinical practice guideline. J Clin Endocrinol Metabol. 2008;93(5):1526– 40. Pivonello R, De Leo M, Cozzolino A, Colao A. The treatment of Cushing’s disease. Endocr Rev. 2015;36(4):385–486. Tritos N, Biller BMK. Medical therapy for Cushing’s syndrome in the twenty- first century. Endocrinol Metab Clin N Am. 2018;47(2):427–40. Adrenalectomy 19 Ole-Petter R. Hamnvik Contents Preoperative Evaluation 230 Review Indications for Adrenalectomy and Consider Appropriateness of a Biopsy 230 Ensure Completeness of Preoperative Endocrine Evaluation 231 Postoperative Management 233 Assess for Hormonal Deficiencies 233 Initiate Replacement Therapy 233 Educate the Patient About Adrenal Insufficiency if Present 234 Organize Follow-Up After Discharge 235 Suggested Reading 235 Abbreviation IV Intravenous O.-P. R. Hamnvik (*) Brigham and Women’s Hospital, Department of Medicine, Division of Endocrinology, Diabetes and Hypertension, Boston, MA, USA e-mail: ohamnvik@bwh.harvard.edu © Springer Nature Switzerland AG 2020 229 R. K. Garg et al. (eds.), Handbook of Inpatient Endocrinology, https://doi.org/10.1007/978-3-030-38976-5_19 230 O.-P. R. Hamnvik Preoperative Evaluation Review Indications for Adrenalectomy and Consider Appropriateness of a Biopsy Most adrenal masses should not be surgically removed. Indications for unilateral adrenalectomy include: • Hormonally secreting adrenal adenomas (such as cortisol- producing or aldosterone-producing adenomas) • Pheochromocytomas • Adrenal masses that are suspicious for primary adrenocortical carcinoma, based on imaging characteristics such as irregular shape, size >4 cm, high unenhanced CT attenuation values (>20 Hounsfield units), irregular enhancement after contrast administration, etc. • As part of a radical nephrectomy for renal cell carcinoma or other rarer tumors such as Wilms tumor or neuroblastomas Bilateral adrenalectomy is usually only performed in the set- ting of ACTH-dependent Cushing syndrome where the source of the ACTH excess cannot be identified or controlled (such as in a widely metastatic ACTH-secreting malignancy). Adrenalectomy is usually not performed for non-adrenal can- cer with metastatic spread to the adrenal gland or for infections causing adrenal masses such as tuberculosis, fungi, etc. Therefore, a fine needle aspiration biopsy may be reasonable if there is concern for metastasis (such as in a patient with a known primary tumor) or infection (such as in a patient with systemic symptoms such as fevers, chills, weight loss, etc.). Biopsy should not be performed until pheochromocytoma has been ruled out biochemically. In addition, biopsy will not distinguish adrenocortical cancer from an adrenal adenoma (a full resection is required) and therefore is not indicated in suspected adreno- cortical cancer. 19 Adrenalectomy 231 The indication for surgery, the surgeon’s experience, and char- acteristics of the patient and the tumor will determine the surgical approach chosen by the surgeon. The standard approach for benign disease is laparoscopic transabdominal adrenalectomy or retroperitoneal endoscopic adrenalectomy. These approaches are used in the vast majority of adrenalectomies and are considered the standard of care for adrenalectomies for benign lesions, par- ticularly in patients who are otherwise at high risk for postopera- tive complications. Open transabdominal adrenalectomy is a more invasive surgical approach that allows the best exposure and visu- alization of the operative field; it is usually the preferred approach in cases of suspected malignancy where a more extensive resec- tion is needed. This includes cases of known adrenocortical carci- noma, suspected adrenocortical carcinoma (such as tumors >6 cm in size, tumors making multiple hormones, or tumors making adrenal androgens), and tumors with local invasion into surround- ing |
structures. However, the open approach to adrenalectomy is associated with more pain and longer postoperative hospitaliza- tion than less invasive approaches, although this is a reasonable trade-off to allow more complete resection in cases of suspected malignancy. Ensure Completeness of Preoperative Endocrine Evaluation All patients with an adrenal mass should have an evaluation for hormonal hypersecretion by history, physical examination, and biochemical testing prior to surgery. If adrenalectomy is performed in a patient without an adrenal mass (such as in a rad- ical nephrectomy), an endocrine evaluation is not required unless the patient has an incidental adrenal mass noted on preoperative imaging. The history and physical examination should focus on symp- toms and signs of Cushing syndrome, primary hyperaldosteron- ism (mainly by assessing blood pressure), androgen excess, and 232 O.-P. R. Hamnvik pheochromocytoma. All patients with an adrenal nodule should have a biochemical assessment for Cushing syndrome (1-mg dexamethasone suppression test or late-night salivary cortisol level) and pheochromocytoma (plasma or 24-h urine metaneph- rines). Patients with hypertension or hypokalemia should also be assessed for primary aldosteronism with an aldosterone-renin ratio. When adrenocortical carcinoma is suspected, andorgen lev- els should be measured: primarily DHEAS, but also consider tes- tosterone and androstenedione. Males and post-menopausal females with features of estrogen excess should have estogen lev- els measured. Assessing the endocrine function preoperatively is essential to avoid unexpected intraoperative or postoperative complications. Patients who have preoperative cortisol excess from a cortisol- secreting adrenal adenoma are at risk for adrenal insufficiency postoperatively due to atrophy of pituitary corticotrophs and of the contralateral adrenal gland; they are also at higher risk of venous thromboembolism, hyperglycemia, hypertension, peptic ulcer disease, and infection. Perioperative management of these patients is discussed in Chap. 18 “Cushing’s Syndrome.” Patients with primary aldosteronism may need preoperative blood pres- sure control and hypokalemia treatment (often with a mineralo- corticoid receptor antagonist such as spironolactone) and are at risk for postoperative hypoaldosteronism with hyperkalemia and sodium wasting with hypotension, as discussed in Chap. 21 “Primary Aldosteronism.” Patients with pheochromocytomas should receive preoperative blockade of alpha- and beta- adrenergic receptors as well as volume expansion, as discussed in Chap. 20 “Pheochromocytoma and Paraganglioma,” to prevent uncontrollable intraoperative blood pressure swings. A finding of hyperandrogenism raises the likelihood that the lesion is an adre- nocortical cancer; benign adrenal adenomas almost never secrete androgens. 19 Adrenalectomy 233 Postoperative Management Assess for Hormonal Deficiencies Postoperatively, adrenal insufficiency may be an expected occur- rence, such as after bilateral adrenalectomy. These patients do not need any further hormonal assessment but should start hormone replacement as discussed below. In patients who have undergone unilateral adrenalectomy for a hormonally silent lesion, as assessed preoperatively, the likelihood of clinically apparent adre- nal insufficiency is low, and routine glucocorticoid replacement is therefore not indicated. However, biochemical adrenal insuffi- ciency on postoperative day 1 (defined by a morning cortisol below 94 nmol/L [3.4 μg/dL]) has been found in around 20% of patients and may represent suppression of the remaining adrenal from subclinical Cushing syndrome or an inadequate adrenocorti- cal reserve in the remaining adrenal. While routine postoperative testing for adrenal insufficiency in these patients is not currently standard of care, close monitoring of the patient’s clinical status (symptoms, blood pressure, electrolytes) should be performed, and there should be a low threshold to assess for adrenal insuffi- ciency. Postoperative endocrine monitoring of patients with secre- tory adrenal masses is discussed in Chap. 18 “Cushing’s Syndrome,” Chap. 20 “Pheochromocytoma and Paraganglioma,” and Chap. 21 “Primary Hyperaldosteronism.” Initiate Replacement Therapy Patients who undergo bilateral adrenalectomy, as well as those patients whose indication for unilateral adrenalectomy is a cortisol- secreting adrenal adenoma or adenocarcinoma, will have adrenal insufficiency postoperatively. Therefore, routine adminis- tration of glucocorticoids is indicated. For patients who have undergone bilateral adrenalectomy, an example of a postoperative hormone replacement strategy is the following: 234 O.-P. R. Hamnvik • Hydrocortisone 50 mg IV every 8 h on the day of surgery and postoperative day 1, with the first dose being administered intraoperatively after the second adrenal gland has been removed. • Then reduce the dose to 25 mg IV every 8 h on postoperative day 2. • On postoperative day 3, if the patient is tolerating oral intake, switch to oral hydrocortisone, 40 mg at 7 am and 20 mg at 3 pm for 1 day and then to 20 mg at 7 am and 10 mg at 3 pm thereafter. When oral intake is tolerated, oral fludrocortisone 0.1 mg daily is also added. • The dose can be weaned further after discharge based on patient symptoms, blood pressure readings and potassium levels. In patients who have undergone adrenal surgery for overt or subclinical cortisol excess, some practitioners prefer to wait with initiation of glucocorticoids until postoperative day 1 after ensur- ing that blood cortisol levels have dropped, confirming surgical cure of the disease. In patients with overt Cushing syndrome, higher supraphysiologic glucocorticoid doses and a slower taper are often needed as the patient can otherwise be very symptomatic from the rapid decline in glucocorticoid levels. Patients who undergo unilateral adrenalectomy for any indication usually do not require mineralocorticoid replacement with fludrocortisone, although they should be monitored for hyperkalemia and hypo- tension which are signs of hypoaldosteronism. Educate the Patient About Adrenal Insufficiency if Present All patients diagnosed with adrenal insufficiency should be informed about their diagnosis and taught how to prevent adrenal crises prior to discharge. This is discussed in further detail in Chap. 17 “Suspected Adrenocortical Deficiency.” 19 Adrenalectomy 235 Organize Follow-Up After Discharge Patients should have a follow-up appointment within 1–2 weeks with their surgeon for routine postoperative follow-up and to dis- cuss the results of the histopathologic examination of the adrenal specimen. Patients who are diagnosed with adrenocortical cancer or patients who are discharged on adrenal hormone replacement should have follow-up with an endocrinologist within 2–4 weeks to discuss whether adjuvant mitotane is indicated and to titrate the hormone replacement dose, respectively. Patients should have a contact number in case symptoms of adrenal insufficiency develop. Suggested Reading Fassnacht M, Arlt W, Bancos I, Dralle H, Newell-Price J, Sahdev A, et al. Management of adrenal incidentalomas: European Society of Endocrinology Clinical Practice Guideline in collaboration with the European Network for the Study of Adrenal Tumors. Eur J Endocrinol. 2016;175(2):G1–G34. Mitchell J, Barbosa G, Tsinberg M, Milas M, Siperstein A, Berber E. Unrecognized adrenal insufficiency in patients undergoing laparo- scopic adrenalectomy. Surg Endosc. 2009;23:248–54. Zeiger MA, Thompson GB, Duh QY, Hamrahian AH, Angelos P, Elaraj D, et al. The American Association of Clinical Endocrinologists and American Association of Endocrine Surgeons medical guidelines for the management of adrenal incidentalomas. Endocr Pract. 2009;15(Suppl 1):1–20. Pheochromocytoma 20 and Paraganglioma Alejandro Raul Ayala and Mark Anthony Jara Contents Before the Admission 238 Preoperative Blood Pressure Control 239 Hydration 240 During Admission 241 Inpatient Diagnosis and Treatment 241 Confounders: Diagnostic Accuracy of Metanephrines 242 Localization of Pheochromocytomas/PPGLs 243 Opportunities to Explore Syndromic Pheochromocytoma: Hints of Genotype 244 Anesthesia in the Patient with Pheochromocytoma 244 Early Postoperative 245 Special Circumstances 247 Suggested Reading 248 A. R. Ayala (*) University of Miami, Miller School of Medicine, Department of Endocrinology and Metabolism, Miami, FL, USA e-mail: aayala2@miami.edu M. A. Jara University of Miami, Miller School of Medicine, Division of Endocrinology and Metabolism, Miami, FL, USA e-mail: maj158@miami.edu © Springer Nature Switzerland AG 2020 237 R. K. Garg et al. (eds.), Handbook of Inpatient Endocrinology, https://doi.org/10.1007/978-3-030-38976-5_20 238 A. R. Ayala and M. A. Jara Before the Admission Because pheochromocytoma and catecholamine-secreting para- gangliomas (PPGLs) might have similar clinical presentations and are treated with similar approaches, many clinicians use the term “pheochromocytoma” to refer to both. The most common inpatient consultation often involves perioperative management of a patient previously diagnosed with a pheochromocytoma. However, catecholamine secreting tumors can also be diagnosed during a hospitalization for unrelated conditions or in the context of a hypertensive crisis. The clinical presentation of patients with PPGLs varies widely from no symptoms or minor discrete symp- toms to catastrophic life-threatening clinical conditions. In gen- eral, 50% of these patients are asymptomatic at presentation. This subgroup is much larger in those patients with incidentally dis- covered adrenal masses or those tested during family screenings. When symptomatic, patients may present with the following: • Pounding headache, approximately 90% of symptomatic patients. • Profuse sweating in 60–70%. • Palpitations that occurs in spells that last from several minutes to 1 h with complete remission of the symptoms between spells. The spells could occur either spontaneously or being provoked by a variety of physical or chemical triggers, such as general anesthesia, micturition, and medications (e.g., β-adrenergic inhibitors, tricyclic antidepressants, glucocorticoids). • Panic attack like symptoms. Approximately 50% of patients have paroxysmal hyperten- sion, often severe, while the remaining either have primary hypertension or are normotensive (5–15%). Other symptoms include tremors, pallor, dyspnea, weakness mostly generalized, and panic attack-type symptoms. On rare occasion, catechol- amine excess can result in decompensated heart failure and/or cardiogenic shock with features of stress-induced (Takotsubo) cardiomyopathy. 20 Pheochromocytoma and Paraganglioma 239 Preoperative Blood Pressure Control The main goal of preoperative management of a pheochromocy- toma patient is to normalize blood pressure, heart rate, and func- tion of other organs; restore volume depletion; and prevent a patient from surgery-induced catecholamine storm and its poten- tially devastating consequences. All patients with a biochemically positive pheochromocy- toma should receive appropriate preoperative medical manage- ment to block the effects of released catecholamines. Medical treatment should be started ideally 14 days preoperatively allowing for blood pressure and pulse normalization. Based on retrospective studies and institutional experience, target goals include a blood pressure of less than 130/80 mm Hg while seated and greater than 90 mm Hg systolic while standing and a heart rate target of 60–70 bpm seated and 70–80 bpm standing. The α-adrenergic receptor blockers are the first-choice agents having significant impact on surgical outcome as patients without α-adrenoceptor blockade experience significant periop- erative complications when compared with those on treatment. Phenoxybenzamine (a noncompetitive, α-adrenoceptor blocker) is most commonly used for preoperative blockade. The initial dose of phenoxybenzamine is usually 10 mg twice a day followed by 10–20 mg increments every 2–3 days until the clinical manifestations are controlled or further increases are limited by side effects. Generally, a total daily dose of 1 mg/kg is sufficient. Additionally, the prolonged action of phenoxybenzamine can contribute to hypotension in the first 24 h after tumor removal. Another option is to administer phenoxybenzamine by infusion (0.5 mg/kg·d) for 5 h a day, 3 days before the surgical intervention in those patients that are hospitalized. Prazosin, terazosin, and doxazosin are specific competitive alpha 1-postsynaptic blocking α-adrenoceptor blocking agents of shorter half-life that can also be used safely. Prazosin is administered in doses of 2–5 mg two or three times a day, terazosin in doses of 2–5 mg per day, and doxazosin in doses of 2–8 mg per day. These three medications could 240 A. R. Ayala and M. A. Jara potentially induce severe postural hypotension immediately after the first dose; thus, they should be given just as the patient is ready to go to bed. Thereafter, the dosage can be increased as needed; titration can be achieved more quickly with much less side effects compared with phenoxybenzamine. Beta-adrenoceptor blocking agents are needed when catecholamine- related or α-blocker-induced tachyarrhythmia occurs but should never be used before an adequate α-blockade has been established as unopposed alpha-receptor stimulation will cause increased vasoconstriction and might lead to hypertensive crisis. Calcium channel blockers may also be used preoperatively. The combination of extended-release verapamil (180–360 mg/ daily), sustained release nicardipine beginning with 30 mg twice daily, amlodipine beginning with 2.5-5 mg daily or extended release nifedipine beginning with 30 mg daily and specific com- petitive alpha 1-p ostsynaptic α-adrenoceptor blocking agents (i.e., doxazosin) may be particularly useful although there is little data to compare the efficacy of one treatment regimen over another. Calcium channel blockers do not cause hypotension or orthostatic hypotension during normotensive period and may also be used as the primary preoperative treatment of choice in normo- tensive patients with pheochromocytoma. These agents may also prevent catecholamine-associated coronary spasm; therefore, they may be useful when pheochromocytoma is associated with cate- cholamine-induced coronary vasospasm. Hydration Adequate oral hydration should be encouraged prior to admission. Catecholamines cause intense vasoconstriction through the |
alpha-1 receptors, and initiation of α-blockade can lead to severe orthostatic hypotension. A patient may need 2–3 L of fluid orally or intravenously with 5–10 g of salt to increase the intravascular volume, reverse catecholamine-induced blood volume contrac- 20 Pheochromocytoma and Paraganglioma 241 tion preoperatively, and prevent severe hypotension after tumor removal. Serial hematocrit measurements give a guide to the effectiveness of volume expansion. Usually, a 5–10% fall in hematocrit is seen in well-prepared patients. During Admission Inpatient Diagnosis and Treatment The diagnosis of a pheochromocytoma in hospitalized patients can be challenging, mainly due to confounders that can result in non-tumoral catecholamine elevation. Coexisting conditions (heart failure, renal failure, and hypoglycemia) increase sympa- thetic activity and may result in a false-positive test. Interfering medications and psychiatric conditions should also be taken into account. Confirmatory biochemical testing should generally pre- cede imaging procedures because only solid evidence of excess production of catecholamines can justify performing expensive imaging procedures. However, a highly suspicious lesion (i.e., markedly hyperintense vascular tumor on T2 MRI images with no signal loss on out-of-phase imaging) should prompt immediate and incisive investigation. Imaging characteristics are particularly important during the evaluation of an incidentally discovered adrenal tumor (adrenal incidentaloma), since the tumor may be in the so called pre-biochemical phase (normal catecholamines/ metanephrines). Initial biochemical testing for PPGLs should include mea- surements of plasma-free metanephrines or urinary fractionated metanephrines by either mass spectrometry, liquid chromatog- raphy with electrochemical, or fluorometric detection (LC-ECD), as they have shown superior sensitivity and accu- racy compared to VMA and urine catecholamines. For mea- surement of plasma metanephrines, it is recommended to test the patient in the supine position and use of reference intervals established in the same position. An elevation of two to four times above the normal reference values often confirms the diagnosis with few exceptions. 242 A. R. Ayala and M. A. Jara Confounders: Diagnostic Accuracy of Metanephrines Plasma (free and total) metanephrines have similar sensitivities of 96% and 95% to urinary fractionated metanephrines. Both tests are equally recommended and combination of tests is not necessary. To avoid false positives, acetaminophen should be avoided for 5 days before blood sampling (HPLC assay). Caffeine intake and cigarette smoking should be discontinued for at least 24 h before a blood sample is obtained. The blood sample should be drawn in lavender or green-top tube, transferred on ice, and then stored at −80 °C until analyzed. The highest diagnostic sensitivity for plasma-free metanephrines is reached if the collection is performed in the supine position after an overnight fast and while the patient is recumbent in a quiet room for at least 20–30 min (Table 20.1). Table 20.1 Drugs that can affect the levels of plasma and urinary catechol- amines or metanephrines and affect test accuracy Medications Effect Tricyclic antidepressants amitriptyline, Increase plasma and urinary imipramine, and nortriptyline NA, NMA, and VMA SSRI Increased NMA Blockers atenolol, propranolol Increase plasma MA Caffeine, nicotine Increase plasma and urinary A and NA Calcium channel antagonists Increase plasma A and NA Amphetamine, ephedrine Increase plasma and urinary A and NA SNRI (venlafaxine) Increase NMA Adapted from Davison AS. Biochemical Investigations in Laboratory Medi- cine. Physiological effects of medications on Plasma/Urine metanephrines. Newcastle upon Tyne NHS Foundation Trust. http://www.pathology.leedsth. nhs.uk/dnn_bilm/Misc/Effectofdrugsonmetanephrines.aspx. (See Suggested Readings) NA noradrenaline, A adrenaline, NMA normetadrenaline, MA metadrenaline, VMA vanillylmandelic acid 20 Pheochromocytoma and Paraganglioma 243 Localization of Pheochromocytomas/PPGLs Localization of PPGLs is only done when there is biochemical diagnosis confirmation. CT or MRI may be used as the usual ini- tial imaging modalities for localization of PPGLs. These studies have high sensitivity but less than optimal specificity. These should be combined with functional imaging studies (nuclear medicine) to rule out extra-adrenal pheochromocytoma or meta- static disease. Gallium-68 PET/C is a promising agent that may offer further advantage in the localization of paragangliomas (Fig. 20.1). Clinical features suspicious for pheochromocytoma Rule out confounders: heart failure, renal failure, medications, caffeine WARD ICU In acute illness hyperadrenergic state, Biochemical testing: catecholamines and Plasma free metanephrines are rarely helpful metanephrines after 30 min of supine rest or 24 h Adrenal CT/MRI urinary fractionated metanephrines Normal Abnormal results results Positive Negative Repeat Elevation 2–3 testing during times above the symptomatic upper limit of episode normal Functional scanning Extradrenal tumor 18F-Dopa PET CT neck, CT chest Negative Ga-68 DOTATE PET Fig. 20.1 Algorithm 1 Biochemical and imaging diagnosis of catecholamine- producing tumors 244 A. R. Ayala and M. A. Jara Opportunities to Explore Syndromic Pheochromocytoma: Hints of Genotype Pheochromocytoma/PPGLs may be inherited and may have dis- tinct characteristic setting them apart from sporadic pheochromo- cytoma. Patients with syndromic lesions and/or positive family history should be tested for appertaining genes. Considerations should be made in patient presenting with: • PPGL at young age, usually before 40 years old • Positive family history • Multifocal PPGLs • Bilateral adrenal tumors Pheochromocytomas are associated with the following famil- ial syndromes: multiple endocrine neoplasia type 2 (MEN 2), von Hippel-Lindau disease (VHL), von Recklinghausen’s neurofibromatosis type 1 (NF 1), and familial paragangliomas (PGLs). Hospitalization represents a unique opportunity to identify such associated syndromic inherited conditions. Furthermore, the presence of family members providing support to the hospi- talized patient represents an opportunity to further explore famil- ial forms and to evaluate family members following appropriate consent. Anesthesia in the Patient with Pheochromocytoma Pheochromocytoma represents an important challenge for the anesthesiologist. By some estimates, 25–50% of hospital deaths of patients with unmanaged or unknown pheochromocytoma occur during induction of anesthesia or during operative proce- dures for other conditions, mostly related to lethal hypertensive crises, malignant arrhythmias, and multiorgan failure. Most patients with pheochromocytoma will require surgical interven- tion, and labile blood pressures, arrhythmias, and tachycardia 20 Pheochromocytoma and Paraganglioma 245 during and after surgery are not uncommon. Risks are much higher for patients with unrecognized pheochromocytoma who undergo anesthesia for unrelated surgery. Multidisciplinary pre- operative evaluation and medical management before surgery are important. Once the diagnosis is confirmed, medical management for sur- gery preparation is recommended as resecting a pheochromocy- toma is a high-risk surgical procedure. Preoperative cardiac evaluation should include an electro- cardiogram (ECG) to evaluate for possible ischemic changes and rhythm disturbances as damage to the cardiovascular sys- tem is the most likely to impact on outcomes in patient requir- ing anesthesia. A number of medications commonly used in anesthesia should be avoided or used cautiously in patients with pheochromocy- toma. Metoclopramide is associated with hypertensive crisis and adrenergic myocarditis with cardiogenic shock in patients with pheochromocytoma. Phenothiazine derivatives, including droper- idol, haloperidol, and chlorpromazine, can result in hypotension in patients with pheochromocytoma. Glucagon has been shown to release catecholamines from the tumor and also linked with hypertensive crisis (Fig. 20.2). Early Postoperative The postoperative management usually requires an intensive care unit admission as once the tumor is removed the withdrawal of catecholamine effect will result in hypotension. The incidence of hypotension is variably described as 20–70% in various reports and may somewhat be dependent on the use of nature of preop- erative alpha-antagonist and intraoperative hypotensive agents. Fluid replacement and vasopressor infusion might be necessary in some patients. After tumor removal, sudden catecholamine with- drawal can lead to severe hypoglycemia, and blood sugar moni- toring, at least for the initial 12–24 h of the postoperative period, is recommended. 246 A. R. Ayala and M. A. Jara Hemodynamics monitor blood pressure Blood glucose monitoring ICU admission Discontinuation of alpha Postopeative at least for 12–24h stimulation can lead to management hyperinsulinemia and hypoglycemia due to disappearance of B-cell suppression. Hydration IV fluids Discharge Instructions Inpatient-ward - Follow up appointment and contacts transfer - Laboratory assessment including BMP, 24 h urine free Blood pressure metanephrines in 2 weeks. monitoring Fig. 20.2 Algorithm 2 Postoperative management of pheochromocytoma 20 Pheochromocytoma and Paraganglioma 247 Special Circumstances The Pregnant Patient Pheochromocytoma has a reported incidence of <0.2 per 10,000 pregnancies. Although a rare disorder, untreated, it carries a risk of mortality for both mother and fetus. Pheochromocytomas have the ability to produce signs and symptoms that mimic other forms of hypertension, including the new-onset hypertensive syndromes in pregnancy, gestational hypertension, and preeclampsia. It may become overt during pregnancy because of increases in intra- abdominal pressure, fetal movements, uterine contractions, the process of delivery, an abdominal surgical intervention, and even general anesthesia. The diagnosis is based on the results of 24-h urinary fraction- ated metanephrines and/or plasma fractionated metanephrines. MRI without gadolinium is the preferred imaging modality for localization as it locates adrenal and extra-adrenal masses and requires no radiation. The management has primary goal to prevent hypertensive cri- sis. Medical treatment with α-blockers must be started as soon as the diagnosis is confirmed and should be given for 10–14 days. The drug of choice is phenoxybenzamine (pregnancy class C), followed by a β-blocker if necessary. Phenoxybenzamine crosses the placenta and may cause perinatal depression in the mother and transient hypotension in the neonate; however, it has been described as generally safe for the fetus. Methyldopa is not rec- ommended, because it may worsen the symptoms of pheochro- mocytoma. Cesarean section is the preferred mode of delivery since it appears to carry less risk of maternal death than vaginal delivery. The definitive treatment is surgery, and tumor resection can be completed either before 24 weeks, as second trimester is the safest period to do surgery during pregnancy, or a few weeks later after uterine involution. The ICU Patient Because critical illness results in a hyperadrenergic state, mea- surements of catecholamines and metanephrines are rarely helpful in the ICU setting. Furthermore, vasoactive amines and 248 A. R. Ayala and M. A. Jara antiarrhythmics may also interfere with diagnostic testing. Therefore, a CT of the abdomen with emphasis on the adrenal gland may be the most convenient test in this situation, as most pheochromocytomas are large (4–5 cm) and have distinct imag- ing characteristics. Renal Failure Measurements of urinary catecholamines and metabolites are less reliable if the patient has advanced kidney disease. In addition, serum chromogranin A levels have poor specificity in these patients. There is very limited literature in this regard. However, one study by Eisenhofer G et al. found that in renal failure, there are up to twofold higher plasma concentrations of catecholamines and free metanephrines. Suggested Reading Amar L, Bertherat J, Baudin E, Ajzenberg C, Bressac-de Paillerets B, Chabre O, et al. Genetic testing in pheochromocytoma or functional paragangli- oma. J Clin Oncol. 2005;23(34):8812–8. Barrett C, van Uum SH, Lenders JW. Risk of catecholaminergic crisis follow- ing glucocorticoid administration in patients with an adrenal mass: a lit- erature review. Clin Endocrinol (Oxf). 2015;83(5):622–8. Davison AS. Biochemical investigations in laboratory medicine. Physiological effects of medications on plasma/urine metanephrines. Newcastle upon Tyne NHS Foundation Trust. http://www.pathology. leedsth.nhs.uk/dnn_bilm/Misc/Effectofdrugsonmetanephrines.aspx. Eisenhofer G, Peitzsch M. Laboratory evaluation of pheochromocytoma and paraganglioma. Clin Chem. 2014;60(12):1486–99. Eisenhofer G, Rivers G, Rosas AL, Quezado Z, Manger WM, Pacak K. Adverse drug reactions in patients with pheochromocytoma: incidence, prevention and management. Drug Saf. 2007;30(11):1031–62. Lenders JW, Duh QY, Eisenhofer G, Gimenez-Roqueplo AP, Grebe SK, Murad MH, et al. Pheochromocytoma and paraganglioma: an endocrine society clinical practice guideline. Endocrine Society. J Clin Endocrinol Metabol. 2014;99(6):1915–42. Manger WM, Gifford RW. Pheochromocytoma. J Clin Hypertens (Greenwich). 2002;4(1):62–72. Pacak K. Preoperative management of the pheochromocytoma patient. J Clin Endocrinol Metabol. 2007;92(11):4069–79. 20 Pheochromocytoma and Paraganglioma 249 Pacak K, Eisenhofer G, Ahlman H, Bornstein SR, Gimenez-Roqueplo AP, Grossman AB, et al. International Symposium on Pheochromocytoma. 2005 Pheochromocytoma: recommendations for clinical practice from the First International Symposium. Nat Clin Pract Endocrinol Metab. 2007;3(2):92–102. Primary Aldosteronism 21 Alejandro Raul Ayala and Mark Anthony Jara Contents Diagnostic Considerations 252 Inpatient Testing for Hyperaldosteronism 252 Factors Affecting Aldosterone/Renin Ratio 253 Special Considerations: Cortisol Co-secretion 254 Disease Subtyping 254 Treatment 255 Early Postoperative Period 255 Special Considerations 256 Primary Hyperaldosteronisms and Pregnancy 256 The Patient with Chronic Kidney Disease 257 Familial Hyperaldosteronism: Contact with the Family Members 258 Suggested Reading 260 A. R. Ayala (*) University of Miami, Miller School of Medicine, Department of Endocrinology and Metabolism, Miami, FL, USA e-mail: aayala2@miami.edu M. A. Jara University of Miami, Miller School of Medicine, Division of Endocrinology and Metabolism, Miami, FL, USA e-mail: maj158@med.miami.edu © Springer Nature Switzerland AG 2020 251 R. K. Garg et al. (eds.), Handbook of Inpatient Endocrinology, https://doi.org/10.1007/978-3-030-38976-5_21 252 A. R. Ayala and M. A. Jara |
Diagnostic Considerations Primary aldosteronism (PA) is the most common cause of endo- crine hypertension. Patients with PA have higher cardiovascular morbidity and mortality compared with age- and sex-matched patients with essential hypertension and the same degree of blood pressure elevation. Case detection screening should be considered in patients with: • Spontaneous hypokalemia, including patients treated with low-dose thiazide diuretics. However, there are patients with primary mineralocorticoid excess who are normokalemic and rarely some who are hypokalemic but normotensive. Only 9–37% of patients with primary aldosteronism are hypokalemic. • Severe or resistant hypertension to three conventional antihypertensive drugs (including a diuretic) or controlled BP (<140/90 mm Hg) requiring four or more antihyperten- sive drugs. • Patients with hypertension and adrenal incidentaloma. • Hypertension and a family history of early-onset hypertension or cerebrovascular accident at a young age (<40 years). • Hypertensive first-degree relatives of patients with PA. Inpatient Testing for Hyperaldosteronism The recommended case detection-screening test is the plasma aldosterone activity (PAC)/plasma renin activity (PRA). An elevated plasma aldosterone activity (PAC)/plasma renin activity (PRA) ratio and an increased PAC are required for the diagnosis of primary aldosteronism. • PAC is inappropriately high for the PRA, usually >15 ng/dL. • PAC/PRA ratio greater than 20. Collecting blood midmorning from seated patients following 2–4-h upright posture improves sensitivity. 21 Primary Aldosteronism 253 In the setting of spontaneous hypokalemia, plasma renin below detection levels plus plasma aldosterone concentration (PAC) >20 ng/dL, further confirmatory testing might not be needed. Confirmatory Testing Usually, elevated PAC/PRA ratio alone does not establish the diagnosis of primary aldosteronism, and the results have to be confirmed by demonstrating inappropriate aldo- sterone secretion, except in situations as spontaneous hypokale- mia, undetectable PRA or PRC, and a PAC >20 ng/dL. Otherwise, aldosterone suppression testing is needed with one of several tests (table of confirmatory test). The patient that presents with hypertensive crisis despite the use of multiple antihypertensives should be screened for primary hyperaldosteronism. Factors Affecting Aldosterone/Renin Ratio False Negatives Genrally limited to the mineralocorticoid recep- tor antagonists, spironolactone and eplerenone. While dietary salt restriction, concomitant malignant or renovascular hypertension, pregnancy, and treatment with diuretics (including spironolactone), dihydropyridine calcium blockers, angiotensin-converting enzyme inhibitors, and angiotensin receptor antagonists can stimulate renin, they generally do not have a sufficiently potent effect to interfere with diagnosing PA. False Positives Beta-blockers, alpha-methyldopa, clonidine, and nonsteroidal anti-inflammatory drugs suppress renin, raising the ARR with potential for false positives. False positives can also occur in patient with advanced age and renal disease. In general, medications other than the minetarlocorticoid antagonists do not need to be discontinued before ARR measure- ment. However, when the diagnosis is not clear, the interfering medications should be discontinued at least 2 weeks before ARR measurement; diuretics should be discontinued ideally 6 weeks before the test, although this is inconvenient, potentially harmful and rarely feasible. Some patients will require substitution of the 254 A. R. Ayala and M. A. Jara interfering medication during the w ashout period until the test is completed. Doxazosin and fosinopril can be used in hypertensive patients who need to undergo aldosterone and PRA measurement for the diagnosis of primary aldosteronism; amlodipine yields a small percentage of false-negative diagnoses, and beta-blockers may only have limited influence on the diagnosis of primary aldo- steronism as they lower PRA and PRC measurements and raise the PAC/PRA ratio, an effect that in most settings is not clinically significant. Other potassium- sparing diuretics, such as amiloride and triamterene, usually do not interfere with testing unless the patient is treated with high doses. Special Considerations: Cortisol Co-secretion There is an increasing awareness of cortisol co-secretion in the context of primary hyperaldosteronism resulting from adrenal tumors. Overt or subtle glucocorticoid hypersecretion may poten- tially interfere with diagnostic studies or result in secondary/ter- tiary adrenal insufficiency after surgical removal of the tumor because of contralateral gland suppression. Patients with adrenal tumors, including those with confirmed hyperaldosteronism, should also be evaluated for hypercortisolism with a 1 mg dexa- methasone suppression test. Disease Subtyping Once the diagnosis of primary hyperaldosteronism has been confirmed, unilateral adenoma or rarely carcinoma must be distinguished from bilateral disease. Disease subtyping is established using adrenal computed tomography (CT) and adrenal vein sampling (AVS) (algorithm). Adrenal vein sam- pling is used to distinguish between unilateral adenoma and bilateral hyperplasia, and it is recommended to confirm unilat- 21 Primary Aldosteronism 255 eral secretion for patients who would likely pursue surgical management. Treatment The curative treatment is surgical: unilateral laparoscopic adre- nalectomy for patients with documented unilateral PA or unilat- eral adrenal hyperplasia. Medical treatment is preferred in patients who are unable or unwilling to undergo surgery or who have bilateral adrenal disease. Mineralocorticoid receptor antagonists are the medical treatment of choice. Spironolactone is the primary agent at doses ranging from 25 to 400 mg/d, with eplerenone as an alternative. Antiandrogen side effects such as gynecomastia and diminished libido in men and menstrual disorders in women can result from spironolactone due to cross-antagonism of the sex steroid receptor. Eplerenone is more specific for the aldosterone receptor and therefore causes less unde- sired side effects but is less potent than spironolactone. In a study comparing these two therapies, spironolactone at doses ranging from 75 to 225 mg/d was more efficacious than eplerenone at doses between 100 and 300 mg/d for hypertension control. Biochemical cure following adrenalectomy as well as hemodynamic improve- ment is seen in over 90% of patients. Hypokalemia typically resolves immediately after surgery, and blood pressure reduction may take months, prompting a reduction in quantity of antihyper- tensive medications in most patients. Early Postoperative Period We suggest the measurement of aldosterone and PRA on the first and second postoperative day. A significant decrease in serum aldosterone levels is detected a few hours after adrenal clipping is performed during adrenalectomy, although plasma renin activity may take weeks to normalize. 256 A. R. Ayala and M. A. Jara In general, when the unilateral adrenalectomy is successful, aldosterone levels achieve a nadir within 24–48 h after the inter- vention, suggesting cure. After surgery, mineralocorticoid recep- tor antagonists should be withdrawn in the first postoperative day to avoid hyperkalemia. Antihypertensives should be administered base on the patient’s postoperative blood pressure readings. One should expect a significant reduction in the number of antihyper- tensives and dosing in most cases. On occasion, normotension is observed in the early postoperative period, particularly in younger patients with less severe preoperative hypertension, although blood pressure normalization may take up to a year to occur. Unless the patient is persistently hypokalemic, postopera- tive hydration should include normal saline without potassium with careful monitoring of renal function, as a decrease in GFR is often seen following resolution of hyperaldosteronism, a con- dition that results in glomerular hyperfiltration. Preoperative renal damage as revealed by elevated serum creatinine and microalbuminuria are significant predictors of postoperative hyperkalemia (hypoaldosteronism). Hence, the combination of worsening renal function and post- surgical hypoaldosteronism that occurs in cured patients treated with unilateral adrenalectomy may result in severe hyperkalemia, requiring close attention not only in the early postoperative period but also following discharge. Because the hypoaldosteronism may be prolonged, we recommend at least weekly electrolyte and renal function testing during postsurgical month, as a minimum. Special Considerations Primary Hyperaldosteronisms and Pregnancy Primary aldosteronism is uncommon in pregnancy, with only few cases reported in the literature, most of them due to aldosterone- producing adenomas. Primary aldosteronism can lead to 21 Primary Aldosteronism 257 intrauterine growth retardation, preterm delivery, intrauterine fetal demise, and placental abruption. The evaluation in the pregnant woman is the same as for non- pregnant patients. For case confirmation, however, the captopril stimulation test is contraindicated in pregnancy, but measurement of sodium and aldosterone in a 24-h urine collection is an option. Subtype testing with abdominal magnetic resonance imaging (MRI) without gadolinium is the test of choice. Computed tomography (CT) and adrenal venous sampling are contraindi- cated in pregnancy. Hypertension may improve or worsen in pregnancy due to the agonist/antagonist function of progesterone on the mineralocorti- coid receptor. The treatment depends on the case presentation including med- ical or surgical options: • Unilateral laparoscopic adrenalectomy during the second tri- mester in clear cases of tumors of >1 cm. • Spironolactone crosses the placenta and is a US Food and Drug Administration (FDA) pregnancy category C (Not proven safe in pregnancy), and eplerenone is an FDA pregnancy category B (There are no adequate and well-controlled studies in preg- nant women. Should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus). Therefore, standard antihypertensive drugs approved for use during pregnancy should be used. • Hypokalemia can be managed with oral potassium supplements. The Patient with Chronic Kidney Disease The diagnosis of primary hyperaldosteronism could be challeng- ing in patient with chronic kidney disease (CKD) as this may 258 A. R. Ayala and M. A. Jara disturb the renin-angiotensin-aldosterone system. The diagnosis of primary PA in the CKD population has not been established as plasma aldosterone concentration, PRA, and ARR can vary sig- nificantly in CKD. As CKD progresses, PAC increases, and the more advanced the CKD, the lesser the effect on PRA, giving rise to a higher ARR. Also in a study, primary aldosteronism patients accompanying chronic kidney disease had high serum aldoste- rone and ARR levels, low PRA, and no clear association of hypokalemia. Familial Hyperaldosteronism: Contact with the Family Members Familial hyperaldosteronism is a group of inherited conditions inhered in an autosomal dominant pattern. Three familial forms of PA have been described: • FH type I or glucocorticoid-remediable aldosteronism, usually associated with bilateral adrenal hyperplasia. • FH type II is not dexamethasone suppressible. • FH type III is caused by germ line mutations in the potassium channel subunit KCNJ5, mostly suspected in patient with mas- sive adrenal hyperplasia and children. The patient and their family should receive appropriate information as well as appropriate counseling for biochemical screening of family members; continuously updated databases of human genes and genetic disorders and traits like OMIM or MalaCards are excellent free educational resources (Fig. 21.1). 21 Primary Aldosteronism 259 - BMP once - Low plasma a week for Unilateral aldosterone four weeks.* adrenalectomy - Reassess BP - Reassess control and BP control Measure: antihypertensive (home Is - Plasma Aldosterone on regime monitoring) adrenalectomy day 2 post surgery Unilateral desired or the disease Preoperative Postoperative - Potassium level, patient a YES management management creatinine candidate? - Discontinue MRA to avoid hyperkalemia - BP control with PRN - Blood pressure antihypertensive (i.e Primary NO - Possiblecontrol: Start MRA hydralazine) aldosteronism persistent- Potassium - Hydration with normal confirmed disease,supplementation if saline (with potassium if Repeat hypokalemic. persistently hypokalemic) plasma Plasma aldosterone >5 aldosterone Start treatment with MRA ng/dl (PRA) and - Spironolactone: 50–400 mg/day Bilateral BMP in one - Eplerenone: if sides effects disease week. (gynecomastia,erectile dysfunction) 50–200 mg/day * May require prolonged monitoring for persistent contraltaeral adrenocorticol supression (hypoaldosteronism) MRA: Mineralocorticoid receptor antagonist BP: Blood pressure PRA: Plasma renin activity Fig. 21.1 Algorithm: inpatient management of primary hyperaldosteronism 260 A. R. Ayala and M. A. Jara Suggested Reading Funder JW, Carey RM, Fardella C, Gomez-Sanchez CE, Mantero F, Stowasser M, Endocrine Society, et al. Case detection, diagnosis, and treatment of patients with primary aldosteronism: an Endocrine Society clinical prac- tice guideline. J Clin Endocrinol Metabol. 2008;93(9):3266–81. https:// doi.org/10.1210/jc.2008-0104. Funder JW, Carey RM, Mantero F, Murad MH, Reincke M, Shibata H, et al. The management of primary aldosteronism: case detection, diagnosis, and treatment: an endocrine society clinical practice guideline. J Clin Endocrinol Metabol. 2016;101(5):1889–916. https://doi.org/10.1210/ jc.2015-4061. Keuer B, Ayala AR, Pinto P. The role of intra- and postoperative serum aldo- sterone levels following adrenalectomy for primary aldosteronism. 64th Annual Meeting of the American Urologic Association (Mid-Atlantic Section), Washington, DC, October 12–15 2006. Mulatero P, Rabbia F, Milan A, Paglieri C, Morello F, Chiandussi L, Veglio F. Drug effects on aldosterone/plasma renin activity ratio in primary aldo- steronism. Hypertension. 2002;40(6):897–902. Parthasarathy HK, Ménard J, White WB, Young WF Jr, Williams GH, Williams B, et al. A double-blind, randomized study comparing the anti- hypertensive effect of eplerenone and spironolactone in patients with hypertension and evidence of primary aldosteronism. J Hypertens. 2011;29(5):980–90. https://doi.org/10.1097/HJH.0b013e3283455ca5. Rossi GP, Auchus RJ, Brown M, Lenders JW, Naruse M, Plouin PF, et al. An expert consensus statement on use of adrenal |
vein sampling for the sub- typing of primary aldosteronism. Hypertension. 2014;63(1):151–60. https://doi.org/10.1161/HYPERTENSIONAHA.113.02097. Savard S, Amar L, Plouin PF, Steichen O. Cardiovascular complications asso- ciated with primary aldosteronism. A controlled cross-sectional study. Hypertension. 2013;62(2):331–6. https://doi.org/10.1161/ HYPERTENSIONAHA.113.01060. Stowasser M, Ahmed AH, Pimenta E, Taylor PJ, Gordon RD. Factors affect- ing the aldosterone/renin ratio. Horm Metab Res. 2012;44(3):170–6. https://doi.org/10.1055/s-0031-1295460. Young WF. Primary aldosteronism: renaissance of a syndrome. Clin Endocrinol (Oxf). 2007;66(5):607–18. Treatment of Hyperglycemia 22 in a Hospitalized Patient Without Hyperglycemic Emergency Rajesh K. Garg Contents Obtain HbA1c Unless Available Within Last 3 Months 262 Assess Preadmission Diabetes Status and Antidiabetic Treatment 262 Assess Current Nutritional Status 262 Assess Other Medications That May Affect Glycemic Status 263 Point of Care (POC) Blood Glucose (BG) Monitoring 263 Insulin Infusion in Critically Ill Patients, Intraoperatively or During Labor/Delivery 264 Critically Ill Patients in Intensive Care Units 264 Labor and Delivery 264 Order Correctional Insulin 265 Order Basal Insulin Therapy 265 Order Nutritional Insulin Therapy 266 Order Hypoglycemia Protocol 267 R. K. Garg (*) Division of Endocrinology, Diabetes and Metabolism, University of Miami Miller School of Medicine, Coral Gables, FL, USA e-mail: rgarg@miami.edu © Springer Nature Switzerland AG 2020 261 R. K. Garg et al. (eds.), Handbook of Inpatient Endocrinology, https://doi.org/10.1007/978-3-030-38976-5_22 262 R. K. Garg Continue Insulin Pump if Patient Can Manage the Pump: Otherwise, Switch to Basal Bolus Insulin 267 Review Blood Glucose (BG) Data Daily and Adjust Insulin Doses to Achieve Target BG Levels 268 Evaluate Diabetes Treatment at Time of Discharge 268 Follow-Up After Discharge 269 Suggested Reading 269 Obtain HbA1c Unless Available Within Last 3 Months All hyperglycemic patients should get an HbA1c at the time of admission. HbA1c helps in diagnosing new-onset diabetes or assessing the preadmission diabetes control. It also helps in advis- ing antidiabetic treatment at the time of discharge. Assess Preadmission Diabetes Status and Antidiabetic Treatment If possible, a detailed history including the duration of diabetes, type of diabetes, presence of complications of diabetes, and pre- admission diabetes treatment, especially the use of insulin, should be obtained. A focused physical examination assessing body weight, presence of neuropathy, and peripheral vascular disease should be conducted. Assess Current Nutritional Status Many hospitalized patients are rendered nothing per-oral (NPO) at the time of admission due to an impending surgery or a diag- nostic procedure or simply due to inability to eat. Make a note of the reason for NPO status and expected duration for this order. 22 Treatment of Hyperglycemia in a Hospitalized Patient… 263 Assess whether the patient will be able to swallow after lifting the NPO status and what type of foods are likely to be swallowed. Any special restrictions or additional requirements for food should be noted. Patients requiring special supplements in- between regular meals may require a modified insulin regimen. If a patient is getting enteral tube feed, note the content, rate, and times of tube feed. Similar data need to be collected for parenteral nutrition. Assess Other Medications That May Affect Glycemic Status Most hospitalized are likely to be receiving one or more medica- tions that can potentially affect BG levels. Most important medi- cations are agents like norepinephrine, dopamine, and glucocorticoids. If possible, medications for intravenous (IV) infusion should be prepared in glucose-free solutions rather than in dextrose water. Point of Care (POC) Blood Glucose (BG) Monitoring BG monitoring is often obtained using POC BG monitoring devices and is adequate for glycemic management in hospital- ized patients. However, in the intensive care unit (ICU) setting, arterial blood glucose monitoring may be available if blood oxy- gen is being monitored at the same time. In a patient eating regu- lar meals, BG monitoring should be ordered before meals and bedtime. In all other situations, blood glucose should be moni- tored at least every 6 h. More frequent monitoring may be appro- priate in critically ill patients or in a rapidly changing clinical situation. POC monitoring devices are less accurate at low BG levels. Therefore, any BG value less than 70 mg/dl should be confirmed by sending a sample for plasma glucose to the central laboratory. 264 R. K. Garg Insulin Infusion in Critically Ill Patients, Intraoperatively or During Labor/Delivery Critically Ill Patients in Intensive Care Units Most critically ill patients are NPO and have a rapidly changing clinical condition. The same may apply to some patients intraop- eratively. Therefore, insulin infusion is the preferred treatment for these patients. All hospitals with an ICU should have an approved insulin infusion protocol that the entire ICU staff are familiar with. It is always better to order continuous insulin infu- sion using hospital approved protocol. Blood glucose should be monitored every 1–4 h and insulin infusion rate adjusted using an algorithm that takes into account the current insulin infusion rate, current BG levels, and the rate of rise or fall of BG level. Blood glucose targets may vary from one hospital to another but are usually in a range of 100–180 mg/dL. As the clinical condition improves, patients should be transitioned from insulin infusion to basal bolus insulin therapy. In most hospitals, general floors are not equipped to administer insulin infusion. Therefore, it is important to switch to basal-bolus insulin before the patient leaves the ICU. Labor and Delivery Hyperglycemia during labor and delivery increases the risk of hypoglycemia in the newborn because of beta cell stimulation by glucose diffusing from the placenta. Therefore, tight glycemic control with BG target 70–110 mg/dL is recommended during labor and delivery. Most women with pregestational type 1 diabe- tes require insulin and glucose infusion to maintain glycemic con- trol. Women with type 2 diabetes and those with gestational diabetes may or may not require insulin infusion, but they need to be monitored hourly. 22 Treatment of Hyperglycemia in a Hospitalized Patient… 265 Order Correctional Insulin Correctional insulin therapy, also called sliding scale insulin therapy, is ordered for almost all hospitalized patients with hyperglycemia who are not on an insulin infusion protocol. There has been much criticism of using correctional insulin alone in a patient with diabetes. It leads to highly fluctuating blood glucose levels with high risk of both hypoglycemia and hyperglycemia. Moreover, in a patient with type 1 diabetes or insulin-requiring type 2 diabetes, using sliding scale insulin alone can be danger- ous because of the risk of diabetic ketoacidosis or hyperosmolar state. Therefore, correctional insulin therapy alone should be avoided, and it should be ordered along with basal or basal-bolus insulin therapy. However, in a non-insulin-dependent patient with mildly high BG levels after admission, it may be appropri- ate to order correctional insulin alone for 1–2 days while assess- ing the need for basal and nutritional insulin. Correctional insulin doses should be administered after each POC BG testing and, if possible, combined with nutritional insulin doses. Thus, insulin formulation used for correctional insulin should be the same as used for nutritional insulin. Correctional insulin doses should be administered in proportion to the total daily insulin doses: a lower scale for patients with total daily dose of insulin <40 units, medium scale for patients with total daily dose of insulin 41–80 units, and higher scale for those with total daily dose of insulin >80 units/day. Avoid using correctional insulin more fre- quently than every 4 h to prevent the stacking effect that often leads to hypoglycemia. Order Basal Insulin Therapy Most hyperglycemic patients should receive basal insulin ther- apy in the hospital. Basal insulin can be an intermediate-acting insulin used twice daily or a long-acting insulin used once daily. Long- acting insulin may be administered in the morning or at 266 R. K. Garg bedtime. The dose of basal insulin can be decided on the basis of preadmission insulin needs or current insulin needs if on IV insu- lin infusion or body weight. In a patient with good glycemic con- trol on insulin at home, total daily dose of insulin may be divided into 50% as basal insulin and 50% as the nutritional insulin need. In general, 80% of the preadmission basal insulin need is an appropriate starting dose. However, full dose or even a higher dose may be used if the admission HbA1c was high. In a patient coming off an insulin drip, insulin infusion rates in the last few hours may guide the basal insulin dose. However, if no informa- tion is available, weight-based basal insulin dose starting at 0.25 unit/kg is appropriate. Order Nutritional Insulin Therapy Once a patient starts receiving nutrition, insulin coverage is needed. Nutritional insulin coverage depends on the type of nutri- tion and it should be customized for each patient. If the patient is on an insulin infusion protocol, insulin infusion rates may be adjusted to cover all the nutritional insulin needs. For parenteral nutrition, regular insulin may be added to the IV nutrition. However, mostly the patients are switched to subcutaneous insu- lin when they start receiving enteral nutrition. In a patient eating regular meals, nutritional insulin doses may be assessed from the total daily dose of insulin and given as three equal premeal doses of a short-acting insulin. Nutritional insulin should be held if a meal is missed. It may be administered after a meal if oral intake is unreliable and reduced in proportion to the food intake. In a patient unable to eat regular meals but able to ingest semisolids or liquids, rapid-acting insulin is given before each meal. In a patient receiving tube feeds, rapid-acting insulin every 4 h or regular insulin every 6 h should be used during the duration of tube feeds. Often a much higher nutritional insulin coverage is needed with tube feeds than with regular meals. In a patient on bolus tube 22 Treatment of Hyperglycemia in a Hospitalized Patient… 267 feeds, a rapid-acting insulin dose at the time of each bolus of tube feed should be ordered. Order Hypoglycemia Protocol All patients on insulin should have an order for hypoglycemia protocol. Treatment for hypoglycemia should start at BG level <70 mg/dL. Any low BG value should be confirmed by sending a stat plasma glucose test unless the patient is symptomatic in which case treatment should be administered immediately. If patients are able to eat, give 4 ounces of juice, non-diet soda, or 8 ounces of nonfat milk. If unable to eat but an IV line is in place, give dex- trose 50% 1 ampule (25 g). If unable to take orally and no IV line is in place, give glucagon HCl 1 mg IM. Check BG every 15–30 min and repeat one of the three treatments till BG level is above 80 mg/dL. Continue Insulin Pump if Patient Can Manage the Pump: Otherwise, Switch to Basal Bolus Insulin Many patients with type 1 diabetes and some with type 2 diabetes may be using insulin pump before admission to hospital. Evaluate patients’ proficiency with insulin pump, their clinical condition to manage their own pump, and the availability of pump supplies. If all conditions are ideal, i.e., the patient is well educated about insulin pump use and clinically (mentally and physically) able to take care of pump and can provide all their supplies for the pump, insulin pump can be continued as inpatient. Basal rates may need to be lowered (generally to about 80% of home dose) to prevent hypoglycemia. If the patient becomes unable to manage pump at any time during hospitalization, he/she should be switched to basal bolus insulin. 268 R. K. Garg Review Blood Glucose (BG) Data Daily and Adjust Insulin Doses to Achieve Target BG Levels It is important to review BG data at least once daily and adjust insulin doses to achieve target BG levels and to prevent hypogly- cemia. Basal insulin should be adjusted to keep the fasting BG <140 mg/dL, and nutritional insulin should be adjusted to main- tain all other BG levels in 100–180 range. Insulin doses should be increased by 10–20% at a time to produce a meaningful effect. A rapid increase in insulin dose may be appropriate depending on the clinical condition and BG levels. Any BG value <100 mg/dL in the previous 24 h should lead to a decrease in insulin dose to prevent hypoglycemia. Any BG <70 mg/dL or symptomatic hypo- glycemia should lead to immediate reevaluation to prevent recur- rence of hypoglycemia. Evaluate Diabetes Treatment at Time of Discharge Clinical condition may |
have changed during hospitalization necessitating changes to preadmission treatment for diabetes. Additionally, changes to diabetes treatment may be indicated due to poor preadmission diabetes control. In general, if HbA1c was <7% at time of admission, the patient should be discharged on the pre-hospitalization treatment. If HbA1s was 7–8%, adjust the pre- hospitalization treatment without making drastic changes to treat- ment. For example, doses of non-insulin agents or insulin may be increased or decreased, but avoid adding additional antidiabetic agents. An HbA1c >8% suggests that changes in treatment are needed but it depends on the glycemic goal for an individual patient. If a change in antidiabetic medications is made, the patient and the outpatient diabetes care provider should be informed of the change and the rationale for it, and a follow-up plan must be developed. 22 Treatment of Hyperglycemia in a Hospitalized Patient… 269 Follow-Up After Discharge Discharge plan should include a timely follow-up visit for contin- ued outpatient diabetes care. An appointment should be made for the patient to see their diabetes care providers within 7–30 days of discharge. Because glycemic control is expected to change after discharge, make sure that the patient is able to contact a diabetes care provider in case of high or low blood glucose levels. Suggested Reading American Diabetes Association. 14. Diabetes care in the hospital. Diabetes Care. 2017;40(Suppl 1):S120–7. Garg R, Hudson M, editors. Hyperglycemia in the hospital setting. New Delhi: JP Brothers; 2014. Umpierrez GE, Hellman R, Korytkowski MT, Kosiborod M, Maynard GA, Montori VM, et al. Management of hyperglycemia in hospitalized patients in non-critical care setting: an endocrine society clinical practice guide- line. J Clin Endocrinol Metabol. 2012;97(1):16–38. Hypoglycemia in Patients 23 with Diabetes Margo Hudson Contents Questions to Ask When a Patient with Diabetes Has Hypoglycemia in the Hospital 272 Defining Hypoglycemia in the Inpatient Setting 272 Detecting Hypoglycemia 272 Frequency of Hypoglycemia in Patients Treated with Insulin 273 Deleterious Effects of Hypoglycemia 274 Identifying Patients Most at Risk for Hypoglycemia 274 Insulin Action 276 Initial Dosing of Insulin to Avoid Hypoglycemia 276 What to Do When Hypoglycemia Occurs 279 Hospital Surveillance and Reporting: Glucometrics 280 Beyond Basal-Bolus Insulin: Glucose Control Without Hypoglycemia 280 Suggested Reading 281 M. Hudson (*) Brigham and Women’s Hospital, Department of Endocrinology, Hypertension and Diabetes, Boston, MA, USA e-mail: mhudson@partners.org © Springer Nature Switzerland AG 2020 271 R. K. Garg et al. (eds.), Handbook of Inpatient Endocrinology, https://doi.org/10.1007/978-3-030-38976-5_23 272 M. Hudson Questions to Ask When a Patient with Diabetes Has Hypoglycemia in the Hospital • Has the patient received insulin or sulfonylurea agent to cause hypoglycemia? • Does the patient have an underlying condition predisposing to hypoglycemia such as renal or hepatic failure or advanced age? • Was the insulin dose weight based or home dose? • Are eating habits different in the hospital compared to home? • Was prandial insulin mismatched to meal time or meal size? • Were continuous tube feedings or TPN held or decreased? • Was correctional insulin “stacked”? • Were glucose checks done at correct times? • Has there been a decrease in medications that cause hypergly- cemia such as glucocorticoids or vasopressors? • Does the hospital have systems in place to help detect, treat, and prevent hypoglycemia? Defining Hypoglycemia in the Inpatient Setting Inpatient hypoglycemia has previously been defined as any glu- cose <70 mg/dl (3.9 mmol/l) and severe hypoglycemia as glucose <40 mg/dl (2.2 mmol/l) independent of symptoms. However, as of 2017, the American Diabetes Association has modified the defini- tion which now applies to inpatients and outpatients. Level 1 hypoglycemia is any glucose ≤70 mg/dL which is sufficiently low to warrant acute treatment with fast-acting carbohydrate as well as to adjust therapy to prevent in the future. Level 2 hypoglycemia is any level <54 mg/dL (3.0 mmol/l) which is sufficiently low to be considered serious and clinically important. Level 3 hypogly- cemia is any glucose low enough to cause severe cognitive impair- ment which requires external assistance. Detecting Hypoglycemia Frequent glucose monitoring is required to detect hypoglycemia with use of insulin. Point of care (POC) testing provides immedi- ate actionable results. Glucose values obtained with venous 23 Hypoglycemia in Patients with Diabetes 273 blood draws sent to the lab are generally less helpful than POC because of the significant time delay for resulting as well as a tendency for glucose levels to decrease in the tube unless sodium fluoride has been added to inhibit glycolysis. However, some medical conditions such as extremes of hematocrit and periph- eral ischemia may render POC testing less accurate and require venous draws. With IV insulin protocols, monitoring should be done at least every 1–2 h. With subcutaneous insulin, monitoring is usually at least four times a day: at meals and bedtime when patients are eating and every 6 h when they are NPO. In the inpa- tient setting, it is important to remember that patients may not manifest usual symptoms of hypoglycemia because of concomi- tant use of drugs that mask symptoms or diminished cognition from underlying medical conditions, so vigilance is important in detecting hypoglycemia. Frequency of Hypoglycemia in Patients Treated with Insulin Rates of hypoglycemia vary by severity of underlying condition (critical or noncritical), type of glycemic treatment (intravenous insulin or basal-bolus insulin or sliding scale alone), and target glucose range. In the Normoglycemia in Intensive Care Evaluation- Survival Using Glucose Algorithm Regulation (NICE- SUGAR) study, patients in the ICU were randomized to IV insu- lin targeting glucose of 80–110 mg/dl or 140–180 mg/dl. Nearly 7% of the patients with the lower glucose targets had at least one episode of BG below 40 mg/dl which was significantly greater than the less than 1% rate in the patients in the higher target range. In another study on a general surgical ward, patients with diabetes were randomized to basal-bolus insulin or sliding scale alone with glucose target ranges of 100–140 mg/dl in both groups. In the basal-bolus group, the mean glucose was 145 mg/dl, and in the sliding-scale-alone group, the mean glucose was 175 mg/dl. Incidence of glucose <70 mg/dl was 23% in the basal-bolus group and 4.7% in the sliding scale group. And, a third study looking at insulin dosing found that rates of hypoglycemia are greater with total daily doses of insulin exceeding 0.6 units/kg/day compared to lower doses. The implication of these studies is not to use 274 M. Hudson sliding scale alone rather than basal-bolus or IV insulin but rather to use basal-bolus therapy or IV insulin with appropriate targets and methods for dose calculation. In order to reduce potential for hypoglycemia, most professional society guidelines suggest glu- cose target goals should be fasting 100–140 mg/dL, premeal <140 mg/dL, and random <180 mg/dL on the general medical ward and 140–180 mg/dl in the ICU setting. Deleterious Effects of Hypoglycemia Hypoglycemia in the inpatient setting is strongly associated with higher mortality. In a review of general ward patients with diabe- tes, each day with any BG <50 mg/dl was associated with an 85% increase in inpatient death, 65% increase in 1-year mortality, and 2.5 extra days of hospitalization. In another retrospective study, inpatients on insulin with an episode of hypoglycemia (BG <50 mg/dl) had an in-hospital mortality rate of 20.3% compared to 4.5% mortality rate in insulin-treated patients without hypogly- cemia. In the NICE-SUGAR study, ICU patients on the lower tar- get insulin drip protocol who had severe hypoglycemia (BG <40) had 79% higher mortality than patients on the same insulin drip protocol who did not experience hypoglycemia. In the subset of patients with diabetes, moderate hypoglycemia was associated with 58% higher mortality and severe hypoglycemia with 85% higher mortality than patients with diabetes who did not have hypoglycemia. Whether hypoglycemia is the driver of higher mortality or a marker of poor health, it is clear that it should be avoided if possible. Identifying Patients Most at Risk for Hypoglycemia Patients admitted to the hospital often have multiple medical problems. The elderly and patients with renal or hepatic failure are at high risk for hypoglycemia because of decreased gluconeo- genesis as well as decreased insulin metabolism. Another risk 23 Hypoglycemia in Patients with Diabetes 275 Table 23.1 High-risk 1. Change in nutrition situations for hypoglycemia (a) H olding TPN, tube feeds, or sudden NPO status (b) Patient off floor at meal time 2. Drop in steroid dose 3. Patients who are on pressors and iv insulin together who then have pressors decreased 4. Acute kidney or liver injury 5. Stress hyperglycemia treated with insulin when stress resolves group is patients with unusually high outpatient insulin doses (over 1 unit/kg/day total daily dose) which may indicate either noncompliance or excess caloric intake, both of which will be corrected in the hospital, and therefore giving 80% of the usual outpatient dose or recalculating with standard weight-based dos- ing may be prudent. Common inpatient situations that lead to an acute drop in insu- lin requirements are listed in Table 23.1. Change in nutrition is responsible for many episodes of hypoglycemia. Patients with insulin “on board” and who are on TPN or enteral tube feeds who have the feedings held or decreased or patients who are eating and are made NPO or do not eat a complete meal are particularly vul- nerable. Other common high-risk scenarios include patients on high-dose steroids who have the steroid dose dropped, patients on high insulin infusion rates due to vasopressors who have them tapered, and patients who develop acute renal, hepatic, or adrenal failure. Patients who are actually improving such as patients with sepsis or MI and secondary acute hyperglycemia (stress hyperglycemia) will see glucose levels drop and insulin require- ments decrease. Hypoglycemia should be anticipated in all these situations and insulin doses dropped preemptively to prevent hypoglycemia. When subcutaneous insulin has already been given, short-term IV glucose infusion may be necessary to avoid hypoglycemia. For patients on continuous tube feeds, for example, that are abruptly discontinued (e.g., patient pulls out NG tube), D5W at the rate of the tube feeds or D10 at half the rate of the tube feeds will usually 276 M. Hudson be adequate to avoid short-term hypoglycemia until beyond the period of active insulin action or the tube feeds can be restored. Communication between nursing and providers is essential to manage these situations that often are unpredictable. Insulin Action Medications that may contribute to hypoglycemia in the inpatient setting include drugs in the sulfonylurea class (glyburide, glipi- zide, glimepiride in the United States), meglitinides (usually repa- glinide), and all insulins. In general, use of oral agents is discouraged in the hospital because of unpredictable and pro- longed action, especially in the setting of hepatic or renal dys- function or interruption of nutritional patterns. Insulin is the most widely used medication to treat hyperglyce- mia in the inpatient setting because the many types of insulin offer a wide range of available action profiles to allow greater flexibility in dosing. However, insulin is also responsible for medication- induced hypoglycemia because of its narrow therapeutic window. Insulin action profiles are shown in Table 23.2. Patients are most at risk for hypoglycemia at the peak action of the insulin. When two types of insulin are used, hypoglycemic potential will be additive. Premixed insulin is not recommended in the hospital set- ting because the faster-acting and longer-acting components can- not be individually adjusted. When regular insulin is given IV either as a bolus or as a continuous drip, the impact is immediate and action can persist for up to an hour after the dose. Initial Dosing of Insulin to Avoid Hypoglycemia In patients naive to insulin who are admitted to the hospital, a framework for prescribing insulin is critical to assist in meeting glucose targets and avoid hypoglycemia. Weight; age; renal, hepatic, and pancreatic functions; and steroid use all impact insu- lin requirements. Generally insulin is prescribed using a combina- tion of intermediate- or long-acting insulin (basal) with short- or 23 Hypoglycemia in Patients with Diabetes 277 Table 23.2 Insulin action profiles (subcutaneously) Type of insulin Name Onset Peak Duration Rapid acting Aspart (Novolog) 5–15 min 1–2 h 4–6 h Lispro (Humalog) Glulisine (Apidra) Short acting Regular (Humulin R, 30–60 min 2–4 h 6–10 h Novolin R) Intermediate NPH (Humulin N, 2–4 h 6–12 h 12–18 h acting Novolin N) 30–60 min 2–4 h 6–8 |
h U-500 regular insulin (only for use in insulin-resistant patients) Long acting Glargine (Lantus) 2–4 h None 22–24 h Detemir (Levemir) 17–24 h Glargine (Toujeo) 6 h None 22–36 h Degludec (Tresiba) 1 h None 42 h Premixed NPH/regular (Humulin 30–60 min 2–12 h 12–18 h insulin 70/30, Novolin 70/30) Lispro protamine/lispro 5–15 min 1–2 h 12–18 h (Humalog 75/25, Humalog 50/50) Aspart protamine/aspart 5–15 min 1–2 h 12–18 h (Novolog 70/30) rapid-acting insulin (nutritional and correctional). The schema in Fig. 23.1 is a handy way to calculate the doses. For patients on TF or glucocorticoid treatment, consider using 60% of TDD as nutri- tional component rather than 50%. Correctional insulin (sliding scale) can be prescribed based on the calculated total daily dose so that if TDD is less than or equal to 40 units, use a correctional scale of 1 unit rapid-acting or short- acting insulin for every 50 mg/dl above goal. For TDD over 40 units a day, consider using 1 unit for every 25 mg/dl above goal. Correctional insulin is generally given with a rapid-acting insulin analog before meals and before bed in patients who are eating and with regular human insulin every 6 h in patients who are on continuous feedings, TPN, or NPO. Outside of hyperglyce- mic emergencies, correctional insulin should not be given more frequently than this to avoid hypoglycemia from overlapping the 278 M. Hudson a Baseline weight-based TDD 0.5 unit/kg/day, adjust by Estimate factors listed below Age > 70 years –0.1 unit/kg/day Renal insufficiency (eGFR < 45) –0.1 unit/kg/day Advanced Cirrhosis –0.1 unit/kg/day Pancreatic deficiency (chronic pancreatitis, cystic fibrosis, s/p –0.1 unit/kg/day pancreatectomy) HbA1c >10% +0.1 unit/kg/day Currently on glucocorticoids with equivalent of prednisone 40 mg/day +0.1 unit/kg/day or greater FINAL TDD estimate ? b TDD Basal Nutritional (40–50%) (50–60%) Example: 60 kg patient with TDD estimate 0.5 unit/kg/day 0.5 X 60 = 30 units TDD with 50% basal and 50% nutritional 30÷2=15 units basal and 15 units prandial (5 units AC) Fig. 23.1 (a) Step 1: initiation of insulin and determination of total daily dose (TDD). Use weight or if patients on insulin as outpatient consider 80% of home dose, but not to exceed 1 unit/kg TDD (b) Step 2: Components of insulin program: basal, nutritional, correctional. (Reprinted from Hudson M.S., Palermo N.E. Diabetes in Older Adults, pp. 1–18, In: Rosenthal R., Zenilman M., Katlic M. (eds) Principles and Practice of Geriatric Surgery, © 2017, with permission from Springer Nature. See Suggested Readings) actions of repeated doses, a phenomenon known as “stacking.” Some institutions give only “half” scale for bedtime correctional insulin to avoid potential for overnight hypoglycemia. 23 Hypoglycemia in Patients with Diabetes 279 What to Do When Hypoglycemia Occurs All hospitals should have protocols in place for managing acute hypoglycemia both on the general wards and in the ICU. Generally, treatment should be started in the hospital when glucose falls below 70 mg/dl. If possible, patients should be treated orally. A nursing protocol should be in place for treat- ment (Fig. 23.2). The art of managing hypoglycemia is to determine which insu- lin dose may be responsible for an episode of hypoglycemia and how much it should be reduced. Knowing the insulin action pro- file (see Table 23.2) is helpful. Generally the early morning glu- cose is the best reflection of the action of basal insulin, but this may not be the case if the patient is receiving rapid-acting insulin late at night (nighttime correctional scales) or overnight (e.g., with continuous enteral nutrition). Premeal or pre-bed hypoglyce- mia may reflect the rapid-acting insulin given with the previous meal. If the hypoglycemia is associated with a significant change in medical condition (stopping steroids, e.g., or acute renal failure), dose adjustments in the range of 30–50% may be necessary. However, if the patient is otherwise clinically stable, a simple cal- culation for adjusting insulin is to decrease the TDD of insulin by Treatment of Hypoglycemia 1. Give 15 g of sugar (no artificial sweetners) as 1/2 cup of fruit juice or 1 cup skim or 3 packs of sugar in water or 3 − 4 commercial glucose tablets (4–5 g glucose each). 2. Wait 15 min and re-test blood sugar. Retreat until glucose is at least over 70 mg/dl. 3. If the patient is unable to take orally for any reason (loss of consciousness, aspiration risk, etc.) glucose should be given IV generally 12.5–25 g of dextrose as D50 IV push. 4. If patient does not have an adequate IV to handle D50W push, then glucagon 1 mg IV or IM can be given. Fig. 23.2 Treatment of hypoglycemia 280 M. Hudson 10% for glucose values running 70–99 mg/dl and to decrease the TDD by 20% for any glucose value below 70 mg/dl. Hospital Surveillance and Reporting: Glucometrics Hospitals should have in place quality improvement programs to monitor glucose values generally and episodes of hypoglycemia specifically so that areas with recurrent problems can be identi- fied and causes addressed. The Society for Hospital Medicine has developed a national Glucose Control Mentored Implementation Program that hospitals can join to report their glucose values. The hospital can then be benchmarked against other institutions for metrics such as days with any glucose below 70 mg/dl. In this way, the institution can assess performance on a national level and hopefully find ways to improve patient care. For more information, go to http://dev.hospitalmedicine.org/Web/Quality_ Innovation/Implementation_Toolkits/Glycemic_Control/Web/ Quality___Innovation/Implementation_Toolkit/Glycemic/ Track_Performance/Introducing_Glucometrics.aspx Beyond Basal-Bolus Insulin: Glucose Control Without Hypoglycemia Because of concern for hypoglycemia and its potentially devastat- ing consequences, improvements on current basal-bolus treat- ment recommendations are being actively studied. A trial comparing basal-bolus insulin to basal plus correctional insulin (i.e., no scheduled mealtime insulin) showed similar average glu- cose values but less moderate hypoglycemia (<70 mg/dl) in the basal plus correctional treatment group. Other trials have looked at using DPP-4 inhibitors or GLP-1 receptor agonist agents in the inpatient setting, but these have not received general acceptance at this time. 23 Hypoglycemia in Patients with Diabetes 281 Suggested Reading American Diabetes Association. Diabetes care in the hospital. Diabetes Care. 2017a;40(Suppl 1):S120–7. American Diabetes Association. Glycemic targets. Sec 6. In Standards of medical care in diabetes–2017. Diabetes Care. 2017b;40(Suppl. 1): S48–56. Garg R, Hurwitz S, Turchin A, Trivedi A. Hypoglycemia, with or without insulin therapy, is associated with increased mortality among hospitalized patients. Diabetes Care. 2013;36(5):1107–10. Hudson MS, Palermo NE. Diabetes in older adults. In: Rosenthal R, Zenilman M, Katlic M, editors. Principles and practice of geriatric surgery. Cham: Springer; 2017. p. 1–18. NICE-SUGAR Study Investigators, Finfer S, Chittock DR, Su SY, Blair D, Foster D, et al. Intensive versus conventional glucose control in critically ill patients. N Engl J Med. 2009;360(13):1283–97. Rubin DJ, Rybin D, Doros G, McDonnell ME. Weight-based, insulin dose- related hypoglycemia in hospitalized patients with diabetes. Diabetes Care. 2011;34(8):1723–8. Society of Hospital Medicine. Quality & innovation. External sources & benchmarking/glycemic control implementation toolkit 2017 https:// www.hospitalmedicine.org/Web/Quality_Innovation/Implementation_ Toolkits/Glycemic_Control/Web/Quality___Innovation/Implementation_ Toolkit/Glycemic/Track_Performance/external_sources_benchmarking. aspx. Turchin A, Matheny ME, Shubina M, Scanlon JV, Greenwood B, Pendergrass ML. Hypoglycemia and clinical outcomes in patients with diabetes hospi- talized in the general ward. Diabetes Care. 2009;32(7):1153–7. Umpierrez GE, Smiley D, Jacobs S, Peng L, Temponi A, Mulligan P, Umpierrez D, et al. Randomized study of basal-bolus insulin therapy in the inpatient management of patients with type 2 diabetes undergoing general surgery (RABBIT 2 surgery). Diabetes Care. 2011;34(2):256–61. Umpierrez GE, Smiley D, Hermayer K, Khan A, Olson DE, Newton C, et al. Randomized study comparing a Basal-bolus with a basal plus correction insulin regimen for the hospital management of medical and surgical patients with type 2 diabetes: basal plus trial. Diabetes Care. 2013;36(8):2169–74. Hypoglycemia in Patients 24 Without Diabetes Rajesh K. Garg Contents Diagnosis of Hypoglycemia in Patients Without Major Acute or Chronic Illness 284 Diagnosis in Patients with Major Illness 284 Symptoms and Signs of Hypoglycemia 284 Causes of Hypoglycemia 285 Medications 285 Organ System Failure Like Cardiac, Renal, or Liver Failure 285 Sepsis and Adrenal or Pituitary Insufficiency Are All Associated with Hypoglycemia 285 Non-islet Cell Tumors 286 Antibody-Induced Hypoglycemia 286 Endogenous Insulin Production 286 Pseudohypoglycemia 287 Laboratory Investigations for Hypoglycemia 287 Prolonged Fasting Test 287 Mixed Meal Test 289 R. K. Garg (*) Division of Endocrinology, Diabetes and Metabolism, University of Miami Miller School of Medicine, Coral Gables, FL, USA e-mail: rgarg@miami.edu © Springer Nature Switzerland AG 2020 283 R. K. Garg et al. (eds.), Handbook of Inpatient Endocrinology, https://doi.org/10.1007/978-3-030-38976-5_24 284 R. K. Garg Differentiating Insulin-Mediated Versus Non-insulin-Mediated Hypoglycemia 289 Imaging Studies for Insulinoma 290 Treatment of Hypoglycemia 291 Suggested Reading 291 Diagnosis of Hypoglycemia in Patients Without Major Acute or Chronic Illness Symptoms and signs of hypoglycemia are often nonspecific. Therefore, Whipple’s triad must be satisfied to make a diagnosis of hypoglycemia. Whipple’s triad includes low blood glucose lev- els, the presence of symptoms or signs of hypoglycemia at the time of low blood glucose levels, and recovery from symptoms or signs by raising blood glucose levels. Diagnosis in Patients with Major Illness Sick patients may not feel symptoms or signs of hypoglycemia. Therefore, any blood glucose <55 mg/dL needs evaluation in a sick person. Spontaneous hypoglycemia in a sick person is often not caused by hyperinsulinemia. Both insulin-mediated and non- insulin- mediated hypoglycemia in the hospital setting are associ- ated with high mortality. Symptoms and Signs of Hypoglycemia Symptoms and signs of hypoglycemia can be divided into auto- nomic or neuroglycopenic. Autonomic symptoms and signs including hunger, palpitation, anxiety, tachycardia, tremor, pallor, and diaphoresis appear early as the blood glucose levels start going down. Neuroglycopenic symptoms and signs including behavioral changes, confusion, loss of consciousness, and seizures appear later and at much lower blood glucose levels. However, in 24 Hypoglycemia in Patients Without Diabetes 285 patients getting frequent hypoglycemic episodes, autonomic symptoms and signs may be suppressed, and as a result they may present with neuroglycopenic symptoms. Causes of Hypoglycemia Medications The most common medications that cause hypoglycemia are insu- lin or insulin secretagogues and alcohol. However, the list of drugs associated with hypoglycemia is long and ever growing. Check all current medications that a patient is taking that may cause hypoglycemia. However, the evidence regarding associa- tion between most drugs and hypoglycemia is rather weak. Therefore, in many cases, diagnosis of drug-induced hypoglyce- mia can only be made after excluding other causes. More often, drugs are a contributing factor to hypoglycemia caused by another major problem, like organ system failure. Organ System Failure Like Cardiac, Renal, or Liver Failure The liver is the main glucogenic organ with the kidney contribut- ing to gluconeogenesis to some extent. Therefore, hypoglycemia is common in the presence of liver failure, and the risk of hypo- glycemia increases in the presence of renal failure. Severe heart failure can cause hypoglycemia due to inanition and liver congestion. Sepsis and Adrenal or Pituitary Insufficiency Are All Associated with Hypoglycemia Major illness is evident in this setting. A high index of suspicion and targeted testing are needed to rule in adrenal and pituitary insufficiency. 286 R. K. Garg Non-islet Cell Tumors Tumors associated with hypoglycemic are mostly large mesen- chymal tumors that secrete IGF-II. In these cases, IGF-II level or its ratio to IGF-I is increased. However, a few reports of IGF-1 secreting tumors leading to hypoglycemia have also been published. Antibody-Induced Hypoglycemia Insulin antibodies can bind endogenous insulin and release it in large amounts periodically to cause hypoglycemia. Antibodies may also directly bind to insulin receptors and cause hypoglyce- mia. In the presence of antibody-induced hypoglycemia, insulin levels are often reported extremely high (>100 mU/L) due to the antibodies interfering with the insulin assay. C-peptide and proin- sulin levels can be high, normal, or low. Endogenous Insulin Production Insulinoma- and non-insulinoma-related hyperinsulinemia are rare but important causes of hypoglycemia. Insulinomas are often small, single, benign tumors with very low recurrence rate after resection. However, they may also occur as part of the MEN-1 syndrome where they can be multiple and have a high recurrence rate. Non-insulinoma-related hyperinsulinemia has been described most often after bariatric surgery. It is due to diffuse islet hypertrophy, sometimes with hyperplasia, also called as nesidio- blastosis. No single lesion can be identified in these cases, making treatment very difficult. Endogenous insulin secretion due to drugs like sulfonylureas or meglitinides must be ruled out before making a diagnosis of insulinoma- and non-insulinoma-related |
hyperinsulinemia. 24 Hypoglycemia in Patients Without Diabetes 287 Pseudohypoglycemia Pseudohypoglycemia can happen in conditions with increased number of red or white blood cells. It may also happen when the blood sample is collected in a tube without an inhibitor of gly- colysis or when the processing of blood sample for glucose mea- surement is delayed. Laboratory Investigations for Hypoglycemia Laboratory investigations for hypoglycemia are necessary unless there is a clear cause of hypoglycemia, in which case it will resolve after the cause is addressed (Table 24.1). Investigations for the cause of hypoglycemia must be performed at the time of the condition. Induction of hypoglycemia may be necessary if the episodes of spontaneous hypoglycemia are infrequent. Blood glu- cose from finger-stick blood samples is appropriate for monitor- ing while waiting for a symptomatic episode of hypoglycemia. However, venous blood samples for the following laboratory tests should be collected at the time of hypoglycemia: glucose, insulin, C-peptide, proinsulin, beta-hydroxybutyrate, and sulfonylureas. After collecting blood, patient should receive an IV injection of 1.0 mg glucagon, and then finger-stick and plasma glucose should be measured at 10, 20, and 30 min after the injection. Prolonged Fasting Test A prolonged fasting test is indicated when the patient complains of fasting hypoglycemia, but it is hard to observe an episode of spontaneous hypoglycemia. A prolonged fast test can take up to 72 h to be diagnostic. A sufficient amount of noncaloric, non- caffeinated beverages may be administered during the test in order to prevent dehydration. Although it can be started at any 288 R. K. Garg Table 24.1 Differential diagnosis of spontaneous hypoglycemia Diagnosis Laboratory tests Comment Endogenous High insulin, C-peptide, and Prolonged fasting may insulin proinsulin be required to induce production: Low beta- hydroxybutyrate hypoglycemia insulinoma and Response to glucagon diffuse islet cell Absence of insulin hyperplasia secretagogue drugs Exogenous High insulin Detailed history may insulin Low C-peptide and proinsulin reveal exogenous Low beta- hydroxybutyrate insulin use Response to glucagon Absence of insulin secretagogue drugs Drug induced: High insulin, C-peptide, and Detailed history sulfonylurea-like proinsulin including examination drugs Low beta- hydroxybutyrate of all drugs and Response to glucagon supplements is Presence of insulin important secretagogue drugs Non-islet tumors: Low insulin, C-peptide, and Presence of tumor producing IGF-II proinsulin may be obvious Low beta- hydroxybutyrate Response to glucagon Absence of insulin secretagogue drugs High IGF-II levels Non-insulin- or Low insulin, C-peptide, and Presence of obvious insulin- like proinsulin severe acute or chronic factor-related High beta- hydroxybutyrate illness condition: organ No response to glucagon system failure, Absence of insulin endocrine secretagogue drugs deficiencies Antibody Very high insulin levels Blood glucose levels mediated High or low C-peptide and highly variable. Other proinsulin autoimmune Low beta- hydroxybutyrate conditions may be Response to glucagon present Absence of insulin secretagogue drugs 24 Hypoglycemia in Patients Without Diabetes 289 time of the day in a patient admitted to hospital, it is best that the prolonged fast test be started in the morning because the majority of patients with significant underlying pathology are likely to become hypoglycemic within the first 8 h and appropriate testing would be possible before the night shift when access to staff and other resources may be limited. However, if hypoglycemia does not develop within 8 h, fasting should continue until the time of symptomatic hypoglycemia or up to 72 h before ending the fast. Patients should be closely monitored for signs and symptoms including mental status checks along with finger-stick blood glu- cose determinations. Low blood glucose values should be con- firmed by laboratory plasma glucose determination. The prolonged fast test should be ended when the patient is symptomatic with plasma glucose <55 mg/dL or the plasma glucose is <45 mg/dL even without symptoms or 72 h have elapsed. Laboratory investi- gations described in previous section should be obtained at this point before ending the prolonged fast test. Mixed Meal Test If hypoglycemia symptoms occur postprandially, a mixed meal test may be able to induce hypoglycemia and allow investigation at the time of hypoglycemia. In general, the meal should be simi- lar to the one that causes spontaneous hypoglycemia. However, if this not practical, a liquid nutritional formula may be used. The test should be conducted in the morning after an overnight fast. Blood glucose should be monitored every 30 min for 4 h. Blood glucose criteria for ending the test are similar to those for the pro- longed fast test. Differentiating Insulin-Mediated Versus Non-insulin-Mediated Hypoglycemia Diagnosis of endogenous hyperinsulinemia depends on demon- strating high insulin, high C-peptide, high proinsulin, low beta- hydroxybutyrate, and absence of sulfonylureas and meglitinides 290 R. K. Garg at the time of hypoglycemia. Because hypoglycemia should nor- mally suppress insulin and C-peptide levels, a plasma insulin level of ≥3.0 microU/ml and a C-peptide level of ≥0.6 ng/ml in the presence of hypoglycemia are considered abnormal. A proin- sulin level of ≥5.0 pmol/L is also highly suggestive of hyperinsu- linism due to insulinoma. If insulin levels are high in the absence of high C-peptide or proinsulin levels, exogenous insulin-induced hypoglycemia should be suspected. Insulin effectively suppresses ketone production, and a beta-hydroxybutyrate level of ≤2.7 mmol/L is indicative of an increased insulin-like effect. An increase in plasma glucose of at least 25 mg/dl after intravenous glucagon also indicates mediation of the hypoglycemia by insulin- like effect. Therefore, low beta-hydroxybutyrate and adequate response to glucagon in the absence of high levels of insulin sug- gest the presence of IGF. Insulin secretagogue drugs like sulfonyl- ureas and meglitinides cause hypoglycemia, and their presence should be ruled out before making a diagnosis of insulinoma or non-insulinoma hyperinsulinism. Non-insulin-mediated hypogly- cemia will be associated with low insulin, low C-peptide, low pro- insulin, high beta-hydroxybutyrate, and inadequate response to glucagon. In severely hypoglycemic patients, glucose require- ment >8 mg/kg/min (normal 4–6 mg/kg min) to maintain normo- glycemia suggests hypoglycemia likely due to excess of insulin or insulin-like growth factor secretion. Imaging Studies for Insulinoma Imaging for insulinoma should be ordered only when the bio- chemical diagnosis has been definitively made. The majority of insulinomas are <2 cm in size. Computed tomography or MRI can identify about 80% of insulinomas. When a lesion is not seen on CT scan or MRI scan, endoscopic pancreatic ultrasonography should be the next modality of imaging because it will detect most remaining insulinomas. Sometimes, an octreotide scan or gallium dotatate PET/CT scan may be ordered. When an insulinoma is not 24 Hypoglycemia in Patients Without Diabetes 291 visible on any of the imaging studies, hepatic venous sampling after selective arterial calcium injections may be required. In this method, calcium gluconate is sequentially injected into the splenic, gastroduodenal, and superior mesenteric arteries, and a twofold increase in insulin levels in the hepatic vein will localize the source of excess insulin to the tail of the pancreas, body of the pancreas, or head of the pancreas. Imaging using 18-FDG PET is of no proven value at this time. However, it may be useful in local- ization of the cause of non-insulin-mediated tumorigenic hypoglycemia. Treatment of Hypoglycemia Treatment of hypoglycemia depends on the cause of hypoglyce- mia, and it may be achieved by treatment of the underlying cause or surgical removal of the cause, e.g., discontinuing the offending drug, hormonal replacement, treating sepsis, or removing an islet cell tumor. In the short term, treatment of hypoglycemia or its prevention is important. Frequent oral feeding or intravenous glu- cose or glucagon may be needed. Most cases of insulinoma are cured after surgery. However, some patients with malignant insu- linoma- or non-insulinoma-mediated hyperinsulinism may need chronic treatment with diazoxide or octreotide or parenteral nutri- tion. Rare patients with nesidioblastosis may require partial or complete pancreatectomy to relieve hypoglycemia. The patient with an IGF-producing malignant tumor may also be difficult to treat. Patients with antibody-induced hypoglycemia may respond to glucocorticoids or immunosuppressive treatment. Suggested Reading Cryer PE, Axelrod L, Grossman AB, Heller SR, Montori VM, Seaquist ER, Service FJ, Endocrine Society. Evaluation and management of adult hypoglycemic disorders: an Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metabol. 2009;94(3):709–28. 292 R. K. Garg Garg R, Hurwitz S, Turchin A, Trivedi A. Hypoglycemia, with or without insulin therapy, is associated with increased mortality among hospitalized patients. Diabetes Care. 2013;36(5):1107–10. Martens P, Tits J. Approach to the patient with spontaneous hypoglycemia. Eur J Intern Med. 2014;25(5):415–21. Salehi M, Vella A, McLaughlin T, Patti ME. Hypoglycemia after gastric bypass surgery: current concepts and controversies. J Clin Endocrinol Metabol. 2018;103(8):2815–26. Diabetic Ketoacidosis 25 and Hyperosmolar Hyperglycemic State Daniela V. Pirela and Rajesh K. Garg Contents Epidemiology 294 Diagnosis of DKA 294 Signs and Symptoms 294 Laboratory Tests 295 Diagnosis of HHS 297 Signs and Symptoms 297 Laboratory Tests 298 Management 298 Most Common Causes to Rule Out 298 IV Fluids 299 Insulin Therapy 299 Electrolytes 300 Monitoring 301 Criteria for Resolution 302 Complications 302 Transition of Care 303 D. V. Pirela Jackson Memorial Hospital/University of Miami Hospital, Division of Endocrinology, Diabetes and Metabolism, Miami, FL, USA R. K. Garg (*) Division of Endocrinology, Diabetes and Metabolism, University of Miami Miller School of Medicine, Coral Gables, FL, USA e-mail: rgarg@miami.edu © Springer Nature Switzerland AG 2020 293 R. K. Garg et al. (eds.), Handbook of Inpatient Endocrinology, https://doi.org/10.1007/978-3-030-38976-5_25 294 D. V. Pirela and R. K. Garg Disposition 304 Suggested Reading 306 Epidemiology According to the CDC data, there were 207,000 emergency depart- ment visits for hyperglycemic crisis in the year 2014. This amounts to 9.5 visits per 1000 persons with diabetes for DKA or HHS. However, these two entities represent an extreme on the spectrum of avoidable hyperglycemic emergencies in patients with diabetes; majority of patients are admitted with hyperglycemia along with another illness. Females, adolescents, ethnic minorities, and patients with high A1c are at higher risk of DKA or HHS. The incidence of DKA has gone up, at least 6% annually from 2009 to 2014 in all age groups. Although DKA is considered pathognomonic of type 1 diabetes, at least one-third of the DKA cases occur in patients with type 2 diabetes. HHS is less common and represents less than 1% of all diabetes-related admissions. Although generally seen in adults with type 2 diabetes, HHS is becoming more frequent among children and young adults. DKA causes almost 50% of all deaths in patients with type 1 diabetes under the age of 24 years. Inpatient DKA mortality is less than 1%, while for HHS, mortality is as high as 16%. Even though the mortality risk has declined, mortality and morbidity related to acute hyperglycemic emergencies remain high, and the health-care costs remain substantial, especially taking into account the increase in incidence. Diagnosis of DKA Signs and Symptoms Evolution of DKA is rather acute. Patients often complain of fatigue and osmotic symptoms like polyuria and polydipsia. Abdominal pain, nausea, and vomiting are present in up to two- 25 Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic State 295 thirds of patients. The severity of symptoms depends on multiple factors including the severity of acidosis, dehydration, and age of the patient. Neurologic symptoms such as lethargy and stupor develop in half of patients when serum osmolarity reaches 320 mOsmol/kg; loss of consciousness occurs in less than 25% of patients. Presence of altered mental status and a serum osmolarity less than 320 should prompt additional neurologic workup. Abdominal pain is more common in younger patients and seems to be related to the severity of the metabolic acidosis, which inter- feres with gastric emptying. In the absence of metabolic acidosis or if abdominal pain persists despite resolution of DKA, pancre- atitis and other gastrointestinal disorders should be considered. Dry mucosa, decreased skin turgor, and low jugular venous pres- sure can be appreciated in most of the patients due to dehydration. The presence of tachycardia and hypotension correlates with the degree of dehydration. Patients may have a fruity odor to their breath due to the exhaled ketones as well as deep hyperventilation (Kussmaul respirations). Laboratory Tests To make a diagnosis of DKA, the triad of hyperglycemia above 250 mg/dL, ketonemia, and metabolic acidosis with elevated anion gap should be present. Plasma glucose is usually between 350 and 500 mg/dL when the patient presents to the emergency department. Some patients with DKA may present with only mild elevations of blood glucose levels. This is known as euglycemic DKA; this can be seen in |
patients with prolonged starvation, alco- hol intake, insufficient insulin dose, and pregnancy and in patients using SGLT-2 inhibitors that lead to glycosuria, blunting the ele- vation of blood glucose level. Hyperglycemia is secondary to the deficit of effective insulin, the excess of counterregulatory hormones, and relative increase in insulin resistance. Insulin normally blocks ketogenesis by inhibit- ing lipolysis and the transport of free fatty acid derivatives into the mitochondrial matrix. Insulin deficiency leads to unrestrained lipolysis and mobilization of triglycerides and amino acids for 296 D. V. Pirela and R. K. Garg energy use instead of glucose. Increased levels of serum free fatty acids are converted to ketones bodies and acids which are mainly acetoacetic acid and beta-hydroxybutyric acid, both strong organic acids. Hepatic gluconeogenesis is stimulated by glucagon excess and excess of other stress hormones, while alanine origi- nated from muscle catabolism and glycerol from lipolysis provide the substrate. The metabolic imbalance is characterized by a low bicarbonate level, usually less than18 mEq/L, and the accumulation of keto acids in blood that cause a drop in the arterial pH to less than 7.3 with an elevation of the anion gap above 12. In DKA, keto acids become circulating unmeasured anions. In addition, lactic acid generated from tissue hypoxia contributes to unmeasured anions further increasing the anion gap. The anion gap is calculated by the following formula: Aniongap Sodium mEq / L Potassium mEq / L Chloride mEq / L HCO3 mEq / L The nitroprusside test can detect ketones bodies, more specifi- cally acetoacetate, in the urine. This test does not correlate with disease severity as it can be negative in severe ketosis when beta- hydroxybutyrate becomes the predominant ketone or when lactic acidosis coexists with the ketoacidosis interfering with the mea- surement of the acetoacetate. Serum ketone levels usually are done when urine ketone test is positive; however, due to the high false-negative and false-positive urine nitroprusside tests, direct measurement of serum beta-hydroxybutyrate is preferred. Hyperglycemia may cause non-hypotonic hyponatremia. Glucose is an osmotically active substance. Therefore, in the pres- ence of hyperglycemia, increased plasma osmolality induces water movement to the extracellular space leading to reduction of serum sodium levels which is also called dilutional hyponatremia. Therefore, corrected serum sodium level should be used to calcu- late an accurate serum anion gap. To correct serum sodium level, add 1.6 mEq/L to the measured serum sodium for each 100 mg/dL of glucose greater than 100 mg/dL. A normal measured sodium 25 Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic State 297 level in the setting of hyperglycemic DKA is suggestive of pro- found hypovolemia. Serum bicarbonate is usually below 10 mmol/l and pH 6.8–7.3. Infrequently, the pH may not be sig- nificantly decreased due to compensatory hyperventilation, which will decrease the partial pressure of carbon dioxide. There is an increased urinary loss of potassium due to the glu- cose osmotic diuresis and the excretion of potassium keto acid anion salts which lead to deficit of the total body potassium. The metabolic acidosis, hyperosmolarity, and insulin deficiency cause a shift of potassium from intracellular fluid to extracellular fluid. Therefore, the serum potassium concentration is usually normal or even elevated initially. Once insulin therapy is introduced, potassium shifts back into cells which rapidly lower the potas- sium concentration and may lead to severe hypokalemia. At presentation, serum phosphate is usually normal or high because both insulin deficiency and metabolic acidosis cause a shift of phosphate out of the cells. However, there is a decreased phosphate intake and phosphaturia caused by osmotic diuresis that result in a net phosphate depletion. Thus, after volume and insulin replacement, hypophosphatemia ensues. Diagnosis of HHS Signs and Symptoms Hyperosmolar hyperglycemic state (HHS) presentation has a less acute presentation than DKA. Symptoms of polyuria, polydipsia, and weight loss are more evident and often start several days or weeks before the hospital admission. Blurred vision and progres- sive decline in mental status are also evident. Severe dehydration and high plasma osmolarity lead to mental obtundation and coma that are proportional to the degree and rate of the development of hyperosmolarity. Decreased skin turgor, dry oral mucosa, low jugular venous pressure, tachycardia, and hypotension are more evident in HHS compared to DKA. Rarely patients can develop abdominal pain. 298 D. V. Pirela and R. K. Garg Laboratory Tests The serum glucose concentration is much higher, frequently exceeding 600 mg/dL, but can be higher than 1000 mg/dL in HHS. The endogenous insulin production is sufficient to suppress ketogenesis. Therefore, ketone levels remain within normal lim- its, which means the pH, the serum bicarbonate, and the anion gap stay normal as well. The glycosuria leads to severe dehydration and an effective plasma osmolarity typically above 320 mOsmol/ kg. Hyponatremia is usually present through the same mechanism as in DKA and is sometimes more severe. Similar to DKA, the serum potassium concentration is usually normal, though in one- third of patients it is elevated up to 5.7 mEq/L on admission. After proper insulin therapy and fluid resuscitation, potassium shifts back into the cells uncovering the total body potassium deficit. Other laboratory results such as leukocytosis, increased BUN, and creatinine are proportional to the degree of hypovolemia. Management Most Common Causes to Rule Out • Medication nonadherence. • Infections. Obtain urine and blood cultures, chest radiograph, and other tests in selected cases. • Pancreatitis. Obtain serum lipase and amylase when pancreati- tis is clinically suspected. The result must be interpreted with caution because some increase in amylase can be associated with DKA itself. • Tissue ischemia such as cardiac ischemia and cerebrovascular accidents. Obtain cardiac enzymes and electrocardiogram, and perform neurologic assessment. • Concomitant medications. Look for medications that may have precipitated the acute hyperglycemic emergency including glucocorticoids, beta-blockers, thiazide diuretics, certain 25 Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic State 299 chemotherapeutic agents, atypical antipsychotics, and SGLT2 inhibitors. • Severe dehydration. Mainly bedridden and elderly patients are in danger of having compromised access to water; this is exac- erbated by the altered thirst response in some of them. Newly diagnosed and even undiagnosed fragile patients, particularly residents of chronic care facilities, may be at risk of delayed recognition of hyperglycemic symptoms and severe dehydra- tion. Administration of insulin, without initial proper fluid replacement, may accentuate hyperosmolality by moving water intracellularly which further aggravate vascular collapse, hypotension, and even death. IV Fluids Intravenous fluid is the mainstay of management of hyperglycemic crises. Fluids improve the clinical and metabolic status by decreas- ing serum glucose through urinary clearance by improving renal perfusion and by intravascular volume expansion. Isotonic saline is initially infused at 500–1000 ml/h for 2–4 h, followed by the infusion of 0.9% or 0.45% saline at 250–500 ml/h depending on the serum sodium level, the state of hydration, and the urine out- put. In general, 0.9% saline is continued in patients with low serum sodium, whereas patients with normal or elevated serum sodium or hyperosmolarity should receive 0.45% NaCl. Intravenous dextrose (5% or 10%) is added once the plasma glucose level is between 200 and 250 mg/dL, to allow continued insulin administration until ketonemia is controlled while avoiding hypoglycemia. Insulin Therapy Insulin is key component of treatment of DKA and HHS. In gen- eral, DKA resolution occurs between 10 and 18 h after initiation of therapy, while HHS resolution can take longer. Intravenous 300 D. V. Pirela and R. K. Garg regular insulin has been the treatment of choice for the manage- ment of acute hyperglycemic emergencies, but the use of subcuta- neous insulin for mild-to-moderate DKA is becoming more common. The time of resolution seems to be equivalent with either option, but the use of subcutaneous insulin mitigates the burden on the nursing staff. Insulin reduces hepatic gluconeogen- esis and suppresses lipolysis and ketogenesis. Insulin therapy will shift extracellular potassium into the intracellular space. Therefore, to avoid severe hypokalemia, serum potassium should be more than 3.3 mEq/L when insulin therapy is started. An intravenous bolus of regular insulin at a rate of 0.1 unit/kg followed by a continuous infusion at a rate of 0.1 U/kg/h (5–10 U/h) vs no bolus and infusion of insulin at a rate of 0.14 U/kg/h has shown similar outcomes. The infusion rate should be adjusted per hour to ensure that serum glucose falls by at least 50 mg/dL/h. The insulin infusion rate may be decreased by 0.05 U/kg per hour until a rate of 0.5 U/h (minimum rate) is reached. Dextrose should be added to the intravenous fluids when the plasma glucose concen- tration reaches <200 mg/dL in patients with DKA and <300 mg/dL in patients with HSS. The insulin i nfusion should be continued to maintain a plasma glucose level of 150–200 mg/dL until ketoaci- dosis has resolved, as evidenced by normalization of pH and anion gap among those with DKA, and until mental status and the hyper- osmolar state are corrected in HHS cases. The use of insulin lispro or aspart in subcutaneous boluses seems to be as effective as IV regular insulin infusion and a safe alternative for patients in situations where insulin infusion is not practical. An initial bolus of 0.2–0.3 U/kg of rapid-acting insulin followed by maintenance boluses of 0.1–0.2 U/kg every hour to 2 h may be used. Once glucose is less than 250, consider reducing the maintenance boluses until resolution of the DKA. Electrolytes Potassium Therapy The initial insulin-deficit state, hypertonic- ity, and acidosis lead to a shift of potassium from the intracellular to the extracellular compartment in the setting of total body 25 Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic State 301 potassium deficit of 3–5 mmol/kg. Fluid and insulin therapy pro- mote a rapid intracellular shift of potassium, which may result in hypokalemia with the risk of arrhythmia and even cardiac arrest. Hence, early IV potassium therapy should be initiated when the serum potassium level is below 5.0 mEq/L with the goal of main- taining a potassium level of 4–5 mEq/L during therapy. An excep- tion to this rule is the case of low urine output or severely decreased renal function whereby potassium should be given only if low and monitored carefully. Bicarbonate Therapy The use of bicarbonate in DKA is contro- versial. The current ADA guidelines recommend bicarbonate therapy for the severe metabolic acidosis with a serum pH <6.9. However, no study has shown benefit from the use of this therapy. Bicarbonate use has some potential side effects including cerebral edema, hypokalemia, rebound acidosis, hypoxia, and hypernatre- mia. In view of the lack of evidence of a therapeutic effect, it should generally be avoided. Phosphate Therapy Replace if serum phosphate is less than 1 mg/dL, especially in a patient with evidence of respiratory or cardiac distress. If the phosphate level is higher than 1 mg/dL, it usually will self-correct once the patient has resumed eating. There is no evidence of a beneficial effect of phosphate replace- ment, and aggressive intravenous phosphate therapy can cause hypocalcemia; therefore, in case of phosphate replacement, cal- cium levels should be monitored closely. Monitoring All patients should get frequent clinical and laboratory reas- sessment to ensure an adequate glycemic control, adequate urine output, and electrolyte correction and avoid fluid over- load. The main assessments include finger-stick blood glucose (every hour to prevent hypoglycemia) and at least basic meta- bolic panel (every 1–4 hours to monitor potassium levels and the anion gap). 302 D. V. Pirela and R. K. Garg Criteria for Resolution Criteria for establishing the resolution of DKA include a serum glucose ≤250 mg/dL and at least two of the following criteria: nor- malization of the anion gap, a venous or arterial pH ≥7.3, and a serum bicarbonate level ≥18 mEq/L. Ketonemia and ketonuria may persist for 24–36 h due to delayed ketone elimination. Patients who recover from ketoacidosis may develop a secondary hyperchloremic non-anion gap metabolic acidosis resulting from aggressive saline administration. The serum bicarbonate may not normalize immedi- ately for this reason as it is temporarily “replaced” by chloride. In HHS, resolution may be declared when a plasma glucose level ≤250 mg/dL and normal effective serum osmolarity <310 mOsmol/ kg are achieved in the setting of a restored baseline mental status. Complications Hypoglycemia: 5–25% of the patients with DKA develop hypo- glycemia. This is due to a significant percentage of patients pre- senting with hyperglycemic emergencies have a defective |
adrenergic response to low blood sugar. Therefore, a lack of fre- quent monitoring, not adjusting the insulin dose appropriately and not adding dextrose-containing solutions when blood sugar is less than 200 mg/dL, can easily lead to hypoglycemia. Hypokalemia can occur when insulin therapy is started with serum potassium less than 3.3 mEq/L because of the mechanisms discussed in electrolyte management section. Cerebral edema is rare in adults. However, the mortality in children, where it is seen more often, can be as high as 20–40%. Fluctuation in the mental status, abnormal verbal or motor response to pain, decorticate or decerebrate posturing, cranial nerve palsy, and abnormal neurogenic respiratory pattern have been described. Onset is usually 4–12 h after starting treatment of DKA. The mechanism of cerebral edema is not well understood. Either mannitol 0.5–1 g/kg IV over 20 min or 3% saline fluid 5–10 ml/kg can be used. After initiating treatment, m onitoring for thrombosis, cerebral infraction and hemorrhage is indicated. 25 Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic State 303 Rhabdomyolysis, more common in HHS than DKA, can lead to renal failure. Checking creatine kinase every 2–3 h in patients with myalgia, weakness, and dark urine is recommended. Transition of Care Transition to a subcutaneous insulin regimen is indicated when the acute metabolic derangement has resolved and the patient is alert and can start oral nutrition. For patients who remain critically ill (e.g., shock requiring pressor agents, mechanical ventilation) or will undergo additional interventions (e.g., sur- gery), insulin infusion therapy should be continued. The half- life of intravenous regular human insulin is less than 10 min. Therefore, when transitioning from IV insulin to subcutaneous insulin, abrupt interruptions of the insulin infusion should be avoided. An overlap for 2–4 h of the insulin infusion and sub- cutaneous basal insulin is absolutely necessary to avoid rebound hyperglycemia and possible reopening of the anion gap from ketoacidosis. To choose a subcutaneous insulin regimen for a patient with controlled diabetes, home insulin regimen can be restarted if appropriate. However, for patients with uncontrolled diabetes and insulin-naïve or newly diagnosed diabetes, insulin can be started at a total daily dose of 0.5–0.8 U/kg/dL, 50% administered as long-acting basal insulin and the other 50% in pre-meal boluses of rapid-acting insulin analogs trying to mimic normal insulin phys- iology. Long-acting insulin analogs seem to have a lower inci- dence of hypoglycemia compared to intermediate-acting insulin (neutral protamine Hagedorn, NPH). Evidence suggests that administration of insulin glargine at a dose of 0.25 U/kg within 12 h of initiation of intravenous insulin infusion may help prevent rebound hyperglycemia following acute management of DKA. Chronic hyperglycemia leads to structural and functional damage in the beta cells decreasing the secretion of insulin and also interferes with the action of insulin in the target tissue c ausing insulin resistance. Therefore once hyperglycemia improves, insulin sensitivity changes quickly, and insulin dose adjustment 304 D. V. Pirela and R. K. Garg may be required after recovery from acute illness, especially in those with renal or pancreatic insufficiency. Disposition With proper treatment, the average time to the resolution of anion gap acidosis is 3 h. If the hyperglycemic crisis itself resolves in the emergency department, these patients may be stable enough for general floor admission to continue subcutaneous insulin, pending improved volume status after resuscitation, closed anion gap, and ability to tolerate fluids by the mouth. Patients with severe DKA or HHS often require ICU admission for adequate treatment, obser- vation, and resolution of sepsis, hypoxia, altered mental status, hypotension, persistent tachycardia, severe acidosis, or electrolyte abnormalities. Acute comorbidities such as myocardial infarction or cerebrovascular accidents may also dictate disposition to an ICU. If the patient has to stay in the emergency department longer than expected, the patient can be managed in the proper-staffed observation unit, and the need of ICU admission can be obviated. It is important to evaluate the cause of acute hyperglycemic emergency and treat it to prevent recurrence. DKA is the initial presentation of diabetes in approximately 15–20% of adults and 30–40% of children with type 1 diabetes. Early identification of new-onset diabetes in the emergency department can prompt the timely inclusion of a multidisciplinary team including an endocri- nologist, dietitian, and social worker with ability to provide diabe- tes education and arrange outpatient follow-up appointment that can prevent future hospital admissions. Visual impairment can lead to inappropriate dosing of insulin specially when using vials of insulin preparation; in these cases, an insulin pen should be considered. For patients with severe visual impairment and, also, for patients with cognitive impairment, super- vised or assisted insulin injection should be arranged with home health care, family members, or assisted living facilities/nursing home admission to prevent readmission with hyperglycemic crisis. Lipodystrophy due to repetitive insulin injection in the same area and malnourished patients with low fat mass should be coun- seled about the appropriate technique and area to inject insulin. 25 Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic State 305 In patients presenting to the emergency department with hyperglycemic emergencies due to medication nonadherence, especially in those with multiple recent readmissions, further questioning should aim to identify the reason behind the medica- tion noncompliance, which in most cases is due to socioeco- nomic issues. In about half of the patients presenting with DKA or HHS due to medication nonadherence, the underlying problem is an inabil- ity to afford medication. In the United States, insulin can be very expensive and almost unaffordable for patients without insurance. For these patients, early social worker involvement may help the patient find community resources for insulin availability. For patients with limited access to health care, for example, undocumented patients, the physician should be aware of inex- pensive options in the community such as state programs, health department free options, and local pharmacies where they can purchase insulin without prescriptions. When prescribing insulin, even patients with insurance can have difficulties obtaining the insulin brand prescribed. Depending on the insurance, prescribing the right brand of insulin with the lowest copayment for the patient can make a big difference in compliance and, therefore, can prevent the next episode of DKA or HHS (Table 25.1). Table 25.1 Differences between DKA and HHS DKA HHS Severe insulin deficiency with excess of Relative insulin deficiency and counterregulatory hormones, promoting inadequate fluid intake, leading gluconeogenesis, glycogenolysis, and to gluconeogenesis and ketone formation glycogenolysis Glucose levels usually 300–500 mg/dL >600 mg/dL Plasma osmolarity <320 >320 Ketones in blood and urine Absent Metabolic acidosis with anion gap Normal pH Elevated beta-hydroxybutyrate Absent Most common symptoms: abdominal Most common symptoms: pain, nausea, vomiting polyuria, polydipsia, and altered mental status Acute onset Subacute onset 306 D. V. Pirela and R. K. Garg Suggested Reading American Diabetes Association. Summary of revisions: standards of medical care in diabetes—2018. Diabetes Care. 2018;41(Suppl 1):S4–6. https:// doi.org/10.2337/dc18-Srev01. CDC. New CDC report: More than 100 million Americans have diabetes or prediabetes. July 18, 2017. Available online https://www.cdc.gov/media/ releases/2017/p0718-diabetes-report.html. Crilly CJ, Allen AJ, Amato TM, Tiberio A, Schulman RC, Silverman RA. Evaluating the Emergency Department Observation Unit for the management of hyperglycemia in adults. Am J Emerg Med. 2018;36(11):1975–9. https://doi.org/10.1016/j.ajem.2018.02.027. Epub 2018 Feb 27. Echouffo-Tcheugui JB, Garg R. Management of hyperglycemia and diabetes in the Emergency Department. Curr Diab Rep. 2017;17(8):56. https://doi. org/10.1007/s11892-017-0883-2. Fayfman M, Pasquel FJ, Umpierrez GE. Management of hyperglycemic cri- ses: diabetic ketoacidosis and hyperglycemic hyperosmolar state. Med Clin North Am. 2017;101(3):587–606. https://doi.org/10.1016/j. mcna.2016.12.011. Management of Preexisting 26 Diabetes and Gestational Diabetes During Hospitalization Gregory P. Westcott and Florence M. Brown Contents Differentiate Between Preexisting Diabetes and Gestational Diabetes 308 Definition of Gestational Diabetes (See Table 26.1) 308 Glycemic Targets (See Table 26.2) 310 Treatment Options 311 Patients with Gestational Diabetes 312 Patients with Type 1 Diabetes 313 Patients with Type 2 Diabetes 314 Diabetic Retinopathy 314 G. P. Westcott Beth Israel Deaconess Medical Center and Joslin Diabetes Center, Department of Endocrinology, Diabetes and Metabolism, Boston, MA, USA e-mail: gregory.westcott@joslin.harvard.edu F. M. Brown (*) Joslin-Beth Israel Deaconess Medical Center Diabetes in Pregnancy Program, Joslin Diabetes Center, Department of Adult Diabetes, Boston, MA, USA e-mail: florence.brown@joslin.harvard.edu © Springer Nature Switzerland AG 2020 307 R. K. Garg et al. (eds.), Handbook of Inpatient Endocrinology, https://doi.org/10.1007/978-3-030-38976-5_26 308 G. P. Westcott and F. M. Brown Special Situations 314 Diabetic Ketoacidosis 314 Betamethasone Therapy 315 Labor and Delivery 315 Glycemic Targets 315 Treatment Strategies 315 Postpartum 316 Postdelivery Insulin Requirements 316 After Discharge and Future Pregnancies 316 Suggested Reading 317 Differentiate Between Preexisting Diabetes and Gestational Diabetes When evaluating patients hospitalized during pregnancy, it is important to determine whether they have preexisting type 1 or type 2 diabetes, or whether they have gestational diabetes. Knowing their preconception diagnosis and treatment as well as the circumstances of their diagnosis provides insights into their current treatment and eventual postpartum care. Definition of Gestational Diabetes (See Table 26.1) As opposed to preexisting diabetes, gestational diabetes mellitus (GDM) is diagnosed during pregnancy. GDM screening is typically performed at 24–28 weeks of gestation when insulin Table 26.1 ADA diagnostic criteria for gestational diabetes Diagnosis of gestational diabetes Glucose in mg/dl One-step 75 g Fasting: ≥92, 1 h: ≥180, 2 h: ≥153 method One abnormal value required Two-step Step 1: 50 g Non-fasting: 1 h: ≥130 to ≥140 method Step 2: 100 g (institutional) Fasting: ≥95, 1 h: ≥180, 2 h: ≥155, 3 h: ≥140, usually two abnormal values required 26 Management of Preexisting Diabetes and Gestational… 309 resistance has increased and hyperglycemia is usually apparent upon testing. Diagnosing GDM has been controversial. Recommendations have shifted over time and differ by organization. The 2018 American Diabetes Association (ADA) guidelines propose two diagnostic protocol options: a one-step fasting 75 g oral glucose tolerance test (OGTT) and a two-step evaluation which includes a 50 g non-fasting screen followed by a fasting 100 g OGTT for those who screen positive. The one-step OGTT employs glucose cutoffs of ≥92 mg/dL fasting, ≥180 mg/ dL at 1 h, and/or ≥153 mg/dL at 2 h with one abnormal value indicating a positive test. The non-fasting 50 g screen, also called a glucose loading test (GLT), uses cutoffs which range from ≥130 mg/dL to ≥140 mg/dL at 1 h, depending on institutional guidelines. The subsequent fasting 100 g OGTT is positive when at least two (or one, depending on the guideline used) of the following cutoffs, proposed by Carpenter and Coustan, are met: ≥95 mg/dL fasting, ≥180 mg/dL at 1 h, ≥155 mg/dL at 2 h, or ≥140 mg/dL at 3 h. The Carpenter-Coustan cutoffs have been demonstrated to confer additional benefit with respect to pregnancy-induced hypertension, shoulder dystocia, cesarean delivery, and macrosomia compared to the less stringent criteria from the National Diabetes Data Group, which uses OGTT cutoffs 5–10 mg/dL higher than Carpenter-Coustan. The one-step method is a more sensitive method to detect gestational hyperglycemia, and data from the Hyperglycemia and Adverse Pregnancy Outcome (HAPO) trial suggested that there is a continuous relationship between maternal glucose and primary cesarean section delivery, neonatal hypoglycemia, birth weight over the 90th percentile, and cord C-peptide over the 90th percentile, and the one-step method is therefore the method endorsed by the International Association of Diabetes and Pregnancy Study Groups (IADPSG). The complexities of the debate between the one-step and two-step methods include discussions of changes in prevalence of diagnosis, effects of outcomes, and medical costs. Women at high risk of abnormal glucose metabolism should be evaluated during the first trimester. The 2018 ACOG Practice Bulletin expanded list of criteria for patients considered high risk are those with: 310 G. P. Westcott and F. M. Brown • High-risk race or ethnicity • Hypertension • HDL cholesterol less than 35 mg/dL or triglyceride level over 250 mg/dL • Polycystic ovarian syndrome or clinical conditions associated with insulin resistance such as acanthosis nigricans • History of cardiovascular disease • Obesity • GDM during a previous pregnancy • Previous baby with birth weight over 9 pounds • Glycosuria • Having a first-degree relative with diabetes • Impaired fasting glucose These women should be evaluated with the one-step fasting 75 g 2 h OGTT. A screening GLT is not indicated in this high-risk population, as the sensitivity of this test is approximately 80% and therefore may be negative in 20% of patients with GDM. Note that alternative measures may also be incorporated in determining fetal and maternal risk. An A1c value ≥5.9 |
during the first trimester is associated with congenital malformations, pre- eclampsia, shoulder dystocia, and perinatal death. Note that while an A1c ≤5.9 has a high negative predictive value for ruling out overt diabetes, it is not highly sensitive in diagnosing gestational diabetes. Therefore, screening should be reassessed at 24–28 weeks of gestation with either the one-step or the two-step method for women with A1c <5.9% on early screening. Glycemic Targets (See Table 26.2) Glycemic targets are the same regardless of whether the patient has preexisting or gestational diabetes. ADA and the American College of Obstetricians and Gynecologists (ACOG) accepted targets are <95 mg/dL fasting and postprandial targets of <140 mg/ dL at 1 h and <120 mg/dL at 2 h after a meal commences (typi- cally patients measure either 1 or 2 h postprandial blood glucose, not both). However, it is noteworthy that in the normal pregnant populations, mean ± SD for fasting blood glucose is 71 mg ± 8 mg/ 26 Management of Preexisting Diabetes and Gestational… 311 Table 26.2 Glycemic targets for pregnant women with diabetes Glycemic targets Glucose in mg/dl Antepartum ACOG and ADA 2018 Fasting: <95, 1 h PP: <140, 2 h PP: Joslin <120 Fetal AC ≥75th percentile (GDM Fasting: <95a or <99b, 1 h PP: <130 only) Fasting: 60–79, 1 h PP: 90–109 Labor and delivery 80–110 Postpartum Fasting: <100, 2 h PP: <140 PP postprandial aGDM bPreexisting DM dl, and post-meal blood glucose at 1 h is 109+/−13 mg/dl and at 2 h is 99.3 ± 10 mg/dl, which are considerably lower than the upper ranges of these targets. So, some institutions advocate low- ering the upper range of targets; for example, Joslin Diabetes Center recommends 1 h postprandial glucose target of 100– 129 mg/dl. For patients with gestational diabetes, more stringent glycemic targets should be considered in patients with a fetus whose Hadlock abdominal circumference (AC) is ≥75th percen- tile prior to 34 weeks of gestation. The fetal AC discriminates low and high risk for large-for-gestational-age newborns. When high- risk fetal AC growth is identified, lower glucose targets signifi- cantly reduce excessive fetal growth. Therefore, fasting glucose target of 60–79 mg/dL and 1 h postprandial target of 90–109 mg/ dL are recommended in these patients. Note that this guidance applies specifically to gestational diabetes, since there is no evi- dence to support similar adjustments in preexisting type 1 or 2 diabetes. In women with preexisting diabetes, these targets may be quite difficult to achieve without increasing the risk of signifi- cant hypoglycemia. Treatment Options There is considerable overlap between outpatient and inpatient management of diabetes during pregnancy. In addition to moni- toring blood glucose while fasting and at peak post meal, patients 312 G. P. Westcott and F. M. Brown diagnosed with gestational diabetes and preexisting diabetes are advised to adhere to consistent carbohydrate intake with small frequent meals, for example: 30 g of carbohydrates for breakfast and 45 g for lunch and dinner with 15–20 g snacks between meals and before bed. Fasting urine ketone measurement in the morning helps identify patients who are over-restricting carbohydrates. Counseling should be provided on the quality of the diet. To con- ceptualize a healthy diet, we recommend the “Healthy Plate” in which half the plate is filled with non-starchy vegetables, one- quarter with whole grains, and one-quarter with lean protein. Fats are derived primarily from plant sources. Low-impact exercise is also encouraged. Patients with Gestational Diabetes Patients with gestational diabetes who maintain blood glucose within target ranges with lifestyle interventions alone are classi- fied as having GDMA1. For patients who are unable to maintain glucose within target range without over-restricting carbohy- drates, insulin is recommended. If there is no history of preexisting diabetes, patients who require insulin to maintain target glucose concentrations are classified as having GDMA2. In gestational diabetes, the pattern of hyperglycemia should guide the choice of insulin. To reduce fasting hyperglycemia, NPH at bedtime is considered standard of care. Insulin analogues aspart and lispro can be dosed before the meal to manage postprandial hyperglycemia, typically via a fixed premeal dose that can be titrated to achieve glycemic target. As mealtime insulin doses are up-titrated to control postprandial glucose peak, hypoglycemia prior to the subsequent meal is common and should be prevented with a small snack 2–3 h after the meal. The use of oral medications during pregnancy has been contro- versial. Until recently, ACOG had endorsed the use of glyburide and metformin for gestational diabetes despite the fact that the FDA has not approved the medications for this indication, while the ADA has stated that insulin is the first-line therapy for GDM 26 Management of Preexisting Diabetes and Gestational… 313 and type 2 diabetes in pregnancy. ACOG has now also embraced this view and considers insulin the preferred treatment for diabetes during pregnancy. Because glyburide crosses the placenta, it can contribute to fetal hyperinsulinemia, and there is evidence that it increases the risk of macrosomia, preeclampsia, neonatal hypogly- cemia, and hyperbilirubinemia. Metformin crosses the placenta, has high failure rates, and achieves therapeutic levels in the fetus, and recently published data from the metformin in gestational dia- betes trial found that at 9 years, offspring of women who received metformin during pregnancy were larger by weight, arm and waist circumference, waist-to-height ratio, BMI, triceps skinfold, and MRI abdominal fat volume. Patients with Type 1 Diabetes Patients with type 1 diabetes typically continue their current regimen with either multiple-dose injections or insulin pump therapy. This includes basal insulin and mealtime insulin admin- istered as fixed doses or determined by a ratio of insulin to cal- culated carbohydrate intake in combination with correctional insulin based on a correction factor or sliding scale. Insulin detemir is non-inferior to NPH insulin for basal dosing based on results from a randomized controlled trial. Glargine is not rec- ommended in pregnant patients or in those planning a preg- nancy, as there is no randomized controlled trial outcome data comparing it to detemir or NPH insulin. There is a six- to eightfold increased affinity of glargine for the IGF-1 receptor, which is of hypothetical concern, although insulin does not cross the placenta and therefore is unlikely to contribute to increased fetal growth. Insulin analogues aspart and lispro are preferred for mealtime dosing as above. Glulisine and degludec have not been studied in pregnancy. Insulin requirements vary throughout pregnancy in all patients on insulin, increasing in the first 9 weeks of gestation, decreasing in weeks 9–16, increasing again until week 37, and then decreasing again in the final month until delivery. Patients with type 1 diabetes may also benefit from continuous glucose monitoring. 314 G. P. Westcott and F. M. Brown Patients with Type 2 Diabetes Patients with type 2 diabetes should be treated exclusively with insulin. There is inadequate safety data regarding the use of GLP-1 agonists, DPP-4 inhibitors, alpha glucosidase inhibitors, and SGLT2 inhibitors in pregnancy. Diabetic Retinopathy In women with preexisting type 1 or type 2 diabetes, a dilated eye exam should be performed in each trimester of pregnancy with the frequency of follow-up depending on the level of baseline reti- nopathy. The level of retinopathy and the timing of the last dilated eye exam should be determined in all hospitalized patients. For patients who require prolonged hospitalization, an ophthalmology consultation may be necessary. Special Situations Diabetic Ketoacidosis DKA may occur at lower glucose levels than what is typically seen in the nongravid state (<200 mg/dl) due to the flux of glucose from the maternal to the fetal circulation via glucose transporter-1 (GLUT-1), the lowered renal threshold for glucose leading to enhanced glycosuria due to reduced tubular reabsorption capacity and increased GFR, and the accelerated starvation state that contributes to ketonemia. Infection, insulin omission or failed delivery, or the use of medications such as terbutaline or glucocorticoids may predispose to DKA. When a patient is seen in triage or as an inpatient due to concern for DKA, insulin pump infusion issues should be ruled-out and insulin given by syringe or intravenously if needed, adequate hydration ensured, and electrolyte abnormalities corrected. Insulin drip protocols should be employed when necessary. Intravenous dextrose may be required to maintain mild hyperglycemia (150–200 mg/dl) to allow for adequate insulin infusion until the anion gap is closed 26 Management of Preexisting Diabetes and Gestational… 315 and the bicarbonate level has normalized. In a recent study, fetal demise occurred in 15.6% of DKA in pregnancy cases; the need for maternal ICU admission and higher serum osmolality were risk factors for fetal demise. Betamethasone Therapy Betamethasone is often given in the setting of preterm labor as it has been shown to reduce perinatal mortality and incidence of respiratory distress syndrome in infants delivered before 34 weeks. It is typically given in two doses of 12 mg 24 h apart. An algo- rithm developed by Mathiesen and others helps proactively adjust insulin dosing to prevent severe glycemic abnormalities. On the day of the first betamethasone dose, the evening insulin dose should be increased by 25%. All insulin doses should be increased (compared to baseline dose) by 45% on day 2, by 40% on day 3, by 30% on day 4, and by 10% on day 5. On days 6 and 7, insulin doses may be reduced toward original dosing, with the caveat that requirements may not return completely to pre-glucocorticoid dosing, as baseline insulin resistance has likely increased as the pregnancy has advanced. Labor and Delivery Glycemic Targets Careful monitoring of blood glucose during labor and delivery is required. Since intrapartum glucose levels affect the risk of neonatal hypoglycemia, the risk is lowest when maternal intrapartum glucose levels average <100 mg/dL while aiming for a range between 80 and 110 mg/dL. Treatment Strategies In the setting of planned induction of labor or preeclampsia requiring magnesium infusion, oral intake may be decreased or 316 G. P. Westcott and F. M. Brown eliminated for several hours. For patients with GDM or type 2 diabetes, basal insulin doses may need to be reduced or held, depending on the timing of expected delivery, and prandial doses likewise held or reduced based on intake status. For patients with type 1 diabetes, an intravenous insulin drip is preferred while the patient is NPO during labor, delivery, and immediately postdeliv- ery. An ideal insulin drip protocol will include insulin and dex- trose infusions that can be titrated hourly by nursing staff based on finger-stick blood glucose data. When oral intake is resumed, the transition back to subcutaneous insulin can be accomplished by overlapping basal (2 h) and prandial insulin (1 h) with the insu- lin drip. An insulin drip can also be used in patients with GDM or type 2 diabetes if intrapartum blood glucose is difficult to control. Postpartum Postdelivery Insulin Requirements Following delivery, there is a significant decrease in insulin resis- tance as placental hormones clear. Patients with GDM typically do not require insulin following delivery, and it should be discon- tinued. Patients with type 2 diabetes who were not on insulin prior to conception may also be trialed off insulin. Oral medications should be held as long as the patient is breastfeeding since these medications distribute to breast milk. Postpartum blood glucose can be monitored following delivery to confirm a return to normal levels (<100 mg/dL fasting and <140 mg/dL at 2 h postprandially). Patients with type 1 diabetes typically require a reduction of insulin doses to approximately 50% of preconception dose. Breastfeeding is considered beneficial due to increased insulin sensitivity and weight loss and should be encouraged for at least 6 months if possible. After Discharge and Future Pregnancies For patients with GDM, the postpartum period is a key opportu- nity for counseling regarding interventions to reduce the risk of 26 Management of Preexisting Diabetes and Gestational… 317 developing type 2 diabetes in the future. The risk of developing type 2 diabetes is approximately 50% at 5–10 years after delivery. Dietary and exercise modifications should be encouraged, and if preconception BMI was ≥25 (or ≥23 for Asians), a goal of 7% weight loss compared to preconception weight will reduce the probability of developing type 2 diabetes in the future. All patients with GDM should undergo a 75 g 2 h OGTT at 6 weeks postpar- tum to assess for impaired glucose metabolism or type 2 diabetes. They |
should also be screened for GDM or undiagnosed type 2 diabetes early in subsequent pregnancies. Prior to discharge, patients with type 1 or type 2 diabetes should be advised to sched- ule appointments 2 weeks and 6 weeks postpartum with their out- patient endocrinologist as insulin sensitivity will be returning to baseline and insulin dosing may require adjustment. The 6 weeks postpartum visit should also include labs for A1c, creatinine, and urine albumin/creatinine ratio, and TSH should be checked given the risk of postpartum thyroiditis particularly in patients with type 1 diabetes and to monitor postpartum levothyroxine dosing changes in patients with type 1 DM who have concurrent chronic lymphocytic thyroiditis. Counseling on contraceptive options and the optimal timing of the next eye exam and endocrinology fol- low- up should be provided. Suggested Reading American Diabetes Association. 13. Management of diabetes in pregnancy: standards of medical care in diabetes—2018. Diabetes Care. 2018;41(Suppl 1):S137–S43. Brown FM, Wyckoff J. Application of one-step IADPSG versus two-step diagnostic criteria for gestational diabetes in the real world: impact on health services, clinical care, and outcomes. Curr Diab Rep. 2017;17(10):85. Committee on Practice Bulletins—Obstetrics. ACOG practice bulletin no. 190: gestational diabetes mellitus. Obstet Gynecol. 2018;131(2): e49–64. Garcia-Patterson A, Gich I, Amini SB, Catalano PM, de Leiva A, Corcoy R. Insulin requirements throughout pregnancy in women with type 1 diabetes mellitus: three changes of direction. Diabetologia. 2010;53(3):446–51. 318 G. P. Westcott and F. M. Brown Harvard School of Public Health. Healthy eating plate & healthy eating pyra- mid. 2011. https://www.hsph.harvard.edu/nutritionsource/healthy-eating- plate. International Association of Diabetes and Pregnancy Study Groups Consensus Panel. International association of diabetes and pregnancy study groups recommendations on the diagnosis and classification of hyperglycemia in pregnancy. Diabetes Care. 2010;33(3):676–82. Joslin Diabetes Center. Joslin diabetes center and Joslin clinic guideline for detection and management of diabetes in pregnancy. 2017. https://www. j o s l i n . o rg / d o c s / P r eg n a n cy - G u i d e l i n e s _ 1 1 - 1 3 - 2 0 1 6 _ c o r- rected_1-11-2017.pdf. Kjos SL, Schaefer-Graf UM. Modified therapy for gestational diabetes using high-risk and low-risk fetal abdominal circumference growth to select strict versus relaxed maternal glycemic targets. Diabetes Care. 2007;30(Suppl 2):S200–5. Mathiesen ER, Christensen AB, Hellmuth E, Hornnes P, Stage E, Damm P. Insulin dose during glucocorticoid treatment for fetal lung maturation in diabetic pregnancy: test of an algorithm [correction of algorithm]. Acta Obstet Gynecol Scand. 2002;81(9):835–9. The HAPO Study Cooperative Research Group. Hyperglycemia and adverse pregnancy outcomes. N Engl J Med. 2008;358(19):1991–2002. Inpatient Insulin Pump 27 Management Maria Vamvini and Elena Toschi Contents Insulin Pump Use in the Hospital in Non-critically Ill Patients 320 Assess Preadmission Diabetes Status 320 Patients Who Can Continue Using Their Insulin Pump 321 Assess Current Nutritional Status 321 Assess Other Medications That May Affect Glycemic Status 322 Medical Orders for Insulin Pump Treatment 322 Insulin Pump Management 323 Insulin Pump Use in the Hospital in Critically Ill Patients 324 Contraindications for Self-Administered Insulin Pump Therapy 324 Special Considerations Regarding Pump Therapy 325 Insulin Pump Use in the Hospital in Patients Undergoing Surgical Procedures 325 During Imaging Studies 326 In Diabetic Ketoacidosis 326 Peripartum 327 Transition from Continuous Subcutaneous Insulin Infusion (CSII) to Multiple Daily Injection (MDI) Insulin Regimen 327 M. Vamvini · E. Toschi (*) Adult Clinic, Joslin Diabetes Center, Harvard Medical School, Beth Israel Deaconess Medical Center, Department of Endocrinology and Diabetes, Boston, MA, USA e-mail: maria.vamvini@joslin.harvard.edu; elena.toschi@joslin.harvard.edu © Springer Nature Switzerland AG 2020 319 R. K. Garg et al. (eds.), Handbook of Inpatient Endocrinology, https://doi.org/10.1007/978-3-030-38976-5_27 320 M. Vamvini and E. Toschi Use of Continuous Glucose Monitor (CGM) in the Hospital 328 In Non-ICU Patients 328 In ICU Patients 328 Sensor-Augmented Insulin Pump and Hybrid Closed-Loop System 329 Evaluate Diabetes Treatment at Time of Discharge 329 Follow-Up After Discharge 330 Suggested Readings 330 Insulin Pump Use in the Hospital in Non-critically Ill Patients Assess Preadmission Diabetes Status The hospital physician should obtain a detailed medical and diabe- tes history including duration of diabetes, type of diabetes, presence of any complications, and review of most recent A1c. If A1c has not been checked in the past 3 months, patient should have a repeat A1c checked at the time of admission. The type of insulin pump and insulin formulation (Humalog or Novolog) as well as pump settings including basal rates, insulin-to-c arbohydrate ratio/s (I:CHO), and the correction or sensitivity factor/s should be clearly docu- mented. Pump settings also include target glucose (see Table 27.1). Table 27.1 Insulin order for the self-administering insulin pump Name of Insulin Pump: Type of Insulin: Target glucose: Settings: Time Basal Time I:CHO Time CF/SF (U/hour) (U/g (U/mg/ carb) dl) MN–6 AM 0.6 MN–6 AM 1:10 MN–8 AM 1:50 6 AM–12 PM 0.8 6 AM–10 AM 1:8 8 AM–8 PM 1:35 12 PM–8 PM 0.7 10 AM–4 PM 1:10 8 PM–MN 1:50 8 PM–MN 0.5 4 PM–8 PM 1:12 Total basal X 8 PM–MN 1:15 27 Inpatient Insulin Pump Management 321 A focused physical examination assessing body weight and skin sites used for pump infusion set should be performed. The pump site should be inspected for possible pump site issues including ecchymosis, hypo- and hypertrophy, infection, and leaking. Careful assessment for diabetic neuropathy and vascular disease should be conducted. Patients Who Can Continue Using Their Insulin Pump Patients on insulin pump therapy are usually knowledgeable about insulin pump technology and management. These patients should be allowed to use their insulin pumps in the hospital set- ting if they are deemed physically, cognitively, and emotionally able to do so. Basal rates may need to be lowered (generally to about 80%) to prevent hypoglycemia. Patient and team should discuss insulin regimen changes recommended while in the hospital. Target glycemic goals may differ between staff team and patient and, therefore, both communication and documen- tation of recommended glucose targets are important for safe and satisfactory care. In non-critically ill hospitalized patients, both the American Diabetes Association (ADA) and Endocrine Society recommend goal for fasting and pre-meal blood glu- cose (BG) is <140 mg/dl and random glucose <180 mg/dl. For contraindications for insulin pump use, see section “Contraindications for Self-Administered Insulin Pump Therapy”. Assess Current Nutritional Status All patients with diabetes should follow a consistent carbohydrate meal plan while in the hospital. Many hospitalized patients are rendered nothing per oral (NPO) for a variety of reasons (impend- ing surgery or diagnostic procedures, gastrointestinal disease, inability to eat). It is important that the reason and anticipated duration of NPO status are documented. Any special dietary restrictions should be noted. If a patient is getting enteral tube feedings, note the content, rate, and times of tube feeds. Similar 322 M. Vamvini and E. Toschi data need to be collected for parenteral nutrition. Based on this information, insulin pump settings may need to be adjusted. In patients who are NPO, it is recommended that the basal rate should be decreased by 20–50%. In cyclical enteral tube feeding, basal rates may need to be increased 2 hours prior to initiation of the feeding cycle, initially by 20%, and then titrated upward as needed. In patients receiving total parenteral nutrition (TPN), basal rate may need to be adjusted depending on the amount of carbohydrates (dextrose) in each TPN bag. Assess Other Medications That May Affect Glycemic Status Most hospitalized patients are likely to be receiving one or more medications that can potentially affect their blood glucose levels. Most commonly used medications are the glucocorticoids. Basal rates as well as insulin-to-carb ratio and sensitivity factor should be adjusted to mitigate glucocorticoid-induced hyperglycemia. If possible, medications for intravenous (IV) infusion should be prepared in glucose-free solutions rather than in dextrose in water. Medical Orders for Insulin Pump Treatment In order to allow a given patient to continue using an insulin pump, a medication order for the insulin pump must be pro- vided by a licensed independent practitioner. A medication order to allow a patient to continue using an insulin pump includes acknowledgment that the patient has been assessed to be competent in operating the pump and that no exclusion criteria apply (see section “Contraindications for Self- Administered Insulin Pump Therapy”). The orders for the self- administering insulin pump should include type of insulin, basal rate, and bolus doses for meals (insulin-to-carb ratio) and for hyperglycemia correction (insulin sensitivity or correction factor) along with glucose targets (Table 27.1). The order 27 Inpatient Insulin Pump Management 323 should also dictate the frequency of blood glucose monitoring. It is optimal that an insulin pump order in the electronic medical record prompts the practitioner to obtain an endocrinology and nutrition consultation, if this is a possibility at a given institution. Insulin Pump Management If a medication order for insulin pump self-administration has been activated, the patient will be considered responsible for programming his/her insulin pump and changing the infusion set as per his/her own regimen (change infusion set is recommended every 2–3 days). Blood glucose should be checked at least four times a day before meals and before bedtime or every 4 hours for NPO patients. Documentation should be completed utilizing an insulin pump flowsheet (see Fig. 27.1). It is important that BG data are reviewed at least once daily by the treating team or endocrinologist for insulin dose adjustments. Basal insulin should be adjusted to keep fasting BG <140 mg/dL, and nutritional insulin should be adjusted to maintain all other BG levels in 100–180 mg/dl range. Insulin doses should be increased or decreased by 10–20% at a time to produce a meaningful effect. The insertion site should be assessed at every shift and if glu- cose values >250 mg/dl. All infusion sets shall be changed by the patient at least every 72 hours. It is good practice to record the date and time of the last infusion set change once the patient is admitted to the hospital. Indications to change infusion sets more frequently may include but are not limited to: • The site is erythematous, swollen, or warm to touch. • Bleeding at insertion site. • Discomfort at insertion site. • Unresolved delivery alarm alerts. • The patient has two consecutive blood glucose readings greater than 250 mg/dl which are refractory to correction boluses. 324 M. Vamvini and E. Toschi 1 2 3 4 5 6AM 7 8 9 10 11 12PM BG (mg/dL) 201 154 Carbs (g) 30 45 Meal Bolus (units) 3 4.5 Correction Bolus (units) 1 0 Basal (u/hr) 0.5 0.7 Fig. 27.1 Insulin pump flowsheet Insulin Pump Use in the Hospital in Critically Ill Patients It is recommended that critically ill patients not use their insulin pump. Instead they should be transitioned to intravenous insulin treatment. Intravenous insulin treatment should start as per usual in-hospital protocol. ADA recommends for most ICU patients glucose targets between 140 and 180 mg/dl. Contraindications for Self-Administered Insulin Pump Therapy • Acute change in conscious state/mental status as assessed by nurse or treating team • Some procedures involving anesthesia that alter the patient’s capability to manage the pump for longer period of time (>12 hours) • Inability to demonstrate competence with pump management • Risk of suicide or suicidal ideation • Recurrent or persistent episodes of hypoglycemia or hypergly- cemia • Patient refusal or inability to participate in pump management • Inability to procure their own supplies (reservoirs and infusion sets should be changed at least every 72 hours) • Unresolved pump failure 27 Inpatient Insulin Pump Management 325 • Unexplained hyperglycemia • Diabetic ketoacidosis and hyperglycemic hyperosmolar state • Unexplained, persistent hypoglycemia • Lack of pump supplies • Health-care decision or lack of trained health-care personnel on management of insulin pump therapy Special Considerations Regarding Pump Therapy Insulin Pump Use in the Hospital in Patients Undergoing Surgical Procedures In procedures and surgeries requiring moderate sedation or anes- thesia, patients have limited or no ability to operate the insulin pump independently throughout the perioperative period. In some cases, it is appropriate to discontinue the insulin pump and provide insulin therapy via an alternative route. Among rea- sons to consider stopping pump use are the length of the proce- dure, postoperative recovery time, and use of imaging perioperatively (i.e., MRI, CT scan, radiation therapy). When use of a self-administering insulin pump is |
contraindicated or must be stopped, the patient may require either subcutaneous insulin via syringe or an insulin drip to maintain glycemic control for the duration of time that the pump is disconnected. Blood glucose monitoring is case dependent but may be done as frequently as 1–2 hours. In other cases, especially when patients undergo ambulatory or short-term surgical procedures lasting a few hours (≤ 2 hours), continuation of the insulin pump at a basal rate administration of insulin may be appropriate. In this scenario, basal rate should be reduced by 20–50% 2 hours pre-procedure and kept at this lower rate up to 4 hours postoperatively. Blood glucose monitoring during procedures is case dependent but may be done as frequently as 1–2 hours. In cases where an insulin pump is to continue while the patient is sedated or under anesthesia, the following is recommended: 326 M. Vamvini and E. Toschi • An order to continue the self-administering insulin pump at the basal rate is written by the primary team if the patient is under an observation status (non-inpatient) and has no existing order in place for the pump. • Blood glucose should be checked before the procedure/sur- gery, hourly during procedure/surgery and following proce- dure/surgery. • IV access is confirmed. • Documentation is completed utilizing the insulin pump flowsheet. • Insertion site is assessed pre- and post-procedure/surgery. If the insertion site is not ideally located due to the anticipated positioning of the patient, it is recommended that the patient should move the site to a more ideal location. Infusion site and tubing should be taped to secure placement and avoid dislodging during procedure. During Imaging Studies During imaging or procedures utilizing x-ray, the pump should be covered by lead apron. Prior to an MRI, insulin pump and metal infusion set, if used, should be disconnected from the patient in the MRI scanning suite (a minimum of 8 feet away from MRI machine) because of incompatibility with the MRI scanning envi- ronment. Interruption of insulin infusion should be overall less than 60 min, and blood glucose levels should be monitored. If duration of the imaging study is long and the pump needs to be discontinued for longer periods of time, the patient may require either subcutaneous insulin administration or an insulin drip to maintain glycemic control and avoid ketosis for the duration of time that the pump is disconnected. In Diabetic Ketoacidosis Insulin pump failure can lead to diabetic ketoacidosis. Pump mal- function can be due to dislodgement of the infusion set and block- 27 Inpatient Insulin Pump Management 327 age or leakage of the tubing system, all causing an interruption of insulin delivery. In patients with diabetic ketoacidosis, the insulin pump must be discontinued, and they should be treated with continuous intravenous insulin administration as per hospital protocol. These patients may be transitioned back to the insulin pump after resolution of the diabetic ketoacidosis when clinically stable and when the acid-base disorder is corrected. The intravenous insulin should be overlapped with the pump restart by at least 2 hours to allow for adequate insulin absorption. Frequent BG monitoring is needed for several hours after the pump is restarted to ensure adequate glycemic control. Peripartum Many women with type 1 diabetes are treated with an insulin pump during pregnancy. It is recommended that the insulin pump be disconnected peripartum. An intravenous insulin drip is pre- ferred while the patient is NPO during labor, delivery, and immediately post-delivery. During labor and delivery, the mater- nal blood glucose level should be kept between 80 and 110 mg/dl. After delivery, insulin requirement falls dramatically, and insulin rate should be decreased. For more details, see Chap. 26, “Management of Preexisting Diabetes and Gestational Diabetes During Hospitalization.” Transition from Continuous Subcutaneous Insulin Infusion (CSII) to Multiple Daily Injection (MDI) Insulin Regimen When use of a self-administered insulin pump or CSII is contra- indicated or must be stopped, the patient will require either sub- cutaneous insulin via syringe or an insulin drip to maintain glycemic control for the duration of time that the pump is dis- connected. When there is no indication for treatment with an insulin drip, insulin should be administered subcutaneously 328 M. Vamvini and E. Toschi through MDI. Because of varying absorption rates, subcutaneous insulin ideally needs to be initiated before discontinuation of the pump. Long- acting (basal) insulin should be administered at least 2 hours and rapid-acting insulin 30 minutes before disconnecting the pump. To transition to MDI insulin regimen, the basal dose should be calculated using the 24 hour basal dose of insulin delivered from the pump. The total basal daily insulin can be given as once-daily or twice-daily injections. Prandial insulin can be calculated as half of a patient’s usual total daily dose of insulin divided by three. Alternatively, the patient, if able, should be allowed to calculate the prandial insulin using his/her insulin-to- carbohydrate ratio from the pump setting. His/ her correctional insulin bolus should be calculated according to the insulin pump correction factor. Capillary blood glucose should be measured before meals and bedtime or every 4 hours if the patient is NPO. Use of Continuous Glucose Monitor (CGM) in the Hospital In Non-ICU Patients There are currently no guidelines for use of CGM in the inpa- tient setting. Some sensors need to be calibrated, and some of them are affected from commonly used drugs such as acetamin- ophen. There is also a lack of evidence on accuracy during hypoxemia, hypotension, or hypothermia. Therefore, sensor readings or trends may not be accurate in the hospital setting. Thus far, the use of this technology in hospital has been largely experimental. In ICU Patients Two CGM systems are FDA-approved for use in hospitals: GlucoScout® (International Biomedical) and OptiScanner 5000®. However, use of CGM in critically ill patients in the ICU 27 Inpatient Insulin Pump Management 329 is not currently recommended. Data from several ICU studies have been conflicting, and there is no clear evidence that use of subcutaneous CGM systems improves the glycemic control of critically ill patients in a clinically significant manner. More large- scale studies are needed to determine potential beneficial effects from CGM use in the ICU. Sensor-Augmented Insulin Pump and Hybrid Closed-Loop System Sensor-augmented insulin pump and hybrid closed-loop systems which feature CGM are now available. Sensor-augmented insulin pumps can suspend insulin delivery based on CGM sensor reading to prevent hypoglycemia. Hybrid closed-loop systems not only can suspend infusion temporarily to prevent episodes of hypoglycemia but can also adjust basal insulin delivery based on sensor reading. However, patients are still required to bolus prior to meals and administer correction boluses as needed to keep these systems operating correctly. Therefore, similar criteria should be used to evaluate if the patient can operate these pumps while in hospital. The sensor-augmented insulin pump and hybrid closed-loop systems should not be used in the ICU settings. Evaluate Diabetes Treatment at Time of Discharge Clinical conditions may change during hospitalization necessitat- ing changes to pre-admission treatment for diabetes. Additionally, changes to diabetes treatment may be indicated due to poor pre- admission diabetes control. If there is a plan to discharge the patient to a rehabilitation or skilled nursing facility, case management should determine the competence of the facility to manage an insulin pump. Prior to patient transfer, the facility will be required to provide their protocol for managing patients on insulin pumps. Discharge paperwork should include the insulin pump treatment plan and a 330 M. Vamvini and E. Toschi contingency plan for insulin management in case the patient is not be able to continue insulin pump therapy. If pump use is not recommended for any reason prior to dis- charge, then a multiple daily injection regimen with long-acting and short-acting insulin for meals and correction doses should be provided. Reasons to be discharged on MDI include patient preference, mental status changes precluding restarting CSII, and lack of additional supplies. Follow-Up After Discharge Discharge plans should include a timely follow-up visit for con- tinued outpatient diabetes care. An appointment should be made for the patient to see their diabetes care providers within 2–4 weeks of discharge. Because glycemic control is expected to change after discharge, make sure that the patient is able to contact a diabetes care provider in case of high or low blood glucose levels. Suggested Readings American Diabetes Association. Diabetes care in the hospital. Diabetes Care. 2017;40(Suppl. 1):S120–7. Garg R, Hudson M, editors. Hyperglycemia in the hospital setting. New Delhi: JP Brothers; 2014. Grunberger G, Abelseth J, Bailey T, Bode B, Handelsman Y, Hellman R, et al. Consensus Statement by the American Association of Clinical Endocrinologists/American College of Endocrinology Insulin Pump Management Task Force. Endocr Pract. 2014;20(5). Joslin Clinical Guidelines at https://www.joslin.org/info/joslin-clinical- guidelines.html. Kannan S, Satra A, Calogeras E, Lock P, Lansang MC. Insulin pump patient characteristics and glucose control in the hospitalized setting. J Diabetes Sci Technol. 2014;8(3):473–8. Mendez CE, Umpierrez GE. Management of type 1 diabetes in the hospital setting. Curr Diab Rep. 2017;17(10):98. Peters AL, Ahmann AJ, Battelino T, Evert A, Hirschn IB, Murad MH, et al. Diabetes technology—continuous subcutaneous insulin infusion therapy 27 Inpatient Insulin Pump Management 331 and continuous glucose monitoring in adults: an endocrine society clinical practice guideline. J Clin Endocrinol Metab. 2016;101(11):3922–37. Thompson B, Korytkowski M, Klonoff DC, Cook CB. Consensus statement on use of continuous subcutaneous insulin infusion therapy in the hospi- tal. J Diabetes Sci Technol. 2018;12(4):880–9. Umpierrez GE, Hellman R, Korytkowski MT, Kosiborod M, Maynard GA, Montori VM, et al. Endocrine society. management of hyperglycemia in hospitalized patients in non-critical care setting: an endocrine society clinical practice guideline. J Clin Endocrinol Metab. 2012;97(1):16–38. Umpierrez GE, Klonoff DC. Diabetes technology update: use of insulin pumps and continuous glucose monitoring in the hospital. Diabetes Care. 2018;41(8):1579–89. Severe 28 Hypertriglyceridemia in the Hospitalized Patient Roselyn Cristelle I. Mateo and Om P. Ganda Contents Define Hypertriglyceridemia (HTG) 334 Risk Factors That Contribute to Elevated TG Levels 335 Physical Examination 336 Laboratory Work-Up 337 Evaluate Need for Insulin and/or Heparin Drip 338 Evaluate Benefit of Plasmapheresis 339 What Is a Safe Therapeutic Target? 339 What Are the Non-pharmacologic Means to Control HTG? 339 Determine the Appropriateness of Starting Fibrate Therapy 340 R. C. I. Mateo Joslin Diabetes Center, Department of Endocrinology, Beth Israel Deaconess Medical Center, Boston, MA, USA e-mail: roselyn.mateo@joslin.harvard.edu O. P. Ganda (*) Joslin Diabetes Center, Department of Medicine, Beth Israel Deaconess Medical Center, Boston, MA, USA e-mail: om.ganda@joslin.harvard.edu © Springer Nature Switzerland AG 2020 333 R. K. Garg et al. (eds.), Handbook of Inpatient Endocrinology, https://doi.org/10.1007/978-3-030-38976-5_28 334 R. C. I. Mateo and O. P. Ganda Determine Appropriateness of Starting Omega-3-Fatty Acid (OM3FA) Therapy 341 Determine Appropriateness of Starting Niacin Therapy 341 Determine Appropriateness of Starting HMG-CoA Reductase Inhibitors (Statins) 342 Evaluate Novel and Potential Therapies of TG-Lowering Agents 342 Suggested Readings 343 Define Hypertriglyceridemia (HTG) Clinical Practice Guidelines (CPG) from major professional societies, including the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (NCEP ATP III), National Lipid Association (NLA), American Association of Clinical Endocrinologists (AACE), and the Endocrine Society (TES), have proposed different criteria for the clinical diagnosis of ele- vated triglyceride levels under fasting conditions, as shown in Table 28.1. Severe HTG, usually >1000 mg/dl, accounts for 10–15% of cases of AP and often occurs in the setting of acute or chronic insulin deficiency. In most cases, AP requires emergency hospital- ization and can be fatal, if not treated promptly, due to severe Table 28.1 Criteria for high fasting TG NCEP ATP III NLA AACE TES Normal <150 mg/dL <150 <150 Normal <150 mg/dL Borderline 150–199 150–199 150–199 Mild 150–199 high High 200–499 200–499 200–499 Moderate 200–999 Very high >= 500 >= 500 >= 500 Severe 1000–1999 Very >= 2000 severe 28 Severe Hypertriglyceridemia in the Hospitalized Patient 335 hemodynamic changes, hypovolemia, and hypotension. AP due to HTG may follow more severe clinical course than that due to other causes. Risk Factors That Contribute to Elevated TG Levels Severe HTG levels are usually associated with genetic traits that are often combined with acquired risk factors such as overweight, physical inactivity, insulin resistance, metabolic syndrome, advanced chronic kidney disease (CKD), or uncontrolled diabetes mellitus (DM). The underlying genetic disorders include familial hypertriglyceridemia, familial dysbetalipoproteinemia, monogenic or polygenic chylomicronemia syndrome (FCS), acquired partial |
lipodystrophy, and familial combined hyperlipidemia (FCH). Pregnancy, hypothyroidism, autoimmune disorders such as para- proteinemia or systemic lupus erythematosus, and certain drugs are also contributing factors to HTG (Table 28.2). Table 28.2 Medications that may affect TG levels Drugs Mechanism of action Thiazide, furosemide Modulate adipocyte differentiation leading to accumulation of plasma TGs in susceptible patients with certain genetic polymorphisms Beta blockers (particularly Peripheral vasoconstriction through atenolol, metoprolol, and peripheral β-adrenergic receptors can propranolol) increase insulin resistance, leading to lowering of HDL-C, and increased TG; induce decreased TG hydrolysis through a reduction in the muscle lipoprotein lipase (LPL) and endothelial dysfunction from peripheral vasoconstriction Estrogen Increase the hepatic secretion of VLDL (continued) 336 R. C. I. Mateo and O. P. Ganda Table 28.2 (continued) Drugs Mechanism of action Bile acid sequestrants (BAS) Activation of phosphatidic acid (cholestyramine, colestipol, phosphatase promotes hepatic TG colesevelam) synthesis and induces secretion of TG-rich VLDL. BAS also act as farnesoid X receptor (FXR) antagonists and activate liver X receptor (LXR), thus increasing TG levels Protease inhibitors, e.g., Increase in VLDL production and ritonavir and lopinavir intermediate-density lipoproteins (IDL); decreased activity of lipoprotein lipase and hepatic lipase; development of insulin resistance and abnormal expression of the apolipoprotein CIII gene Second-generation Cause weight gain, insulin resistance, antipsychotic medications such and worsening of the metabolic as clozapine, olanzapine, syndrome risperidone, and quetiapine Immunosuppressants Inhibit LPL, stimulate hepatic (interferon, tacrolimus, lipogenesis sirolimus, others) Isotretinoin Slows down the metabolism of triglyceride-r ich lipoproteins (TRL), such as chylomicrons, and remnant particles Physical Examination Relevant physical examination should include measurements of body mass index (BMI) and blood pressure (BP); assessment of carotid and peripheral pulses; palpation of the liver and thyroid; and inspection of palms, soles, and extensor surfaces of the arms, buttocks, trunk, and tendinous attachments. Clinical features may include eruptive xanthomas, lipemia retinalis, hepatosplenomeg- aly, focal neurologic symptoms such as irritability, and recurrent epigastric pain consistent with pancreatitis. Eruptive cutaneous xanthomas are filled with foam cells that appear as yellow morbil- liform eruptions that measure 2–5 mm in diameter, often with ery- 28 Severe Hypertriglyceridemia in the Hospitalized Patient 337 thematous areolae. Palmar crease xanthomas, typically seen in familial dyslipidemia syndrome, appear as yellow deposits within palmar creases. Lipemia retinalis is a characteristic milky appearance of the retinal vessels and pink retina. Samples of lipe- mic plasma develop a creamy supernatant when refrigerated overnight. Laboratory Work-Up Order a glucose test, thyroid function tests, and a renal panel and liver panel to detect or rule out diabetes, hypothyroidism, and renal and liver disease. Thyroid hormone plays a role in the regulation of the synthesis, metabolism, and mobilization of lipids. Patients with hypothyroidism have increased levels of total cholesterol, low- density lipoprotein cholesterol, apolipoprotein B, lipoprotein(a) levels, and triglyceride levels. Hypertriglyceridemia and reduction and dysfunction of high-density lipoprotein are also common lipid disturbances in chronic kidney disease, caused mainly by the decreased efficiency of lipoprotein lipase (LPL)-mediated very Low Density Lipoprotein-TG (VLDL-TG) lipolysis. The liver, too, plays a crucial role in the synthesis, secretion, catabolism, and storage of lipids and lipoproteins. Alcoholic and nonalcoholic liver disease affects lipid metabolism differently. High alcohol consumption can cause excessive synthesis of triglycerides, hypercholesterolemia, defective esterification of plasma cholesterol, and decreased level of high-density lipoprotein cholesterol. Order a fasting lipid panel including total cholesterol, HDL-C, direct LDL, and TG. Hemoglobin A1c should be ordered to assess control of diabetes in the appropriate patient. Patients with HTG may present with acute pancreatitis (AP) and relatively low amylase levels. This is brought about by inter- ference caused by triglyceride-rich lipoprotein (TRL) that can result in falsely low amylase levels. Centrifugation before labora- tory testing can remove chylomicrons from plasma and eliminate artifacts in lipemic specimens. HTG can also interfere with bio- chemical measurement of glucose, leading to falsely lower levels in these patients. 338 R. C. I. Mateo and O. P. Ganda The Endocrine Society not only recommends against the rou- tine measurement of lipoprotein particle heterogeneity in patients with hypertriglyceridemia but also recognizes that measurement of apolipoprotein B (Apo B) or lipoprotein(a) [Lp(a)] levels can be of value in assessing cardiovascular (CV) risk in selected cases, such as those with familial combined hyperlipidemia. Evaluate Need for Insulin and/or Heparin Drip HTG can contribute to adverse CV events, including acute coro- nary events, and AP. During AP episodes, insulin promotes synthe- sis and activation of lipoprotein lipase (LPL), thereby accelerating chylomicron degradation. Treatment with insulin infusion, along with hemodynamic support, can dramatically improve the hydro- lysis of chylomicrons and large VLDL particles in patients with DM and uncontrolled hyperglycemia. Heparan sulfate proteoglycan chains normally bind LPL to the capillary endothelium. Heparin, administered as a bolus dose, has a stronger affinity for the LPL binding site than heparan sulfate, leading to the dissociation of heparan-LPL complexes from the endothelium to the plasma. This surge of free LPL is then able to bind to and metabolize chylomicrons and VLDL at an accelerated rate, thus lowering serum TG levels. In case reports, heparin was used in conjunction with an insulin drip or if triglyceride lowering is insufficient despite Nil Per Os (NPO) status, intravenous fluids, and insulin infusions. If heparin is needed despite other interventions, it is safe to start with a standard weight-based infusion to keep the International Normalized Ratio (INR) at 1.5–2 times the upper limit of normal. However, the use of heparin should be limited to short term in order to limit the depletion of LPL stores. There have been numerous reports of the use of heparin and insulin for acute reduction of triglycerides, although there are no established guidelines for efficacy of these modalities, and heparin could pos- sibly be detrimental in the setting of hemorrhagic pancreatitis. In a nondiabetic patient with severe HTG, a bolus dose of regu- lar insulin (0.1 U/kg) given subcutaneously can decrease serum TG rapidly after a few hours. It has been shown in case reports to be effective either as monotherapy or in conjunction with heparin 28 Severe Hypertriglyceridemia in the Hospitalized Patient 339 drip. However, there is insufficient evidence for the benefits of this approach, compared to hemodynamic supportive measures alone. Evaluate Benefit of Plasmapheresis Plasmapheresis involves the removal of units of whole blood anti- coagulated with heparin followed by centrifugation to separate the blood into the cellular elements and plasma. The cellular ele- ments are then mixed with a replacement for the discarded plasma and reinfused. Various studies through the years have repeatedly concluded that plasmapheresis is an effective treatment for reduc- ing the serum TG concentration. However, due to the lack of ran- domized and controlled trials, it is currently unknown if plasmapheresis may improve morbidity and mortality in the clini- cal setting of HTG-AP. There are currently no consensus clinical guidelines in the management of HTG-AP. What Is a Safe Therapeutic Target? An elevated TG level is not a target of therapy per se, to prevent AP, except when very high (>= 500 mg/dL). When TG levels are between 200 and 499 mg/dL, the targets of therapy are non-HDL- C and LDL-C for CV risk reduction. When the TG concentration is very high (>= 500 mg/dL), reducing the concentration to <500 mg/dL to prevent AP becomes the primary goal of therapy. However, some guidelines have concluded that risk of AP decreases if plasma TG concentration is decreased to levels below 1000 mg/dL. Below this level, the treatment goal should be directed toward prevention of premature atherosclerosis. What Are the Non-pharmacologic Means to Control HTG? Alcohol consumption should be reduced or eliminated. Lifestyle therapy, including dietary counseling to achieve appropriate diet composition to include foods with low glycemic index, physical activity, and a program to achieve weight reduction in overweight 340 R. C. I. Mateo and O. P. Ganda and obese individuals, is recommended as the initial treatment of mild-to-moderate hypertriglyceridemia. For severe and very severe hypertriglyceridemia (>1000 mg/ dl), combining reduction of total dietary fat and simple carbohy- drate intake with prophylactic drug treatment to reduce the risk of AP is recommended. Dietary modification should decrease weight, overall energy intake and intake of all fat (including saturated, unsaturated, and trans fats), and refined carbohydrates. NCEP and NLA advise a carbohydrate intake of 55%–60% and a protein intake of 15%–20% of the daily dietary intake. However, reduction in total fat intake is the cornerstone of treatment for preventing AP and should be limited to less than 15–20% of total calories. Plasma TG response to diet and weight loss is about 25%, with marked variation among patients. Medium-chain triglycerides (MCTs) may be added to make up caloric intake in patients with recurrent AP, as MCTs are not dependent on LPL for hydrolysis. Determine the Appropriateness of Starting Fibrate Therapy Treatment with fibrates has been found to be cost-effective as both monotherapy and combination therapy for lowering TG in the prevention of AP. However, the role of fibrates in the prevention of atherosclerotic cardiovascular disease (ASCVD) outcomes in statin-treated patients with optimal LDL-C remains controversial, with some evidence supporting their role in ASCVD event reduc- tion in those with TG concentrations of 200–499 mg/dL and HDL-C concentrations <40 mg/dL. A more potent fibrate, pemafi- brate, currently not available, is undergoing a long-term clinical trial for ASCVD event reduction. Fibrates decrease triglyceride levels by 30–50%. Fibrates may act by multifactorial mechanisms including increased fatty acid oxidation, increased LPL synthesis, reduced expression of Apo CIII, decreased VLDL-TG production, and increased LPL- mediated catabolism of triglyceride-rich lipoproteins (TRL). 28 Severe Hypertriglyceridemia in the Hospitalized Patient 341 Determine Appropriateness of Starting Omega-3-Fatty Acid (OM3FA) Therapy Use of OM3FAs is an effective TG-lowering treatment option, frequently in combination therapy, in the prevention of AP in high-risk patients with TG levels ≥500 mg/dl. The long-chain marine OM3FA [eicosapentaenoic acid, C20:5n-3 (EPA), and docosahexaenoic acid, C22:6n-3 (DHA)] can lower fasting and postprandial TG levels in a dose-dependent fashion. Doses of roughly 3–4 g/d of EPA plus DHA are neces- sary to reduce HTG by 20–40%. OM3FAs are available by pre- scription in capsules that contain >90% of OM3FA in variable proportion of EPA and DHA. In contrast, over-the-counter prepa- rations of OM3FA have variable quantities of EPA and DHA ranging from 20 to 50%, depending on the products, and gener- ally are not recommended for this purpose. A recently completed large cardiovascular trial, REDUCE-IT, employed 4 g daily of pure EPA vs placebo in patients with type 2 diabetes, with or without preexisting CVD, with TG 150–499 mg/dl at baseline. All subjects were on statin therapy and optimally controlled LDL-C. In this trial, there was an impressive 25% reduction in major CV end points. However, the CV outcomes were unrelated to the magnitude of TG reduction. This study points to some unique CVD benefits of pure EPA. Determine Appropriateness of Starting Niacin Therapy Niacin therapy is recommended principally as an adjunct for reducing TG, if fibrates and OM3FA are not adequately effective. At doses of 500–2000 mg/d, niacin lowers triglycerides by 10–30%, increases HDL cholesterol by 10–40%, and lowers LDL cholesterol by 5–20%. Patients with glucose intolerance and those with DM on oral medications or insulin, who have moderate to good glycemic control, can safely use niacin at moderate dosage, as an adjunct to keep TG in safe range. 342 R. C. I. Mateo and O. P. Ganda However, niacin should not be used for ASCVD event reduc- tion in individuals aggressively treated with a statin due to an absence of evidence for additional CV benefits in those with well- controlled LDL-C (<70–80 mg/dl). In the pre-statin era, high- dose niacin was found to reduce plaque progression in several clinical trials, but given the adverse effects including worsening of glucose control at higher dosage, it is currently not recom- mended for CVD reduction. Determine Appropriateness of Starting HMG-CoA Reductase Inhibitors (Statins) HMG-CoA reductase inhibitors, also known as statins, have a weak TG-lowering effect. They should not be used as monother- apy for HTG. They can have a synergistic TG-lowering effect in combination with fibrates and may be considered in patients in whom HTG is not controlled on fibrates or other TG-lowering agents. In combination therapy of statins with fibrates, fenofibrate is preferred over gemfibrozil, to prevent the risk of myositis. Evaluate Novel and Potential Therapies of TG-Lowering Agents Apolipoprotein CIII inhibitors are a novel class of |
drugs available for patients with familial chylomicronemia syndrome (FCS) for TG reduction. Apolipoprotein CIII (Apo CIII), which is primarily synthesized in the liver, is a key regulator of lipoprotein metabo- lism and plasma TG levels. It has a role in inhibiting the LPL- mediated hydrolysis of triglyceride-rich lipoproteins (TRL). It also affects the receptor-mediated hepatic uptake of remnants of TRL. It can also inhibit the activity of hepatic lipase at higher concentrations. Apo CIII is an independent risk factor for CVD and is associated with both impaired lipolysis and impaired clear- ance of TRL from the circulation. 28 Severe Hypertriglyceridemia in the Hospitalized Patient 343 Apo CIII inhibitors are second-generation, single-stranded, DNA-like antisense oligonucleotides designed specifically to bind to a specific RNA sequence. These then elicit degradation of the RNA through RNase H1 and allow the antisense drugs to selectively inhibit Apo CIII synthesis. Reductions in Apo CIII and TG levels have been reported in a small number of patients with the familial chylomicronemia syn- drome who were treated with Apo CIII inhibitors. These patients had defective LPL, and the mechanism of lowering of plasma TG levels was shown to be from an enhanced removal of TRL in a dose-dependent manner. These drugs are currently in phase III studies. Whether targeted reduction of Apo CIII will confer such a benefit in patients at high risk for CVD, including patients with DM and HTG, remains to be determined. Other novel approaches, in development, to reduce HTG include gene therapy for LPL deficiency and antibody-based therapies. Acknowledgments OG was partially supported by NIDDK grant # P30-DK036836. Suggested Readings Berglund L, Brunzell JD, Goldberg AC, et al. Evaluation and treatment of hypertriglyceridemia: an endocrine society clinical practice guideline. J Clin Endocrinol Metab. 2012;97:2969–89. Bhatt DL, Steg PG, Miller M, Brinton EA, Jacobson TA, Ketchum SB, et al. REDUCE-IT investigators. Cardiovascular risk reduction with icosapent ethyl for hypertriglyceridemia. N Engl J Med. 2019;380:11–22. Brahm AJ, Hegele RA. Chylomicronaemia--current diagnosis and future therapies. Nat Rev Endocrinol. 2015;11:352–62. Chait A, Eckel RH. The Chylomicronemia syndrome is most often multifac- torial: a narrative review of causes and treatment of the chylomicronemia syndrome. Ann Intern Med. 2019; https://doi.org/10.7326/M19-0203. Jacobson TA, Maki KC, Orringer CE, et al. National lipid association recom- mendations for patient-centered management of dyslipidemia: part 2. J Clin Lipidol. 2015;9:S1–122. 344 R. C. I. Mateo and O. P. Ganda Nakhoda S, Zimrin AB, Baer MR, Law JY. Use of the APACHE II score to assess impact of therapeutic plasma exchange for critically ill patients with hypertriglyceride-induced pancreatitis. Transfus Apher Sci. 2017;56:123–6. Rocha NA, East C, Zhang J, McCullough PA. ApoCIII as a cardiovascular risk factor and modulation by the novel lipid-lowering agent volane- sorsen. Curr Atheroscler Rep. 2017;19:62. Scherer J, Singh VP, Pitchumoni CS, Yadav D. Issues in hypertriglyceridemic pancreatitis: an update. J Clin Gastroenterol. 2014;48:195–203. Hypomagnesemia 29 Alan Ona Malabanan Contents Hypomagnesemia Should Be Considered in Patients with Hypocalcemia or Hypokalemia, Cardiac Dysrhythmias (Torsades de Pointes), Alcoholism, Diabetes, Diarrheal Illnesses, Renal Tubular Disorders and Use of Medications Associated with Hypomagnesemia such as Proton Pump Inhibitors, Diuretics, Cisplatin, and Amphotericin B 346 Serum Magnesium Does Not Reflect Total Body Magnesium Stores and a Total Body Magnesium Deficit May Exist Even with a Normal Serum Magnesium Level 347 A 24-Hour Urine Magnesium and Creatinine or a Fractional Excretion of Magnesium May Be Useful in Establishing the Etiology of Hypomagnesemia 347 A 24-Hour Urine Magnesium and Creatinine May Be Useful in Confirming Adequacy of Total Body Magnesium Stores 348 Hypocalcemia or Hypokalemia with Concomitant Hypomagnesemia Will Not Correct with Calcium or Potassium Therapy Alone 348 A. O. Malabanan (*) Beth Israel Deaconess Medical Center, Harvard Medical School, Division of Endocrinology, Diabetes and Metabolism, Boston, MA, USA e-mail: amalaban@bidmc.harvard.edu © Springer Nature Switzerland AG 2020 345 R. K. Garg et al. (eds.), Handbook of Inpatient Endocrinology, https://doi.org/10.1007/978-3-030-38976-5_29 346 A. O. Malabanan A Concomitant Assessment of Urinary Calcium Can Help Identify the Portion of the Nephron Affected in Hypomagnesemia 349 Severe Hypomagnesemia (Mg <1 mEq/L) and Symptomatic Hypomagnesemia Should Be Treated with Intravenous Magnesium Therapy 349 Oral Magnesium Oxide Therapy Is Limited by Diarrhea and Often Intravenous Magnesium Sulfate Therapy Is Necessary 349 In Addition to Replacement Magnesium Therapy, Addressing the Etiology of the Hypomagnesemia Is Necessary to Maintain Magnesium Homeostasis 350 Suggested Readings 352 Hypomagnesemia Should Be Considered in Patients with Hypocalcemia or Hypokalemia, Cardiac Dysrhythmias (Torsades de Pointes), Alcoholism, Diabetes, Diarrheal Illnesses, Renal Tubular Disorders and Use of Medications Associated with Hypomagnesemia such as Proton Pump Inhibitors, Diuretics, Cisplatin, and Amphotericin B Magnesium is an important intracellular cofactor for a multitude of cellular processes, and deficiency can disrupt several organ sys- tems. The human body has approximately 25 g of magnesium, 50–60% of which is found in the bone. Magnesium homeostasis is maintained by balancing dietary magnesium absorption and urinary magnesium losses. Up to 60–70% of a dietary magnesium load is absorbed in the gut, the majority in the ileum, with its absorption aided by high gastric acidity. Intestinal magnesium absorption is not regulated. Diarrheal illnesses cause increased magnesium losses and disrupt intestinal magnesium absorption. Serum magnesium levels are controlled primarily through reab- sorption by the kidneys. Illnesses or medications causing diuresis, such as alcoholism, diabetes mellitus or insipidus, or diuretics, lead to increased urinary losses of magnesium. Proton pump inhibitors decrease intestinal magnesium absorption. Cisplatin and amphotericin B may cause renal tubular dysfunction leading 29 Hypomagnesemia 347 to urinary magnesium losses. Magnesium is important for para- thyroid hormone release and action, which can disrupt calcium homeostasis. In addition, it is a cofactor for the sodium-potassium ATPase, and deficiency leads to hypokalemia. As such, hypomag- nesemia may cause neuromuscular and cardiac irritability. Serum Magnesium Does Not Reflect Total Body Magnesium Stores and a Total Body Magnesium Deficit May Exist Even with a Normal Serum Magnesium Level Extracellular magnesium represents only 1% of the total body magnesium. As a result, serum magnesium is not an accurate measure of total body magnesium stores and cannot accurately demonstrate successful repletion of body magnesium stores. A test for red blood cell magnesium is available, but due to pro- longed turnaround time as well as artifact related to improper specimen processing, it is of limited utility in the inpatient setting. Magnesium treatment should be considered, even with a normal serum magnesium level, if there is hypocalcemia, hypokalemia, or drugs/conditions associated with hypomagnesemia. A 24-Hour Urine Magnesium and Creatinine or a Fractional Excretion of Magnesium May Be Useful in Establishing the Etiology of Hypomagnesemia Body magnesium is controlled by a balance between gastrointes- tinal magnesium absorption, skeletal magnesium storage, and uri- nary magnesium losses. Most cellular food (i.e., of animal or plant origin) have significant amounts of magnesium, which are typically readily absorbed, although there are concerns of decreas- ing magnesium content of the Western diet. Gastrointestinal dysfunction, either with increased motility leading to diarrhea or problems with absorption such as inflammatory bowel disease, will lead to decreased magnesium absorption. A daily 24-hour urine magnesium excretion, in the setting of hypomagnesemia, of 348 A. O. Malabanan more than 10–30 mg or a fractional excretion of magnesium (FEMg = ((UMg × PCr)/(0.7 × PMg × UCr)) × 100%) of >2% argues for renal magnesium wasting. A daily 24-hour urine mag- nesium excretion, in the setting of hypomagnesemia, of <10 mg or an FEMg <2% argues for gastrointestinal losses. A 24-Hour Urine Magnesium and Creatinine May Be Useful in Confirming Adequacy of Total Body Magnesium Stores Magnesium sufficiency will lead to increased urinary magne- sium losses. Diuresis, either from drugs or conditions, will lead to increased magnesium ultrafiltration and decreased reabsorp- tion of magnesium. Hungry bone syndrome, after parathyroid- ectomy, will increase the bone uptake of magnesium, as well as calcium and phosphate. The normal physiologic response to hypomagnesemia is an increase in renal reabsorption of magne- sium, so an inappropriately normal or high urinary magnesium points to a renal etiology of the hypomagnesemia. In addition, assessing a 24-hour urine magnesium after an intravenous mag- nesium bolus is helpful. A high 24-hour urine magnesium excretion indicates magnesium sufficiency, although this assessment is not typically practical in most hospitalized patients. Hypocalcemia or Hypokalemia with Concomitant Hypomagnesemia Will Not Correct with Calcium or Potassium Therapy Alone Magnesium is an important cofactor for the Na-K ATPase and is also important for parathyroid hormone release and action. Persistent or recurrent hypokalemia or hypocalcemia is frequently associated with magnesium deficiency, and consideration of magnesium repletion should be pursued even in the presence of normal serum magnesium. 29 Hypomagnesemia 349 A Concomitant Assessment of Urinary Calcium Can Help Identify the Portion of the Nephron Affected in Hypomagnesemia Conditions affecting the loop of Henle, such as loop diuretic use, Bartter’s syndrome, or nephrotoxins, will cause hypercalciuria in the setting of hypermagnesiuria. Conditions affecting the early distal nephron, such as Gitelman’s syndrome, are associated with hypocalciuria with hypermagnesiuria. Normocalciuria and hyper- magnesiuria (i.e., isolated magnesiuria) may be seen in mutations of the pro-epidermal growth factor (pro-EGF) gene or as a result of cetuximab therapy. Severe Hypomagnesemia (Mg <1 mEq/L) and Symptomatic Hypomagnesemia Should Be Treated with Intravenous Magnesium Therapy The presence of torsades de pointes should be treated emergently with 1–2 g of IV magnesium sulfate over 30–60 seconds. It may be repeated in 5–15 minutes if the arrhythmia does not resolve. For asymptomatic severe hypomagnesemia, 1–2 g of IV magne- sium sulfate may be given over 3–6 hours. For both situations, continuous IV magnesium sulfate infusion should be ordered (4–8 g magnesium sulfate over 12–24 hours in those with normal renal function and 50% dose reduction if chronic kidney disease). Oral Magnesium Oxide Therapy Is Limited by Diarrhea and Often Intravenous Magnesium Sulfate Therapy Is Necessary Oral magnesium acts as a laxative and at higher doses can cause diarrhea. Oral magnesium can be tried, at small doses (i.e., 250 mg), as tolerated. Small doses every few hours are much bet- ter tolerated than larger doses at one time. If the oral magnesium 350 A. O. Malabanan is not tolerated or there is already diarrhea, intravenous magnesium sulfate should be considered. Symptomatic hypomagnesemia, i.e., neuromuscular irritability or cardiovascular dysrhythmias, should be treated urgently with intravenous magnesium sulfate. An ongoing intravenous magnesium sulfate drip should be con- sidered in patients with normal renal function to help replete depleted intracellular magnesium. Table 29.1 shows magnesium preparations and elemental magnesium content. In Addition to Replacement Magnesium Therapy, Addressing the Etiology of the Hypomagnesemia Is Necessary to Maintain Magnesium Homeostasis The causes of hypomagnesemia are listed in Table 29.2 and involve either inadequate magnesium intake or absorption or excessive urinary magnesium losses. Assuring adequate intake Table 29.1 Magnesium preparations Route of % Elemental Preparation administration magnesium mg/mEq Magnesium sulfate IV 10% 100 mg/8.1 mEq (1 gm) Magnesium chloride PO 12% 64 mg/5.33 mEq (535 mg) Magnesium oxide PO 60% 241.3 mg/20.1 mEq (400 mg) Magnesium PO 5.4% 27 mg/2.25 mEq gluconate (500 mg) Magnesium PO 42% 500 mg/41 mEq hydroxide (1200 mg/15 mL) Magnesium citrate PO 16% 279 mg/23 mEq (1.745 g/30 mL) Magnesium lactate PO 12% 84 mg/7 mEq (Mag-Tab SR caplet) Magnesium PO 9.9% 61 mg/5 mEq L-aspartate (615 mg) 29 Hypomagnesemia 351 of magnesium and treating diarrhea is important. If the small intestine has been resected, a parenteral source of magnesium may be necessary. Proton pump inhibitor therapy may need to be discontinued and an alternative acid-lowering therapy substituted. Table 29.2 Causes of hypomagnesemia Inadequate intake Excessive urinary losses Redistribution Malnutrition Drugs Ethanol withdrawal Inadequate Diuretics Insulin absorption administration Diarrhea Aminoglycosides Hungry bone syndrome Short bowel Cisplatin (Platinol-AQ) Pancreatitis syndrome Celiac disease Amphotericin B Trisodium (Fungizone) phosphonoformate (Foscarnet) Inflammatory Tacrolimus (Prograf) Blood transfusion bowel disease in liver transplant recipients Laxative abuse Cyclosporine (Sandimmune) Drugs Cetuximab (Erbitux) Proton pump Pentamidine (Nebupent) inhibitors Genetic Primary tubular disorder Primary familial Primary renal wasting hypomagnesemia Renal tubular acidosis Diuretic phase of acute tubular necrosis Post-obstructive diuresis Post renal transplantation (continued) 352 A. O. Malabanan Table 29.2 (continued) Inadequate intake Excessive urinary losses Redistribution Hormone-induced Aldosteronism Hypoparathyroidism and Hyperparathyroidism Hyperthyroidism Genetic Gitelman’s syndrome Autosomal dominant hypercalciuric hypocalcemia Miscellaneous (Na-K- ATPase, HNF1B, KCNA1, EGF) Induced tubular losses Hypercalcemia Volume expansion Glucose, urea, mannitol diuresis Phosphate depletion Alcohol ingestion Suggested Readings Agus ZS. Mechanisms and causes of hypomagnesemia. Curr Opin Nephrol Hypertens. 2016;25:301–7. Ayuk J, Gittoes NJL. Treatment of hypomagnesemia. |
Am J Kidney Dis. 2014;63:691–5. de Baaij JHF, Hoenderop JGJ, Bindels RJM. Magnesium in man: implications for health and disease. Physiol Rev. 2015;95:1–46. Guerrera MP, Volpe SL, Mao JJ. Therapeutic uses of magnesium. Am Fam Physician. 2009;80:157–62. Ismail Y, Ismail AA, Ismail AAA. The underestimated problem of using serum magnesium measurements to exclude magnesium deficiency in adults; a health warning is needed for “normal” results. Clin Chem Lab Med. 2010;48:323–7. Index A diagnosis, 205 Abaloparatide, 149, 152, 154 etiology, 207 Abnormal thyroid stimulating treatment, 210, 213 hormone levels stress dosing, 213, 214 causes, 69–71 Adrenal vein sampling, 254 central hypothyroidism, 65–69 Adrenalectomy immune checkpoint inhibitors, 63 postoperative management laboratory detection, 58–63 adrenal insufficiency, 234 nonthyroidal illness, 64, 65 follow-up appointment, 235 physiologic causes of variations, hormonal deficiency 56, 58 assessment, 233 tyrosine kinase inhibitors, 63 replacement therapy, 233, Acetoacetic acid, 296 234 Activated vitamin D, 162–164 preoperative evaluation Addison’s disease, see Primary bilateral adrenalectomy adrenal insufficiency indications, 230 Adrenal insufficiency, 285 endocrine function adrenal gland assessment, 232 cortex, 200 fine needle aspiration biopsy, medulla, 200 230 critically ill patients, 206 history and physical primary adrenal insufficiency examination, 231 clinical presentation, 203, hormonal hypersecretion 204 evaluation, 231 definition, 203 laparoscopic transabdominal diagnosis, 204 adrenalectomy/ etiology, 207 retroperitoneal signs and symptoms, 203 endoscopic treatment, 208 adrenalectomy, 231 secondary adrenal insufficiency open surgery, 231 clinical presentation, 205 unilateral adrenalectomy definition, 203 indications, 230 © Springer Nature Switzerland AG 2020 353 R. K. Garg et al. (eds.), Handbook of Inpatient Endocrinology, https://doi.org/10.1007/978-3-030-38976-5 354 Index Adrenocortical deficiency Calcium disorders in end stage renal normal cortisol level, 202 failure primary adrenal insufficiency, 204 activated vitamin D and Adrenocorticotropic hormone cinacalcet use, 163 (ACTH), 200–207, 210, 1,25-dihydroxyvitamin D, 160 213 hypocalcemia, 162 Albuterol nebulizer, 192 ionized calcium levels, 161 Aldosterone, 200–204, 208 outpatient dialysis, 162 α-adrenergic receptor blockers, 239 PTH resistance, 161 α-blocker-induced tachyarrhythmia, secondary hyperparathyroidism, 240 dietary phosphate American Diabetes Association restriction/phosphate (ADA) guidelines, 309 binding, 163 Amiloride, 254 serum bone specific alkaline Amiodarone-induced phosphatase, 161 hypothyroidism, 110 serum phosphate, 161 Amiodarone-induced thyrotoxicosis serum PTH, 161 (AIT), 102 tertiary hyperparathyroidism, Angiotensin converting enzyme 164 (ACE)-inhibitors, 194 Calcium gluconate, 191, 192 Anion gap, 296 Captopril stimulation test, 257 Antidiuretic hormone (ADH), 202 Carbimazole, 96 Aquaporin 2 (AQP2) water Cardiac disease channels, 177 hyperthyroidism/thyrotoxicosis Arginine vasopressin (AVP), 167 amiodarone treatment, 108 Arrhythmias, 104 amiodarone-induced Atypical femur fracture (AFF), 155 thyrotoxicosis, 102 Autoimmune hypophysitis, 18 angina, 105 arrhythmias, 104 congestive heart failure, 105 B diagnostic evaluation, 102 Basal bolus insulin, 267 etiology, 102, 105 Beer potomania, 175 subclinical thyrotoxicosis, Betahydroxybutyrate, 288, 290 107, 108 Beta-hydroxybutyric acid, 296 treatment, 103, 106, 107 Betamethasone therapy, 315 hypothyroidism Bicarbonate therapy, 301 amiodarone-induced Bilateral adrenalectomy, 223, 225 hypothyroidism, 110 Bilateral parathyroid exploration, capillary permeability, 103 136 cardiovascular risk factors, Burch-Wartofsky score, 36 108, 109 diagnosis, 103, 110, 111 heart failure and arrhythmias, C 109, 110 Calcitriol, 141, 142 hemodynamics, 109 Calcium channel blockers, 240 perioperative care, 104 Index 355 risk factors, 103 pregnancy, 226 systemic vascular resistance tumor-directed surgery, 223 (SVR), 103 Cytochrome P450 (CYP450) treatment, 103, 111, 112 inhibitors, 218 Catecholamines, 239–242, 245, 247, 248 Central hypothyroidism, 65–69 D Cerebral edema, 302 Denosumab, 150, 153–155 Cholecalciferol, 141 Dexamethasone suppression test Cholestyramine, 98 (DST), 218 Chvostek’s sign, 139 Diabetes insipidus (DI), 5, 10, 11 Cinacalcet, 163, 164 Diabetic ketoacidosis (DKA), 314, Cobicistat, 218 315 Congestive heart failure incidence, 294 (CHF), 105 laboratory tests, 296 Correctional insulin, 277 anion gap, 296 Correctional insulin therapy, 265 nitroprusside test, 296 Cortex, 200 plasma glucose, 295 Corticotropin-releasing hormone plasma osmolality, 296 (CRH), 180, 201–203 serum phosphate, 297 Cortisol co-secretion, 254 serum potassium C-peptide, 286 concentration, 297 Cushing’s syndrome, 29, 30 urine ketone test, 296 adrenal imaging, 222 mortality, 294 bilateral adrenalectomy, signs and symptoms, 294, 295 refractory CS, 225 Diabetic retinopathy, 314 causes of endogenous CS, 219 Diarrheal illnesses, 346 dexamethasone suppression test, Dietary phosphate restriction, 163 218 1,25-dihydroxyvitamin D, 160 diagnostic testing, outpatient Dilutional hyponatremia, 296 setting, 220 Disease subtyping, 254 exogenous glucocorticoids, 218 Doxazosin, 254 features of, 217 DPP-4 inhibitors, 280 glucocorticoid exposure, Dysnatremia iatrogenic CS, 226 causes, 172 hypercortisolism clinical history, 171 consequences and imaging, 172 comorbidities, 222, 223 laboratory findings, 172 evaluation, 220 symptoms, 172 test characteristics, 220, 221 pharmacotherapy, 223–225 pituitary-directed MRI, 222 E pituitary-directed radiotherapy, Ectopic Cushing’s syndrome, 218, 225 219, 222, 223, 225 plasma ACTH measurement, Effective plasma osmolality, see 221 Plasma tonicity 356 Index Endogenous hyperinsulinemia, 289 diabetic retinopathy, 314 Eplerenone, 255 diagnosis, 308–310 Ergocalciferol, 141 discharge and future Esmolol, 96 pregnancies, 316, 317 Euglycemic DKA, 295 glycemic targets, 310, 311 Euvolemic hyponatremia, 180–182 insulin analogues, 312 Exogenous glucocorticoids, 218 labor and delivery, 315, 316 lifestyle interventions, 312 oral medications, 312, 313 F postdelivery insulin Familial hyperaldosteronism, 258 requirements, 316 Familial hypocalciuric vs. preexisting diabetes, 308 hypercalcemia (FHH), treatment, 312 134, 137 type 1 and 2 diabetes, 313, 314 Familial paragangliomas, 244 Glomerulosa (ZG), 200 Fibrate therapy, 340 GLP-1 receptor agonist agents, 280 Fibroblast growth factor 23 Glucocorticoid receptor (GR), 200 (FGF-23), 160 Glucocorticoid therapy, 40 Fludrocortisone, 197, 234 Glucocorticoids, 80, 81, 97, 200, Fosinopril, 254 206, 207, 210, 212, 213 Fracture liaison services (FLS), 156 Glucometrics, 280 Fragility fracture GlucoScout®, 328 follow-up discharge, 156 Glucose Control Mentored hip fracture, 147 Implementation Program, inpatient management 280 anabolic agents, 152 Glucose loading test (GLT), 309 non-pharmacological Gynecomastia, 255 interventions, 148 pharmacologic therapy, 148–150 H pre-hospitalization Hemolysis, 190 osteoporosis medications, Hepatic gluconeogenesis, 296 154, 155 Hip fracture, 147 vitamin D deficiency, 151 Horizon Recurrent Fracture Trial, laboratory evaluation, 153 148–151 mortality rates, 146 Hungry bone syndrome, 140, 141 prevalence, 146 Hydrocortisone, 180, 234 prevention, 156 11β-hydroxysteroid dehydrogenase vertebral fragility, 147 type 2 (11βHSD2), 201 Free water deficit, 186 Hypercalcemia causes, 116 clinical presentation, 117, 118 G diagnosis, 118, 119 Gestational diabetes (GDM) etiologies, 116, 117 betamethasone therapy, 315 treatment, 119, 120 diabetic ketoacidosis, 314, 315 bisphosphonates, 120, 121 Index 357 intravenous hydration and criteria for resolution, 302 calcitonin, 120 disposition, 304, 305 salmon calcitonin, 120 electrolytes Hypercalciuria, 143 bicarbonate therapy, 301 Hyperglycemia and Adverse phosphate therapy, 301 Pregnancy Outcome potassium therapy, 300, 301 (HAPO) trial, 309 infections, 298 Hyperglycemic hyperosmolar state insulin therapy, 299, 300 (HHS) intravenous fluid, 299 incidence, 294 laboratory tests, 298 mortality, 294 monitoring, 301 Hyperkalemia pancreatitis, 298 albuterol nebulizer, 192 severe dehydration, 299 calcium gluconate, 191, 192 signs and symptoms, 297 electrocardiogram, 191 tissue ischemia, 298 history assessment, 193 transition of care, 303 inpatient management Hyperparathyroidism-jaw tumor fludrocortisone, 197 syndrome (HPT-JT), 137 hemodialysis, 196, 197 Hyperphosphatemia, 160, 161, 163 low potassium diet, 195 Hyperprolactinemia, 17 medication discontinuation, Hyperthyroidism management 195 anti-thyroid medications, 74–79 oral loop diuretics, 195 beta-adrenergic-blocking drugs, sodium polystyrene 75, 80 sulfonate, 196 cardiovascular symptoms, 93 insulin administration, 192 clinical judgment, 94 laboratory tests, 193 elective surgery potassium excretion, 193, 194 overt hyperthyroidism, 95 symptom evaluation, 191 subclinical hyperthyroidism, Hypernatremia 94, 95 causes, 176, 184 glucocorticoids, 80, 81 definition, 184 iodine, 80 hypervolemic hypernatremia, mortality rate, 93 184, 185 urgent surgery hypovolemic/euvolemic overt hyperthyroidism, hypernatremia, 185, 186 87–88, 95–98 thirst mechanism, 184 subclinical hyperthyroidism, treatment, 186 95 Hyperosmolar hyperglycemic state Hypertriglyceridemia (HTG) (HHS) adverse CV events, 338 complications alcohol consumption, 339 cerebral edema, 302 apolipoprotein CIII inhibitors, hypoglycemia, 302 342, 343 hypokalemia, 302 clinical diagnosis, 334 rhabdomyolysis, 303 Clinical Practice Guidelines, 334 concomitant medications, 298 dietary modification, 340 358 Index Hypertriglyceridemia (HTG) (cont.) serum parathyroid hormone, 127 fibrate therapy, 340 signs and symptoms of heparan sulfate proteoglycan postsurgical chains, 338 hypocalcemia, 139 HMG-CoA reductase inhibitors, thiazide therapy, 129 342 with tetany and muscle laboratory work up, 337, 338 cramping, 125 lifestyle therapy, 339 total serum calcium, 125 medium-chain triglycerides, 340 Hypoglycemia patients with niacin therapy, 341, 342 diabetes, 302 in non-diabetic patient, 338 basal-bolus treatment, 280 OM3FAs therapy, 341 definition, 272 physical examination, 336, 337 deleterious effects, 274 plasmapheresis, 339 DPP-4 inhibitors, 280 risk factors, 335–336 frequency of hypoglycemia, therapeutic target, 339 insulin treatment, 273, Hypervolemic hypernatremia, 184, 274 185 frequent glucose monitoring, Hypervolemic hyponatremia, 177, 272 178 GLP-1 receptor agonist agents, Hypoalbuminemia, 161, 162 280 Hypoaldosteronism, 194 glucometrics, 280 Hypocalcemia high risk patients, 275 acidemia, 126 hospital surveillance and alkalemia, 126 reporting, 280 anti-resorptive therapy, 129 inpatient setting, 272 bisphosphonates, 129 insulin action, 276, 277 calcium disorders in end stage insulin dosing, 276, 278 renal failure, 162 insulin program components, calcium gluconate, 127, 128 278 cardiovascular irritability, 125 levels, 272 causes, 128 point of care testing, 272, 273 electrocardiographic QT questions for, 272 interval, 126 TPN/enteral tube feeds, 275, 276 free ionized serum calcium, 125 treatment, 279 laboratory evaluation, 127 Hypoglycemia without diabetes long-term parathyroid hormone, adrenal and pituitary 132 insufficiency, 285 medications, 130–131 antibody induced hypoglycemia, postoperative monitoring, 138 286 post-parathyroidectomy, 126 autonomic symptoms and signs, post-thyroidectomy, 126 284 prevention and treatment, 141, cardiac, renal/liver failure, 285 142 diagnosis with major illness, 284 Index 359 diagnosis without acute/chronic hyperglycemia, 174 illness, 284 hypervolemic hyponatremia, insulin mediated versus 177, 178 non-insulin mediated hypovolemic hyponatremia, 178, hypoglycemia, 289, 290 179 insulinomas, 286, 290, 291 low solute intake, 175 laboratory investigations, 287 plasma osmolality, 173 medications, 285 primary polydipsia, 176, 177 mixed meal test, 289 treatment, 182–184 neuroglycopenic symptoms and urine osmolality, 173 signs, 284 urine osmolality to assess ADH non-insulinoma related activity, 175 hyperinsulinemia, 286 Hypoparathyroidism, 139, 140 non-islet cell tumors, 286 Hyporeninemic hypoaldosteronism, prolonged fasting test, 287, 289 194 pseudohypoglycemia, 287 Hypothalamic-pituitary-adrenal sepsis, 285 axis, 202, 210, 212, 213 treatment, 291 Hypothyroidism management, 80, Hypogonadism, 153 83 Hypokalemia, 302 clinical judgment, 89 Hypomagnesemia elective surgery calcium homeostasis, 347 overt hypothyroidism, causes, 351–352 90, 91 cisplatin and amphotericin B, 346 subclinical hypothyroidism, diarrheal illnesses, 346 89, 90 etiology, 347, 348 preoperative patient assessment, extracellular magnesium, 347 86 intravenous magnesium therapy, surgery, 86 349 surgical outcomes, 89 Na-K ATPase, 348 urgent surgery oral magnesium oxide therapy, overt hypothyroidism, 91–93 349, 350 subclinical hypothyroidism, proton pump inhibitors, 346 91 red blood cell magnesium, 347 Hypovolemic hyponatremia, replacement magnesium therapy, 178–180 350, 351 Hypovolemic/euvolemic total body magnesium stores, hypernatremia, 185, 186 348 urinary calcium assessment, 349 Hyponatremia, 4 I beer potomania, 175 Iatrogenic CS, 226 definition, 173 Immunotherapy-induced euvolemic hyponatremia, hypophysitis, 18 180–182 Inorganic iodine, 97 360 Index Inpatient hyperglycemia long-acting (basal) insulin, 328 anti-diabetic treatment, 262 medical orders, 322, 323 basal bolus insulin, 267 in non-critically ill hospitalized basal insulin therapy, 265, 266 patients, 321 BG levels, 268 nutritional status, 321, 322 correctional insulin therapy, 265 prandial insulin, 328 diabetes at time of discharge, pre-admission diabetes status 268 assessment, 320 follow-up after discharge, 269 during pregnancy, 327 HbA1c, 262 pump settings, 320 hypoglycemia protocol, 267 recommendations, 325, 326 insulin infusion in critically ill sensor-augmented insulin pump, patients 329 intensive care units, 264 target glycemic goals, 321 labor and delivery, 264 Insulinoma, 286, 290, 291 insulin pump, 267 Interfering medications, 253, 254 medications affecting glycemic International Association of status, 263 Diabetes and Pregnancy nutritional insulin therapy, 266, Study Groups (IADPSG), 267 309 nutritional status, 262, 263 Iso-osmotic hyponatremia, 174 point of care blood glucose monitoring, 263 preadmission diabetes status, 262 J Insulin mediated versus non-insulin Jod-Basedow effect, 97 mediated hypoglycemia, 289 Insulin pump management, 267 K during ambulatory/short-term Kayexalate, see Sodium polystyrene surgical procedures, 325 sulfonate blood glucose monitoring, 325 Ketoconazole, 223 closed-loop systems, 329 Kidney Disease Improving Global continuous glucose monitor Outcomes (KDIGO) in ICU patients, 328, 329 guidelines, 161 in non-ICU patients, 328 contraindications, 321, 324, 325 in critically ill patients, 324 L diabetes treatment, 329, 330 Late-night salivary cortisol (LNSC), in diabetic ketoacidosis, 326, 327 220, 221, 226 follow-up after discharge, 330 Lipodystrophy, 304 glycemic control, 327 Liquid chromatography with glycemic status affecting electrochemical or medications, 322 fluorometric detection during imaging studies, 326 (LC-ECD), 241 indications, 323 Low solute intake, 175 insulin pump flowsheet, 323, 324 Lymphocytic hypophysitis, 18 Index 361 M Nitroprusside test, 296 Medication-induced hypophysitis, Non-insulinoma related 18 hyperinsulinemia, 286 Medulla, 200 Non-islet cell tumors, 286 Megestrol acetate, 218 Normoglycemia in Intensive Care Melanocyte stimulating hormone Evaluation-Survival (MSH), 203 Using Glucose Algorithm Metanephrines, 241–243, 247, 248 Regulation (NICE- Methimazole (MMI), 74 SUGAR) study, 273 Methyldopa, 247 Metoclopramide, 245 Metyrapone, 223 O Mifepristone, 226 Omega-3-Fatty Acids (OM3FAs) Mineralocorticoid receptor (MR), therapy, 341 200–202, 255–257 OptiScanner 5000®, 328 Mixed meal test, 289 Oral glucose tolerance test (OGTT), Multiple endocrine neoplasia 309 (MEN) syndrome, 137, Oral loop diuretics, 195 244 Order iodine therapy, 40 Myxedema coma Osmotic demyelinating syndrome adrenal insufficiency, 49 (ODS), 175, 182 bowel wall edema, 48 Osteoporosis cardinal features, 45 definition, |
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The publisher shall not be liable for any special, consequential, or exemplary damages resulting, in whole or part, from the readers’ use of, or reliance upon, this material. Printed in the United States of America 1 2 3 4 5 XX 11 10 09 Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. Dedicated to the memory of John Pryor: Paramedic, surgeon, father, husband, brother, and son. On Christmas Day, 2008, while serving his country in Iraq, Dr. Pryor was tragically killed in the line of duty. Dr. Pryor felt compelled to join the U.S. Army Reserve after witnessing the effects of September 11, 2001, from the rubble pile at Ground Zero. As a member of the U.S. Forward Army Surgical Unit, Dr. Pryor volunteered for not one, but two tours of duty in Iraq, believing that he needed to be there to help others, especially his fellow soldiers. Dr. Pryor’s history as a volunteer in medical service started at age 17 with the Clifton Park–Halfmoon Volunteer Ambulance Corp., where he became an Emergency Medical Technician and later a Paramedic. These early beginnings in EMS may have led Dr. Pryor to a career as a widely respected trauma surgeon in Philadelphia. Dr. Pryor often wrote eloquently about his view of the human condition, whether he observed it in war–torn Iraq or the streets of Philadelphia. In one letter he wrote to the family of a mortally wounded Marine, he described his struggle to save the soldier. He expressed that he, his fellow physicians, and especially the Paramedics and EMTs who had the honor of serving with the dead Marine “more than anyone else, know he was a true American hero.” The life of service, love for others, and spirit of devotion of Dr. John Pryor is an example for us all. We, his fellow Paramedics, more than almost anyone else, know he was a true American hero. Dedication v Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. Foreword ........................................................xvi Architecture of EMS Systems .................................... 28 Information Systems ................................................. 30 Preface .........................................................xviii Integration of Health Services ................................... 30 SECTION I: FRAMEWORK FOR Medical Direction ..................................................... 31 Finance Systems ....................................................... 31 PARAMEDIC PRACTICE National Healthcare Systems ............................ 32 1. Roles and Responsibilities of the Professional Paramedic 2 3. Workforce Safety and Wellness 38 What Is Paramedicine? .......................................4 Wellness .......................................................... 40 Hallmarks of a Profession ..................................5 Benefits of Wellness ................................................. 40 Education Systems .............................................6 Methods Used to Achieve Wellness ............................ 40 Commission on Accreditation of Allied Health Stress .............................................................. 41 Education Programs .................................................6 Symptoms of Stress ................................................... 42 National Registry of Emergency Medical The Crisis Process .................................................... 43 Technicians .............................................................6 Stress Management ................................................... 43 National Association of Emergency Medical Specif ic Stressful Situations ...................................... 43 Technicians .............................................................6 National Institute of Medicine Report ..........................7 Personal Injury Prevention ............................... 45 Back Injury ............................................................... 46 Core Values .......................................................7 Risk Management ..................................................... 46 Roles of a Paramedic .........................................8 Safety ....................................................................... 46 Healer .........................................................................8 Infection Control ............................................. 49 Clinician .....................................................................8 Infectious Disease Exposure ...................................... 51 Researcher ................................................................ 10 Teacher ..................................................................... 10 4. research and ems 56 Patient Advocate ....................................................... 11 Paramedics as Physician Extenders ............................ 11 Practice, Protocols, and Procedures ................. 58 2. Introduction to Emergency Evidence-Based Practice .................................. 58 Medical Service Systems 16 Performing a Literature Search .................................. 59 Reviewing the Literature ........................................... 59 The Evolution of EMS ..................................... 18 Types of Research ............................................ 60 Historical Evolution of American Health Care ........... 18 Descriptive Studies ................................................... 60 Observational Studies ............................................... 60 The History of Emergency Medical Service ...... 20 Experimental Studies ................................................ 61 Emergence of Civilian EMS ...................................... 21 Prehospital Research ................................................. 61 Changing Paradigms ................................................. 21 Economic Research ................................................... 62 The White Paper ....................................................... 22 Absence of Research ................................................. 63 Prehospital Coronary Care ........................................ 22 Emergency Hits TV Screens ...................................... 23 SECTION II: ETHICS AND LAW EMS Act of 1973 ...................................................... 23 Federal EMS Efforts in the 1980s .............................. 23 IN EMS EMS Agenda for the Future .............................. 25 5. Ethics and the Paramedic 70 National EMS Education Agenda for the Future ......... 26 Mission of the EMS System ............................. 27 Ethics Defined ................................................. 72 Legislation and Regulation ........................................ 28 Public Access ............................................................ 28 Medical Ethics ................................................. 72 Communication Systems ........................................... 28 Foundations for Value Judgments .............................. 73 vi Table of Contents Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. 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Foundations of Bioethics ........................................... 74 Limited Disclosure .................................................... 98 EMS Code of Ethics .................................................. 76 Health Insurance Portability and Accountability Act ... 98 Moral Rules and Particular Circumstances ........ 76 Disclosure to Law Enforcement ................................. 98 Ethical Obligation ..................................................... 76 Employment Law ............................................. 98 Allocation of Scarce Medical Resources .................... 76 Americans with Disabilities Act ................................ 98 Ethics and EMS Research .......................................... 77 Title VII.................................................................... 99 End-of-Life Decisions ............................................... 77 Ethics Committees .................................................... 78 SECTION III: EMS AND PUBLIC 6. The Law and Paramedics 82 HEALTH Origin of Law .................................................. 84 7. Public Health and the Paramedic 106 Criminal Law versus Civil Law ........................ 84 Criminal Law ............................................................ 84 Civil Law .................................................................. 85 What Is Public Health? .................................. 108 Elements of a Tort Action ................................. 85 Public Health in History ................................. 108 Duty to Act ............................................................... 85 Traditional Public Health Missions .......................... 109 Good Samaritan Act .................................................. 86 Public Health Organization ..................................... 109 Breach of Duty ......................................................... 86 Public Health Management ............................. 110 Damages ................................................................... 87 International ........................................................... 110 Proximate Causation ................................................. 87 The American Public Health Movement ................... 111 Borrowed Servant Doctrine .............................. 87 Public Health and EMS .................................. 112 The Process of a Civil Lawsuit ......................... 87 Healthcare Access ................................................... 112 Pretrial Discovery ..................................................... 88 Disaster Response ................................................... 113 Quality Assurance and Discoverability ...................... 88 Immunity and Defense .............................................. 88 8. Illness and Injury Prevention 118 Motions in Court ....................................................... 89 Patient Consent ................................................ 89 Public Health ................................................. 120 Disclosure................................................................. 89 Impact of Public Health Prevention Programs .......... 120 Understanding ........................................................... 90 Public Health Prevention Initiatives ......................... 120 Voluntariness ............................................................ 90 Injury Surveillance ................................................. 120 Permission ................................................................ 90 EMS and Injury Prevention ............................ 121 BARNACLE ............................................................. 90 Injury Prevention Theory and the Emergency Exception ................................................ 90 Haddon Matrix ................................................... 121 Therapeutic Privilege ................................................ 91 Injury Countermeasures .......................................... 122 Waiver of the Right to Consent .................................. 91 Injury Prevention Strategies .................................... 123 Advantages of Consent .............................................. 91 Assessment ............................................................. 123 Types of Consent....................................................... 91 Implementation ....................................................... 124 Medical Restraint ............................................. 92 Teaching Injury Prevention ............................ 124 Positional Asphyxia ................................................... 93 EMS Injury Prevention Programs ............................ 124 Refusal of Medical Assistance .......................... 94 Outcomes ................................................................ 125 Against Medical Advice ............................................ 94 Destination ...................................................... 94 SECTION IV: SCIENTIFIC Advanced Directives ........................................ 96 PRINCIPLES Case of Karen Ann Quinlan ....................................... 96 Case of Nancy Cruzan ............................................... 96 |
9. Lifespan Development 130 Principles of Advanced Directives ............................. 96 Patient Self-Determination Act of 1990 ..................... 97 Types of Advanced Directives .................................... 97 Personal Development .................................... 132 Do-Not-Resuscitate Orders ........................................ 97 Theories of Personal Development ................. 132 Physician’s Order of Life-Sustaining Treatment ......... 97 Theories of Psychosocial Development .................... 132 Confidentiality ................................................ 97 Topics in Human Development ....................... 133 Breaches of Patient Confidentiality ........................... 98 Table of Contents vii Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). 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Conception to Childbirth ................................ 133 Stress and the Endocrine System ............................. 166 Genetics and Human Development .......................... 133 Stress and the Immune System ................................ 167 Pregnancy ............................................................... 134 Cellular Adaptation ........................................ 167 Childbirth ............................................................... 135 Atrophy .................................................................. 167 The Newly Born............................................. 135 Hypertrophy ............................................................ 167 Cell Replacement .................................................... 167 The Infant ...................................................... 135 Dysplasia ................................................................ 167 Physical Development ............................................. 135 Apoptosis ............................................................... 168 Cognitive Development ........................................... 138 Psychosocial Development ...................................... 138 Parent–Child Relationships ..................................... 138 Preschool Children: Early Childhood .............. 139 11. Principles of Physical Development ............................................. 139 Pathophysiology 174 Cognitive Development ........................................... 140 Psychosocial Development ...................................... 140 Pathophysiology Defined ............................... 176 School-Aged Children: Middle Childhood .................................... 141 Disease: Defined ........................................... 176 Physical Development ............................................. 141 Etiologies of Disease ..................................... 176 Cognitive Development ........................................... 141 Known Causes of Disease........................................ 176 Psychosocial Development ...................................... 141 Risk Factors ............................................................ 177 Adolescence .................................................. 142 Prognosis ................................................................ 178 Physical Development ............................................. 142 Iatrogenic Disease .......................................... 178 Adolescent Health Concerns.................................... 143 Cognitive Development ........................................... 143 Disease as a Process....................................... 178 Psychosocial Development ...................................... 143 Morbidity and Mortality ................................. 179 Early Adulthood ............................................. 144 Chemical Causes of Cell Injury ...................... 179 Physical Development ............................................. 145 Hypoxic Injury ........................................................ 179 Cognitive Development ........................................... 145 Reperfusion Injury and Free Radicals ...................... 180 Psychosocial Development ...................................... 145 Toxins ..................................................................... 180 Middle Adulthood .......................................... 146 Physical Causes of Cellular Injury .................. 181 Physical Development ............................................. 146 Mechanical Injury ................................................... 181 Cognitive Development ........................................... 146 Heat or Cold Injury ................................................. 181 Psychosocial Development ...................................... 146 Burn Injury ............................................................. 182 Late Adulthood .............................................. 147 Barotrauma ............................................................. 183 Life Expectancy ...................................................... 147 Physical Development ............................................. 147 Metabolic Disorders ....................................... 184 Cognitive Development ........................................... 147 Genetic Disorders .......................................... 184 Psychosocial Development ...................................... 148 Death and Dying ..................................................... 148 Infection ........................................................ 184 Immune Reactions ......................................... 185 10. Basic Human Physiology 156 Effect: Systemic Defense ............................... 185 Nonspecif ic Defenses.............................................. 186 Physiology ..................................................... 158 Inflammatory Response ........................................... 186 Cellular Milieu .............................................. 158 Immune Response ................................................... 189 Homeostasis .................................................. 158 Outcomes: Shock Syndrome ........................... 190 Cellular Physiology ........................................ 158 Classif ications of Shock .......................................... 190 Sodium Potassium Pump ......................................... 159 Pathophysiology of Shock ....................................... 190 Glucose Storage ...................................................... 159 Organs in Shock ...................................................... 190 Fluid Balance ................................................ 160 Shock: Vital Organs ................................................ 191 Decompensated Shock............................................. 192 Temperature Regulation ................................. 162 Axioms of Shock Treatment .................................... 192 Temperature and the Oxyhemoglobin Curve ............. 163 Pathological Cell Injury ................................. 193 Stress ............................................................ 163 Stress and Cellular Response ................................... 163 Patterns of Necrosis ....................................... 193 Stress and the Autonomic Nervous System .............. 164 Death ............................................................. 193 viii Table of Contents Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. 12. Medical Terminology 200 15. History Taking 242 Medical Terminology ..................................... 202 History Taking ............................................... 244 Medicalese .................................................... 202 The Art and Science of History Taking ........... 244 Anatomy of Medical Terminology .................. 202 Setting the Stage ..................................................... 244 Combining Forms ................................................... 204 Starting the Interview ............................................. 245 Plural Forms ........................................................... 204 The Structure and Content of the Patient History ..... 246 The Focused History ............................................... 246 Reading Medical Terminology ........................ 205 Clinical Reasoning .................................................. 248 Pronunciation.......................................................... 205 Spelling .................................................................. 205 Special Challenges to History Taking ............. 249 Abbreviations ......................................................... 205 Sensitive Topics ...................................................... 249 Topographic Anatomy .................................... 208 Silence.................................................................... 249 Overly Talkative Patients ......................................... 249 SECTION V: PRINCIPLES OF Patients with Multiple Symptoms ............................ 249 Anxious Patients ..................................................... 249 CLINICAL PRACTICE Reassurance ............................................................ 249 Anger and Hostility ................................................. 249 13. Scene Size-Up and Primary The Intoxicated Patient ........................................... 250 Assessment 212 Crying .................................................................... 250 Depression .............................................................. 250 Seductive Patients ................................................... 250 Patient Assessment ......................................... 214 Confusing Behaviors or Histories ............................ 250 Limited Intelligence ................................................ 250 Scene Size-Up ............................................... 214 Language Barriers ................................................... 250 Scene Safety ........................................................... 214 Hearing Impaired Patients ....................................... 250 Body Substance Isolation ........................................ 215 Vision Impaired Patients ......................................... 251 Mechanism of Injury or Nature of Illness ................ 215 Family and Friends .................................................. 251 Number of Patients ................................................. 216 The Primary Assessment ................................ 216 16. Physical Examination General Impression ................................................. 216 and Secondary Assessment 256 Mental Status .......................................................... 217 Airway .................................................................... 218 Breathing ................................................................ 218 Physical Examination ..................................... 258 Circulation .............................................................. 221 Physical Examination Techniques ................... 258 Sick or Not Sick: Priority Decision Making .... 222 Inspection ............................................................... 258 Focused History and Physical Exam ............... 223 Auscultation ........................................................... 259 Palpation ................................................................ 259 14. Therapeutic Percussion .............................................................. 260 Vital Signs Measurement ......................................... 260 Communications 228 Concern-Based Physical Exam ....................... 272 Focused Exam Matrix .............................................. 272 Therapeutic Communications ......................... 230 Examination Matrix ................................................ 273 Human Communications ................................ 230 General Exam ......................................................... 273 Chest Pain .............................................................. 274 Encoding ................................................................ 230 Shortness of Breath ................................................. 277 Transmission........................................................... 230 Abdominal Pain ...................................................... 279 Reception ............................................................... 231 Syncope .................................................................. 282 Decoding ................................................................ 231 Altered Mental Status ............................................. 287 Feedback ................................................................ 231 Extremity Pain ........................................................ 289 Hermeneutics .......................................................... 231 High Blood Pressure ............................................... 290 Improving Communications ........................... 232 HEENT ................................................................... 292 Interview Techniques .............................................. 232 Fever ...................................................................... 293 Behaviors Detrimental to Dialogue .......................... 237 Pregnancy ............................................................... 296 Special Communication Situations .......................... 238 Trauma ................................................................... 297 Table of Contents ix Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. 17. Clinical Decision Making SECTION VI: CLINICAL and Teamwork 310 ESSENTIALS Clinical Decision Making ............................... 312 20. Airway Anatomy and Physiology 352 Medical Intelligence ...................................... 312 The Method of Paramedic Practice ................. 313 Airway Anatomy ............................................ 354 Initial Impression .................................................... 313 The Upper Airway ................................................... 354 Differential Diagnosis ............................................. 314 The Lower Airway ................................................... 356 Barriers to Effective Clinical Bony Thorax Anatomy ............................................. 361 Decision Making ...................................... 315 Respiratory Physiology .................................. 363 Improved Clinical Decision Making ............... 315 Lung Volumes and Capacities .................................. 363 Treatment ............................................................... 316 The Bony and Muscular Thoracic Structures Evaluate .................................................................. 316 and the Pleura...................................................... 364 Neurological Control of Breathing ........................... 365 Disposition .................................................... 316 Oxygen and Carbon Dioxide Metabolism ................. 366 Pediatrics ....................................................... 368 18. Communications 320 Pediatric Anatomy ................................................... 368 Physiology .............................................................. 369 Communications and Teamwork ..................... 322 History of Radio ............................................ 322 21. The Algorithmic Approach Radio Technology ................................................... 323 to Airway Management 378 Radio Systems ........................................................ 326 Alternative Communication Devices ........................ 328 Airway Management ...................................... 380 Public Safety Communications ....................... 328 Algorithms .................................................... 380 Early EMS Radio Communications .......................... 329 Development of Algorithms ..................................... 381 Phases of EMS Communications ............................. 329 Assessment of an Algorithm’s Impact ...................... 381 Prehospital Airway Management Algorithms ............ 382 19. Documentation 336 22. Non-Intubating Purpose of EMS Documentation ..................... 338 Airway Management 394 Elements of a PCR ......................................... 339 Documentation Standards ........................................ 339 Basic Airway Management ............................. 396 Errors and Omissions .............................................. 340 The Basic Airway Management Algorithm ...... 397 Confidentiality .............................................. 340 Preoxygenation ....................................................... 397 Oxygen Delivery Devices ........................................ 397 Forms of Documentation ................................ 340 Equipment for Basic Airway Management ............... 398 Electronic Documentation ....................................... 340 Suction ................................................................... 402 On-Scene Medical Records ..................................... 341 Opening the Airway ................................................ 403 Problem-Oriented Medical Recordkeeping ............... 341 Cricoid Pressure ...................................................... 404 EMS PCR Formats ......................................... 341 Face-Mask Ventilation ............................................. 405 Continuing Ventilatory Care .................................... 409 CHEATED ..................................................... 342 Assisted Ventilation ....................................... 412 Early EMS Documentation Formats ......................... 342 CHEATED Format .................................................. 342 Continuous Positive Airway Pressure .............. 413 Special Documentation .................................. 346 Pediatric Considerations in Basic Airway Refusal of Medical Assistance Documentation ......... 346 Management............................................. 415 Hazardous Materials Operations Documentation ...... 346 Documentation of Multiple Casualties ..................... 347 23. Intubating Airway Documentation of Pregnancy and Childbirth ............ 347 Management 424 Special Incident Report ........................................... 347 Legal Proceedings .......................................... 347 The Intubating Airway Management Algorithm ................................................ 426 x Table of Contents Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. Equipment for Intubating Airway Medication-Facilitated and Rapid Management............................................. 427 Sequence Intubation ............................................ 477 Endotracheal Tubes ................................................. 427 Pharmacological Adjuncts for Intubation ................. 477 The Laryngoscope ................................................... 429 The 9 P’s for Medication Facilitated Intubation Stylet ...................................................................... 431 and Rapid Sequence Intubation ................. 483 Securing Devices .................................................... 431 Preparation ............................................................. 483 Secondary Confirmation Equipment ........................ 431 Predict the Degree of Diff iculty .............................. 483 Rescue Devices ....................................................... 433 Preoxygenate .......................................................... 484 Elastic Gum Bougie ................................................ 435 Pretreat ................................................................... 484 Lighted Stylettes/Translaryngeal Cricoid Pressure ...................................................... 484 Illumination Intubation ........................................ 436 Paralyze .................................................................. 484 Surgical Airways ..................................................... 436 Pass the Tube .......................................................... 484 Patient Preparation ......................................... 437 Position (Confirm) and Secure ................................ 484 Oral Endotracheal Intubation ......................... 439 Post-Intubation Care ............................................... 485 Visualizing the Vocal Cords..................................... 440 Passing the Endotracheal Tube ................................. 441 25. Ventilation 490 Confirming Endotracheal Tube Placement ............... 442 Securing the Endotracheal Tube ............................... 443 Respiration and Oxygen Transportation .......... 492 Nasotracheal Intubation ................................. 444 Oxygen Transport ................................................... 492 Patient Preparation .................................................. 444 Carbon Dioxide Transport ....................................... 494 Intubation ............................................................... 444 Acid–Base Balance ........................................ 495 Confirming Placement ............................................ 444 Buffering Systems ................................................... 495 Securing the Endotracheal Tube ............................... 444 Effects of an Acidic Environment ............................ 497 Failed Intubation ............................................ 444 Acid–Base Disorders ............................................... 497 Digital Intubation .......................................... 445 Assessment of Oxygenation and Ventilation.... 500 The Elastic Gum Bougie ......................................... 445 Pulse Oximetry ....................................................... 500 Translaryngeal Illumination .................................... 445 Capnography ........................................................... 503 Fiberoptic Stylettes/Bronchoscope ........................... 446 Co-oximetry............................................................ 507 Supraglottic Airway Devices .......................... 446 Arterial Blood Gas .................................................. 507 King LTS-D Airway ................................................ 446 The Laryngeal Mask Airway .................................... 446 26. Principles of Medication The Esophageal-Tracheal Combitube ....................... 447 Administration 514 Bag-Valve Mask and Automatic Transport Ventilator Face-Mask Ventilation .............. 447 Medication Administration ............................. 516 Surgical Airway ............................................. 448 Surgical Cricothyroidotomy ..................................... 448 Forms of Medication ...................................... 516 Needle Cricothyroidotomy....................................... 448 Liquid Medication Forms ........................................ 516 Percutaneous Devices .............................................. 449 Solid Medication Forms .......................................... 516 Injected Medications ............................................... 517 Post-Intubation Care ...................................... 450 Post-Intubation Ventilation ...................................... 450 Drug Measurement and Dosing ...................... 518 Orogastric and Nasogastric Tube Placement ............. 451 Systems of Measurement ......................................... 518 Tracheobronchial Suctioning ................................... 452 Measurement Devices ............................................. 519 Special Circumstances ................................... 452 Mathematical Conversions ...................................... 519 Concentration ......................................................... 520 Stoma Management ................................................. 452 The Trauma Patient ................................................. 453 Elements of a Drug Order .............................. 521 The Pediatric Patient ...................................... 453 Standard Drug Order ............................................... 521 Best Practice ........................................................... 453 Weight-Dependent Drug Order ................................ 521 The Advanced Airway Management Algorithm ........ 453 Pediatric Dosing ..................................................... 522 Intravenous Infusions ..................................... 522 24. Medication-Facilitated Continuous Infusion ................................................ 522 Intubation 474 Intravenous Drug Infusion ....................................... 523 Weight-Dependent Intravenous Drug Infusion .......... 523 Medication-Facilitated Intubation ................... 476 Temperature Measurement ............................. 524 Prehospital Provider Use of Paralytics ..................... 476 Administration of Medication ........................ 524 Table of Contents xi Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed |
content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. Medication Routes ......................................... 525 Access of a Central Venous Access Device .............. 585 Preparation for Medication Administration .............. 525 Implanted Vascular Access Devices ......................... 585 Local Routes ........................................................... 526 Routes for Systemic Medications ................... 527 28. Blood Products Enteral Drug Administration ................................... 527 and Transfusion 598 Parenteral Drug Administration ............................... 530 Injections ....................................................... 534 History of Transfusions .................................. 600 Tools for Injections ................................................. 534 Blood Components ......................................... 601 Hypodermic Needle ................................................ 535 Routes of Injection .................................................. 537 Blood Products .............................................. 603 Packed Red Blood Cells .......................................... 603 27. Intravenous Access 552 Fresh Frozen Plasma ............................................... 604 Cryoprecipitate ....................................................... 604 Platelets .................................................................. 604 Intravenous Access and Paramedics ................ 554 Blood Groups and Compatibility .................... 604 Physiology Review ......................................... 554 Blood Grouping ...................................................... 604 Compatability ......................................................... 605 Medical vs Trauma ......................................... 554 Transfusion Terms ................................................... 606 Sources of Fluid Loss .............................................. 554 Identif ication and Management Past Medical History ............................................... 555 of Transfusion Reactions .......................... 606 Physical Examination for Dehydration ..................... 555 Transfusion-Associated Circulatory Overload .......... 606 Intravenous Fluids ................................................... 556 Allergic Reaction .................................................... 606 Tonicity .................................................................. 556 Febrile Non-Hemolytic Reaction ............................. 607 Intravenous Fluid Administration ................... 556 Acute Hemolytic Reaction ....................................... 607 Administration Sets................................................. 558 Bacterial Contamination .......................................... 607 Preparing the Intravenous Administration Set .......... 561 Transfusion-Related Acute Lung Injury ................... 607 Intravenous Access......................................... 562 Treatment of Transfusion Reactions ......................... 607 Peripheral Venous Access Devices ........................... 562 Transfusion Procedure and Documentation ..... 608 Categories of Venous Access Devices ...................... 563 Prior to Transfer ...................................................... 608 Needle Safety ......................................................... 563 During the Transfer ................................................. 608 Peripheral Site Selection ......................................... 563 After the Transfer .................................................... 609 Site Preparation and Disinfection ............................ 567 Venipuncture ........................................................... 568 29. Introduction to Continuous or Intermittent Infusion ......................... 570 Securing the Intravenous Catheter ........................... 570 Pharmacology 612 Adjusting the Infusion Rate ..................................... 571 Intravenous Injection ..................................... 573 Paramedic Pharmacology ............................... 614 Obstruction of Intravenous Flow ............................. 574 Historical Development Complications of Intravenous Infusions ................... 574 of Pharmacology ...................................... 614 Infusion-Induced Hypothermia ................................ 576 Sources of Drugs ........................................... 615 Removing Intravenous Access ................................. 576 Plants ..................................................................... 615 Intraosseous Access ....................................... 576 Minerals, Chemicals, and Salts ................................ 616 Anatomy and Physiology of the Long Bones ............ 576 Animal ................................................................... 616 Intraosseous Devices ............................................... 577 Synthetic ................................................................ 616 Indications and Contraindications ............................ 577 Genetic Engineering ................................................ 616 Intraosseous Placement ........................................... 577 Drug Terminology .......................................... 617 Medication Administration ...................................... 577 Drug Classif ication ........................................ 617 Phlebotomy .................................................... 577 Pediatric Phlebotomy .............................................. 578 Herbal Remedies ............................................ 619 Blood Cultures ........................................................ 579 Sources of Drug Information .......................... 619 Pediatric Intravenous Access ................................... 579 Historical Legal Developments in Central Venous Access ................................... 582 Pharmacology .......................................... 620 Types of Central Venous Access Devices ................. 582 Controlled Substances Legislation ........................... 620 Field-Placed Central Venous Access Device ............. 583 Drug Misuse versus Drug Abuse.............................. 621 xii Table of Contents Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. New Drug Development ................................. 622 Diuretic Agents ....................................................... 668 FDA IND Status ...................................................... 623 Vasodilator Therapy ................................................ 669 Patented Drugs........................................................ 623 Cardiac Glycosides ................................................. 670 Medicine Errors ...................................................... 624 Acute Heart Failure ................................................. 672 Catecholamines ....................................................... 672 Principles of Pharmacology ............................ 624 Pharmacokinetics ........................................... 624 31. Pharmacological Absorption .............................................................. 624 Therapeutics for Medical Distribution ............................................................ 627 Detoxif ication ......................................................... 628 Emergencies 682 Elimination ............................................................. 629 Pharmacodynamics ........................................ 629 Drugs That Affect the Central Drug-Receptor Interaction ....................................... 630 Nervous System ....................................... 684 Drug-Enzyme Interaction ........................................ 630 Blood-Brain Barrier ................................................ 684 Nonspecif ic Drug Interaction .................................. 630 Central Nervous System Sedatives ........................... 684 Biological Response ................................................ 630 Withdrawal from Central Nervous Adverse Drug Reaction ........................................... 630 System Depressants ............................................. 686 Allergic Reaction .................................................... 631 Pain Management........................................... 688 Idiosyncratic Reaction ............................................ 631 The Experience of Pain ........................................... 688 Concepts in Pain ..................................................... 688 30. Pharmacological Interventions Physiology of Pain .................................................. 689 for Cardiopulmonary Analgesics ..................................................... 689 Emergencies 636 Opiates ................................................................... 689 Non-Opioid Analgesics ........................................... 692 The Nervous System ...................................... 638 Convulsions ................................................... 694 The Central Nervous System ................................... 638 Anticonvulsant Medication ...................................... 694 The Peripheral Nervous System ............................... 638 Parkinson’s Disease ................................................. 696 Autonomic Nervous System .................................... 638 Drugs That Affect the Endocrine System ........ 697 Neurotransmission ......................................... 639 Hormones and Pharmacy ......................................... 697 Cholinergic Receptors ............................................. 640 Diabetes ........................................................ 698 Cholinergic Agents ................................................. 640 Drugs That Are Used to Treat Diabetes .................... 698 Anticholinergic Agents ............................................ 640 Drugs That Are Used to Treat Diabetic Adrenergic Neurotransmitters .................................. 641 Emergencies ........................................................ 698 Adrenergic Agents .................................................. 641 Hypoglycemia ......................................................... 699 Pharmacological Interventions during Drugs That Are Used to Treat Adrenal a Respiratory Emergency .......................... 644 Disorders ................................................. 700 Overview of Pulmonary Pathophysiology ................ 645 Synthetic Glucocorticoids ....................................... 700 Beta-Selective Drugs ............................................... 645 Mineralocorticoids .................................................. 701 Pharmacological Interventions during Antiadrenal Medications ......................................... 701 a Cardiac Emergency ................................ 647 Adrenal Medulla ..................................................... 701 Coronary Artery Disease ......................................... 647 Acute Coronary Syndrome ...................................... 652 Drugs That Are Used to Treat Ovarian Dysrhythmia ........................................................... 654 Disorders ................................................. 701 Estrogen Therapy .................................................... 701 Vaughn-Williams Antidysrhythmic Drug Classif ications ......................................... 657 Drugs That Are Used to Treat Pituitary Class I Drugs .......................................................... 657 Disorders ................................................. 702 Class II Drugs ......................................................... 659 Vasopressin ............................................................. 702 Class III Drugs ....................................................... 662 Drugs That Are Used to Treat Thyroid Class IV Drugs ....................................................... 662 Disorders ................................................. 702 Unclassif ied Antidysrhythmic Agents ...................... 663 Drugs That Are Used to Treat Anaphalaxis ..... 702 Heart Failure .................................................. 665 Antihistamines ........................................................ 703 Angiotensin-Converting Enzyme (ACE) Inhibitors ....666 Therapeutic Approaches to Heart Failure ................. 666 Drugs That Are Used to Treat Diuresis .................................................................. 667 Gastrointestinal Disorders ........................ 703 Table of Contents xiii Copyright 2010 Cengage Learning. 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Ulcer Medicines ...................................................... 703 Descriptive Analysis ............................................... 741 Emetics ................................................................... 704 Emergency Decision Making ................................... 742 Antiemetics ............................................................ 704 Determining the Isoelectric Line ............................. 742 Antidiarrheal .......................................................... 704 Identify the QRS Complex ...................................... 743 Laxatives ................................................................ 705 Determine Rhythm .................................................. 744 Drugs That Are Used to Treat Bleeding Calculate Heart Rate ............................................... 744 Disorders ................................................. 705 QRS Width ............................................................. 745 P Waves .................................................................. 746 Antihemophilic Drugs ............................................. 705 AV Relationships .................................................... 746 Anemia ................................................................... 706 Intervals ................................................................. 746 Drugs That Are Used to Treat Psychiatric Normal Sinus Rhythm .................................... 747 Disorders ................................................. 706 Sinus Tachycardia ................................................... 747 Psychosis ................................................................ 706 Sinus Bradycardia ................................................... 747 Anxiety ................................................................... 707 Sinus Dysrhythmia .................................................. 748 Antidepressant Medication ...................................... 707 Mania ..................................................................... 708 Out-of-Hospital ECG Monitoring Equipment................................................ 750 Drugs That Are Used to Treat Childbirth Emergencies ............................................. 708 At-Home ECG Monitoring ............................. 750 Eclampsia ............................................................... 709 Labor ...................................................................... 709 34. Diagonostic ECG— Drugs That Are Used to Combat Infection ...... 709 The 12-Lead 754 Antimicrobials ........................................................ 710 Antifungals ............................................................. 711 Chief Concern ............................................... 756 Antiprotozoal .......................................................... 711 Atypical Presentations of ACS ....................... 756 Antihelmintics ........................................................ 711 Rhythm Strip ................................................. 756 Drugs Used to Treat Cancer ........................... 711 Palliative Care ........................................................ 711 Origins of the Electrocardiogram ................... 757 Standard Limb Leads .............................................. 757 32. Principles of Precordial Leads ..................................................... 757 Augmented Leads—A More Complete Picture ......... 758 Electrocardiography 718 Acquisition of the 12-Lead ECG .................... 759 Diagnostic 12-Lead ECG versus Rhythm Anatomy ........................................................ 720 Monitoring .......................................................... 759 Cardiac Cycle ................................................ 721 12-Lead ECG Artifact ............................................. 759 Conduction System ................................................. 722 Patient Preparation ......................................... 760 Impulse Formation .................................................. 723 Electrode Placement ................................................ 761 Properties of Cardiac Cells ...................................... 725 Dextrocardia ........................................................... 762 Electrocardiographic Principles ...................... 726 12-Lead ECG Tracing .................................... 762 Leads ...................................................................... 726 Standard Leads ....................................................... 726 Electrocardiographic Assessment Waves ..................................................................... 727 of Left Ventricular Function ..................... 763 Intervals and Spaces ................................................ 728 Contiguous Leads ................................................... 763 Relationship to Coronary Arteries ........................... 764 33. The Monitoring ECG 734 Interpretation .......................................................... 764 12-Lead ECG Identif ication of Myocardial The Monitoring ECG ..................................... 736 Injury ....................................................... 765 Portable ECG Equipment ........................................ 736 Normal Depolarization and Repolarization .............. 765 ECG Tracing ........................................................... 736 Ischemic Patterns .................................................... 766 Monitor Features ..................................................... 737 Injury ..................................................................... 767 Monitor Adjustments ............................................... 737 Electrocardiographic Diagnosis Wire Systems .......................................................... 738 of Acute Myocardial Infarction ................. 769 Electrodes ...................................................... 739 Reciprocal Changes ................................................ 769 Electrode Placement ................................................ 739 R Wave Progression ................................................ 770 New Onset Left Bundle Branch Block ..................... 770 Systematic Approach to ECG Rhythm Right Bundle Branch Block ..................................... 771 Interpretation ........................................... 741 xiv Table of Contents Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. Nondiagnostic ECG ................................................ 771 12-Lead ECG Interpretation .................................... 777 Alternative Etiologies for ECG Abnormalities ......... 772 Further 12-Lead ECG Interpretation ........................ 777 Special Case of Pericarditis ..................................... 773 Evaluation .............................................................. 781 Nonspecif ic ST Changes ......................................... 774 15-Lead ECG ................................................. 782 Approach to 12-Lead ECG Interpretation ....... 775 Calibration .............................................................. 775 Acronyms ...................................................... 787 Speed...................................................................... 775 Glossary ........................................................ 792 Diagnostic Quality .................................................. 775 12-Lead ECG Analysis ............................................ 775 Index ............................................................. 831 Table of Contents xv Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. EMS is a practice of medicine. . . . In medicine, there is an art and a science to everything. The science is what we need to do to improve our patient’s condition. In its purest form, what we do is based on rigorous scientifi c scrutiny and all the available evidence applicable to the conditions we treat. The art of medicine is how we apply the science to our patients in a way that maximizes the potential for an improved outcome. Ironically, the science is often much easier to master than the art. This is perhaps no more pronounced than in the ever-changing, often unpredictable world of EMS. One thing is very clear: A good practitioner must be accomplished at both the art and the science of medicine. Edward M. Racht, MD This is a fascinating time to work in emergency health care. EMS is undergoing tremendous evolution. Not only do we know more about the conditions we treat, but more and more of our clinical practices are now based on sound scientifi c evidence that applies specifi cally to our patient population. In the early days of EMS, we adapted evidence from inpatient studies or the laboratory environment and applied it to what we did in the fi eld. While that was certainly appropriate for much of what we did, the challenges of the fi eld and the unique environment of medical care outside the hospital created the need for very targeted research in out-of-hospital medicine. Fortunately, we have more academic initiatives focused on the fi eld than ever before in our brief history. The more we study, the more we learn. We also understand much more about the seemingly insignifi cant details that can have a dramatic impact on patient outcomes. Paying attention to those details and focusing on what’s truly important in the fi eld practice of medicine is another characteristic of the EMS evolution. For example, there are major changes in the way we attempt to resuscitate our patients. A very consistent, focused attention to perfusion is at the core of everything we do during resuscitation |
attempts. While many would say we’ve always believed that to be true, the fact is we didn’t always focus on those details during patient care. During those critical moments of assessing and repairing altered physiology and broken anatomy, paying attention to details can often mean the difference between life and death. As we learn more about the amazing science of the human body and how it behaves when it’s “broken,” we appreciate that the best approach to management of illness and injury requires more than just memorizing facts. It requires us to put together everything we know, use all our available resources, and develop a plan of action that incorporates clinical care, different modes of transport, and different receiving facilities that have different capabilities. EMS, as a unique practice of medicine, is charged with making complex decisions in short periods of time, often with only limited data. The educational toolbox you hold in your hand will follow you throughout your career and guide you in making the tough calls. Our role in the Big Picture of Medicine is also evolving. The devastating and unfortunate events of September 11th and the emerging challenges of terrorism, intentional violence, and newer, unpredictable threats have forever focused the American public’s attention on the importance of emergency medical care. EMS providers must have the knowledge and ability to deal with an entire spectrum of out-of-hospital problems, ranging from the simple to the unimaginable. Because of the potential for rapidly changing scenarios, we as Paramedics must now know where to go to get the right information and how to rapidly access data we need to make our decisions. Our ability to rapidly deploy our resources throughout a xvi Foreword Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. community has also highlighted the value of using EMS providers and systems to disseminate emergency medications and immunizations in the event of a need for rapid public health interventions. As economic conditions change, our society is retooling healthcare delivery and our patients are using EMS in different ways than they have historically. While that creates some new stresses on EMS, it’s a vitally important part of our EMS culture. We are the safety net for many communities suffering from inadequate healthcare resources. Regardless of the number of facilities, patients still get sick and hurt. We should be very proud of our collective ability to care for our fellow human beings regardless of their ability to afford it or our community’s ability to provide it. It’s who we are. The newly promulgated Educational Standards are the result of thousands of hours of work from the most accomplished EMS educators, clinicians, and administrators in the profession. The standards provide us with a new approach to delivering the tools that perfect the out-of-hospital delivery of medical care. Rich Beebe, Jeff Myers, and their colleagues have done a spectacular job of presenting the latest evidence in a very comprehensible manner. As you embark on your educational journey to master the art and science of fi eld medicine, you will continuously discover the valuable educational approach of the Professional Paramedic Series. Volume I provides a solid foundation in the knowledge and clinical skills a Paramedic needs to expertly assess and treat patients. In Volumes II and III, the clinical material is presented in a unique way that facilitates the development of critical thinking skills (remember the art?). These volumes use an interrupted case format that narrows a patient’s chief concern into a paramedical diagnosis. Volume III also discusses the wide range of operational issues faced by the Paramedic and presents students with the many niches within EMS. In addition, the accompanying student resources and instructor curriculum provide additional cases and avenues to test student knowledge, further refi ne critical thinking skills, and enhance the teaching and learning experience. Throughout the learning process, students will not only understand what’s important, they will also learn how to think their way into the diagnosis and develop an approach that has the best opportunity to improve a patient’s condition. That is critical thinking. Enjoy. Enjoy this part of your journey. Enjoy taking care of people when they need you the most. Enjoy learning about the fascinating intricacies of the human body, and enjoy the impact you will have on people’s lives every day. Always remember how important your knowledge, skills, and compassion are for those at the other end of the 9-1-1 call. Edward M. Racht, MD Foreword xvii Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. The Intent of This Book nature of the Paramedic fi eld demanded a fresh You are about to embark on an exciting career as a approach. We wanted our textbook to challenge Paramedic! Within these pages we will present to you Paramedic students to think about the application of the knowledge, skills, and practical advice needed medical knowledge to fi eld practice. This approach to become a skilled and profi cient Paramedic. changed the focus of a Paramedic textbook from With a focus on future Paramedics and the being the center of a Paramedic’s education to Paramedics of today, the Professional Paramedic one in which it serves as an authoritative resource Series was designed as a comprehensive resource that implores the student to explore the current for Paramedic students during their education state of the science. and as a source for life-long learning. This series As part of our vision in writing this series, we seeks to prepare aspiring Paramedic students wanted to recognize the practice of paramedicine. in community colleges, universities, and other What is paramedicine? Paramedicine is a unique educational programs by not only providing the practice of emergency medicine that happens in knowledge needed to become a Paramedic, but the out-of-hospital setting. First described in the also developing the ability to think critically and EMS Agenda for the Future in 1996, paramedicine decisively when seconds count. Beyond the basic is the result of the growth of EMS over almost one foundation of information and skills, this series half of a century. It encompasses the complete helps the Paramedic student reach a higher level of roles and responsibilities of the Paramedic within understanding. For this reason, the series is also an the domains of health care, public health, and essential source for recertifi cation and continuing public safety systems. We offer this series as a education for practicing Paramedics. guide to prehospital emergency medical care and In January 2009, the new National EMS Education the practice of paramedicine, providing learners Standards were released to the EMS community, with a reference for the often complex, at setting an academic standard for all Paramedic times ambiguous, and always challenging fi eld of education programs. This series was specifi cally emergency medicine. developed with the National EMS Education We understand that often the best Paramedics Standards in mind, yet can also be used in Paramedic are those who start with a natural curiosity about programs that have not yet transitioned to the new emergency medicine and inquisitiveness about how standards. Each of the three volumes, as a series, that medical knowledge could be practically applied meet and exceed these new education standards in the streets. These students know it is important by not only teaching the essential information and to be street smart as well as book smart. This book skills, but also by preparing each student in how to seeks to help answer their questions through a think like a Paramedic. As Paramedics who started conversation with the student. in the streets and who continue to practice in the streets, we support the vision of the National EMS The Professional Paramedic Education Standards, and have created this aptly Series named Professional Paramedic Series. This series is designed to follow a logical progres- sion of learning, in which information and skills Why We Wrote This Book are presented fi rst in Volume I, followed by the As educators, we challenge our learners—the application of those skills in emergency situations students of this series—to be the best Paramedics in Volume II, and trauma and special response they can be. While there are other Paramedic considerations in Volume III. The framework of each textbooks available, we felt that the evolving book is practical in approach: introducing principles, xviii Preface Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. skills, and terminology; presenting a typical case; This volume is divided into six sections. walking through critical response steps; and again reviewing key concepts to ensure understanding for Section I: Framework For successful application on the job. Paramedic Practice The series is inclusive of all of the content areas All things must be built on a solid foundation, listed in the National EMS Education Standards and and the practice of EMS is no different. What contains material on most of the critical and emergent do Paramedics do, why do they do it, and how did disorders listed in the EMS core content, as well as many the fi eld develop? How are EMS systems put to- of the lower acuity conditions. This coverage helps gether and why? How do we remain safe at what ensure the student prepares for the National Registry we do? What is research, how do I read it, and or state Paramedic certifi cation examinations. More why is it important during my daily practice in the importantly, the series helps prepare the Paramedic street? The four chapters in this section answer student for professional Paramedic practice. these questions and examine these subjects in Volume I: Foundations depth. As the fi eld of paramedicine becomes more evidence based, understanding research and how it of Paramedic Care applies to our practice becomes more important. ISBN: 978-114283-2345-2 Section II: Ethics and Law in EMS The public as a whole—and each individual patient and family—entrusts Paramedics with their lives and expects them to provide appropriate care. Some situations pose a dilemma for the Parame-dic, whether it is with a patient, family member, partner, supervisor, or medical director. A strong sense of ethics, displayed by following accepted ethical and legal practices, helps Paramedics maintain the trust and privilege that is placed in them by society. Section III: EMS and Public Health Since September 11, 2001, the EMS community has recognized that there is a strong link between EMS and public health. In some areas of the United States, Paramedics are utilized to augment the public health system, whether as part of a response team to a public health emergency or to assist with day-to-day public health activities in areas of need. These chapters provide a foundation in the fi eld of public health and illness and injury prevention. This allows the Paramedic to fulfi ll these important roles To be able to make a diagnosis, the Paramedic in the healthcare system. must be well grounded in the basics of medicine including anatomy and physiology as well as pa- Section IV: Scientifi c Principles thophysiology. Volume I: Foundations of Paramedic The four chapters in this section provide a basic Care begins with the basics. This fi rst volume in the foundation in lifespan development, physiology, series introduces the fundamental information and pathophysiology, and medical terminology. These skills needed for success, as well as the |
necessary areas again help lay a solid foundation for the tools to begin developing a professional approach to Paramedic to build upon in the later technical and emergency medicine and Paramedic care. clinical chapters. Preface xix Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. Section V: Principles of Clinical Practice various diseases and disorders, from gynecological Communication with and assessment of the patient is concerns to neonatal resuscitation, from the essential to every encounter. Through this process, chronically ill to the victims of domestic violence the Paramedic gains the information needed to form and sexual assault. Each chapter walks you a differential diagnosis and develop an appropriate through a typical emergency that a Paramedic treatment plan for the patient. These seven chapters might encounter in the fi eld—each case associated provide the Paramedic with the base skills to obtain with the subject of the chapter–presenting an effective history and perform a thorough physical critical information that leads you to develop examination. a Paramedic’s diagnosis from the information provided. Section VI: Clinical Essentials It should be understood that each case repre- The fi nal section of this volume includes the essen- sents only one potential patient presentation. tial material regarding airway management, moni- To that end, we have included additional cases in the toring devices, intravenous access, pharmacology, accompanying Study Guide. It is the responsibility ECG monitoring, and acquisition that forms the of the student and the instructor to explore these basis for our assessment and treatment. This section other cases, and other real world examples, to fully provides the foundational material nece-ssary to appreciate other potential patient presentations. progress into the clinical chapters in Volume II. Even so, this cannot possibly cover the entire universe of potential patient presentations. This Volume II: Medical Emergencies, fact makes Paramedic emergency care exciting Maternal Health & Pediatrics and refreshing. These cases are intended to ISBN: 978-1-4283-2351-3 reinforce the commonalities of presentation As Paramedic students, you must learn to for the different disorders and syndromes that apply the skills introduced in the fi rst volume will permit the Paramedic to make a diagnosis, within Volume II of the series. Through introduction regardless of the individual patient-specifi c of an interrupted case approach, this book conditions. walks you through a wide range of emergency Volume II is divided into four sections: response situations, from cardiac emergencies to ■ Section I: Medical Emergencies ■ Section II: Maternal Health ■ Section III: Pediatric Medicine ■ Section IV: Special Patients Volume III: Trauma Care and EMS Operations ISBN: 978-1-4283-2348-3 Volume III highlights special response conside- rations and a broad range of operational medical topics needed to prepare readers with the complete spectrum of knowledge required to succeed as a Paramedic. These aspects of Paramedic practice help to make paramedicine unique and help make paramedicine a profession. Volume III is divided into four sections: ■ Section I: Trauma Care ■ Section II: Environmental Medicine ■ Section III: EMS Operations ■ Section IV: Emergency Incident Management xx Preface Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. and instructor within the classroom. By portraying realistic emergency situations that a Paramedic is likely to encounter on the job, the book introduces the student to the material in a meaningful manner. This presentation also encourages the decision-making process involved in making a fi eld diagnosis, and outlines a plan of treatment that meets the standard of care within the scope of practice for the patient—for prehospital care and transport to the hospital. Each case is designed to encourage a Paramedic thought process, relates to the subject under discussion within the chapter, and includes follow-up Case Study Questions at the end of the chapter. Case Study Questions: Please refer to the Case Study at the beginning of the chapter and answer the questions below. 1. W hat should be included in the radio report to the medical control physician? 2. H ow important was the fi rst-due report given by the Features fi rst member of the public safety team on-scene? Along with an appealing design, this series has many features intended to motivate the student to read CHEATED Method and learn the content and skills presented in each This method follows the standard medical intelligence volume. of a Paramedic (sometimes called “medic think”), and encourages students to engage in the critical Comprehensive Coverage thinking process needed for a proper fi eld diagnosis The complex depth and comprehensive breadth of and treatment—Chief concern, History, Examination, information required for a working knowledge of Assessment, Treatment, Evaluation, and Disposition. Paramedic practice, for Paramedic certifi cation, and, ultimately, for success on the job are all provided in Professional Paramedic an engaging and reader-friendly manner. Students Integrated throughout the book, this advice high- will be properly prepared for these challenges li23g45h7_t18s_ ch1t8h_p3e20 -33p5.irndod f 3e34ssional attitudes that signify the with evidence-based information presented within difference between a competent Paramedic and the content that meets and exceeds National EMS a profi cient Paramedic—one fellow Paramedics Education Standards. respect and look to as a leader. Key Concepts Presented in the beginning of each chapter, the key Professional Paramedic concepts set learning goals for students and prepare The professional Paramedic does not blame the readers for both the didactic and psychomotor skills presented in the chapter. patient for the disease. For example, tobacco smoking is now known to be a risk factor for lung Case Studies diseases such as emphysema and cancer. However, tobacco smoking was encouraged by the U.S. The case studies included in each chapter facilitate government in World War II and tobacco companies the conversation—both the internal dialogue within advertised that tobacco was an aid to digestion. the student and the dialogue between the student Preface xxi Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. Street Smart Skill 23-5 King Airway Placement Street Smart tips, lessons learned by the authors while in practice in the fi eld, focus on practical information that can help new Paramedic students perform in less-than-ideal or unusual situations. Street Smart 1 Grasp tongue and jaw, lifting toward ceiling. Place tip of tube 2 Rotate the airway counterclockwise as it is advanced. To differentiate a pericardial rub from a pleural rub, toward oropharynx, approaching from the patient’s right. have the patient hold his breath. Pleural rubs are heard when the patient is breathing while pericardial rubs occur with each heartbeat. Cultural/Regional Differences 3 Advance until the orogastric port is at the level of the teeth. 4 Infl ate balloon, bag-ventilate the patient, and auscultate Important considerations are pointed out for respond- breath sounds. ing to patients of different cultural backgrounds. This prepares students for the diverse patient population that the Paramedic will encounter in emergency situa- tions. Understanding these cultural/regional differences increases the Paramedic’s effectiveness in the fi eld. 5 Slowly withdraw while listening until breath sounds are the 6 Confi rm placement and secure airway. loudest. Cultural / Regional differences Review Questions It should be noted that while younger and better Review Questions at the end of each chapter are educated patients prefer to share clinical decision helpful for evaluating student knowledge of the con- making, cultural and ethnic differences may decrease cepts presented in the chapter. Review Questions patient cooperation. This lack of cooperation should are followed by Case Study Questions that encourage not be viewed as resistance to care but rather as a students to apply critical thinking skills to the case trust in the Paramedic’s decision. studies that are presented at the beginning of each chapter. 10/2/09 12:41:26 AM Step-by-Step Skills References and an Photos and descriptions are combined to present critical information on the fundamental skills of Evidence-Based Approach Paramedic practice. Each skill is included at the end of The content each student learns must be substantiated the chapter to avoid interrupting the fl ow of learning, by science and medicine. Each chapter is thoroughly and is referenced in the applicable discussion within researched and includes documentation of references the chapter. that support the content presented in the chapter. Conclusion and Key Points References: Critical points in the chapter are covered and 1. Kelly CG. The ways and whys of documentation. Good provide a basis of review for the student. While documentation is more than what’s on a PCS form. Emerg Med the Conclusion provides an overall summary of the Serv. 2007;36(7):30. 2. Perkins TJ. Tell me a story. The importance of good chapter’s main theme, the Key Points provide a documentation. Emerg Med Serv. 2007;36(9):30, 32–33. bulleted list of important information that is helpful 3. Krentz MJ, Wainscott MP. Medical accountability. Emerg Med for study or review. Clin North Am. 1990;8(1):17–32. xxii Preface Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. The Professional Paramedic Series Curriculum Plan We are proud to present a robust curriculum plan for the Paramedic student and instructor. As part of this plan, we offer resources that work hand-in-hand with each volume in the series, serving to further enhance both the teaching and the learning experience. For the students, resources are available that will help them review important concepts through practical application, develop and practice critical thinking skills, and guide them toward further research and discovery. For the instructors, we offer tools that will help them effi ciently prepare for classroom instruction, manage and track student progress of didactic and skill requirements, keep informed of new advances in the EMS fi eld, and overall, engage students in learning both in and out of the classroom. For the Student Study Guides For the Instructor Volume I Study Guide, ISBN: 978-1-4283-2346-9 Instructor Resources (CD-ROM) Volume II Study Guide, ISBN: 978-1-4283-2352-0 Volume III Study Guide, ISBN: 978-1-4283-2349-0 Volume I Instructor Resources, ISBN: 978-1-4283-2347-6 Bridging the gap between knowledge and application, Volume II Instructor Resources, one Study Guide accompanies each volume to offer ISBN: 978-1-4283-2353-7 learners additional case studies for each chapter, Volume III Instructor Resources, along with multiple types of practice questions ISBN: 978-1-4283-2350-6 and activities required for comprehension of the material. The Instructor Resources for each volume are designed to help instructors effectively prepare Online Companions students to become well-rounded, street-smart Students are provided with FREE access to our Paramedics within the guidelines of the new National website with an Online Companion to accompany EMS Educational Standards. The Instructor Resources each volume. This website invites students to on CD-ROM includes tools that help instructors and further study and explore the concepts presented in administrators prepare their Paramedic program in a each volume. The website includes articles and up- timely and effi cient manner. Each CD-ROM includes to-date information on the EMS fi eld, related links the following features: to important industry organizations and resources, ■ Administration: This section includes information information related to national guidelines, illustrated on setting up the program, as well as practical glossaries, and bonus content. Each Online Companion advice for transitioning your program to the new |
is uniquely designed to the corresponding volume in National EMS Educational Standards. In addition, the series, and contains information relevant to the it includes the following tools: topics covered within that volume. ● Equipment Checklist: The checklist provides Visit www.cengage.com/community/ems to access a resource for instructors to ensure that these Online Companions! they have the necessary tools for classroom Preface xxiii Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. revise them according to local practice variations and regional/state medical protocols. ■ PowerPoint Presentations: Correlated to the accompanying Lesson Plans, these presentations combine key points with photos, graphics, and video to serve as a basis for either interactive classroom instruction or as augmentation of an asynchronous distance learning program. ■ Computerized Test Banks: Containing over 1,000 questions and covering the content in each chapter, these Test Banks in ExamView format allow instructors to manage test administration in the classroom. Instructors may create or edit tests based on existing questions, edit questions, and add or delete questions to fi t local practice variations and regional/state medical protocols— all in this user-friendly program. ■ Teaching Sheets: Highlighting the Paramedic skills necessary for Paramedic practice, these Teaching Sheets provide a baseline for skills learning. Each Teaching Sheet provides a break- down of the critical principles for the skill, and is included in Word format to allow instructors to add specifi cs based on their local requirements and/or regional/state protocols and procedures. ■ Clinical Logs: Based on the Teaching Sheets, instruction and for setting up and running skill these Clinical Logs provide forms for tracking sequences. student accomplishment of prehospital (fi eld) ● Concept Maps: Highlighting the decision- and in-hospital (clinical) skills. These forms, making process, these Concept Maps offer complete with a signature page, are provided in a way for instructors to help students Word format to allow instructors to edit them in conceptualize ideas in the classroom and order to meet local requirements. develop the critical thinking skills necessary ■ Research and Discovery—Instructor Reference for determining a fi eld diagnosis. Each Concept Guide: Paramedicine, like medicine, has an ever- Map, utilizing a typical emergency scenario, changing body of knowledge. To remain current, walks students through the critical thinking the Paramedic must be a life-long learner. In steps used during an EMS response. addition to the listing of references that appears ● Correlation to National EMS Education at the end of chapters in each volume in the Standards and D.O.T Paramedic Curriculum: series, this Instructor Reference Guide provides These guides map out Paramedic content and additional resources—including articles, websites, provide students with the volume, chapter, organizations, and other reference materials—to and pages where this content is covered in fi nd information on specifi c topics. This ensures the Professional Paramedic Series. that instructors remain informed of current ■ Lesson Plans: Including an outline of each practices in the EMS fi eld. chapter, with correlations to the accompanying PowerPoint presentations, skill sheets, and helpful Online Companions teaching tips, these Lesson Plans provide a helpful Linked to the student Online Companions, these guide for classroom instruction. These plans are resources provide instructors FREE access to provided in Word format so that instructors may bonus content, including podcasts, articles on xxiv Preface Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. new information and technology, links to EMS During his tenure as a Paramedic Educator, community websites, information related to Mr. Beebe has served in the capacity as lecturer, national guidelines, and additional classroom instructor-coordinator, and Paramedic program materials. Each Online Companion is uniquely director. He continues to speak at local, regional, designed to the corresponding volume in the series, state, and national conferences on topics of and contains information relevant to the topics importance to both the EMT and the Paramedic. covered within that volume. Mr. Beebe is presently a clinical assistant pro- fessor at the State University of New York at Cobleskill and Paramedic program director for Web Tutor on WebCT and Blackboard Bassett Healthcare’s Center for Rural Emergency Providing a content-rich, Web-based teaching and Medical Services Education. learning aid, this tool helps to emphasize and clarify Mr. Beebe has been published in several journals, complex concepts, provides a forum for discussion, including the Journal of Emergency Medical Services and offers a venue for tracking course syllabus and and Fire-Engineering, as well as being a co-author other program-related activities. for Delmar’s Fundamentals of Basic Emergency WebTutor on Blackboard Course allows instructors Care, now in its third edition. to quickly and easily jump-start their on-line course Mr. Beebe has contributed to the previous editions development. Whether you want to Web-enable of the National Standard Curriculum for Paramedic, your class or put an entire course on-line, WebTutor Intermediate, and Basic; to the national EMS delivers! Education Agenda for the Future; to the national EMS Scope of Practice; and served as content leader for the National EMS Education Standards. Mr. Beebe About the Authors is also a charter member of the National Association of EMS Educators. Richard Beebe, MSEd, BSN, RN, NREMT-P Richard Beebe started his EMS career in 1974 as an Jeff Myers, DO, EdM, NREMT-P, FAAEM Explorer Scout with the Moyers Corners Volunteer Fire Dr. Myers has been involved in EMS for over 20 years, Department in upstate New York. Since obtaining his including 12 years in the prehospital environment and Emergency Medical Technician certifi cation in 1975, 18 years as an EMS educator. Dr. Myers began his EMS Mr. Beebe has continuously maintained his certifi cation journey in 1988 in upstate New York by volunteering and his practice. During his career Mr. Beebe has for his college ambulance (RPI Ambulance) and a local served in fi re/EMS, commercial EMS, volunteer EMS, community ambulance (North Greenbush Ambulance and as a municipal Paramedic. During that time, he Association). He began teaching in 1990 for the has served as a volunteer crew chief, a squad captain, Rensselaer County Ambulance and Rescue Association, and Paramedic supervisor. Mr. Beebe currently serves eventually becoming a state Certifi ed Instructor as a civilian Paramedic for the Guilderland Police Coordinator. Dr. Myers ran the EMT-Basic original Department, outside of Albany, New York. course in Rensselaer County for three years before Mr. Beebe has also been a critical care nurse leaving to attend medical school. During the early since 1985, having practiced for 10 years in both 1990s, he also served as a Rensselaer County Deputy the Emergency Department and the Intensive Care County EMS Coordinator for four years, responding Unit. During these years, Mr. Beebe developed to multi-ambulance and multi-agency incidents. His his knowledge of medicine and—perhaps, more fi eld experience includes volunteer, commercial, and importantly—an appreciation of the potential combination paid-volunteer agencies as a Paramedic impact that prehospital advanced life support could in upstate New York and in southern Maine. have on patient morbidity and mortality. Dr. Myers attended medical school at the Consistent with that belief, Mr. Beebe became a University of New England College of Osteopathic Paramedic in 1988 and, in hopes of advancing the Medicine in Biddeford, Maine. While in medical practice of his fellow Paramedics, started his career school, he continued to teach ACLS and BCLS classes as a Paramedic Educator. through the local hospital. Preface xxv Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. Dr. Myers then moved to Buffalo, New York, Anthony Billittier, IV, MD, Commissioner of Health, completing his residency in Emergency Medicine at Erie County, New York; Assistant Professor SUNY-Buffalo in 2004. In his fi nal year of residency, Emergency Medicine, Department of Emergency he served as Chief Resident. He stayed at SUNY- Medicine, School of Medicine and Biomedical Buffalo for a two-year EMS Fellowship through the Sciences; Assistant Professor, Department of Erie County Medical Center and completed a Masters Social and Preventative Medicine, School of Public in Education at the University of Buffalo. He is board Health and Health Professions, State University of certifi ed in Emergency Medicine and a Fellow of the New York at Buffalo American Academy of Emergency Medicine. Jonnathan Busko, MD, MPH, EMT-P, Emergency He is currently on faculty at SUNY-Buffalo as a Physician, Eastern Main Medical Center, Bangor, clinical assistant professor and serves as the associate Maine system EMS medical director and EMS fellowship Steve Carson, BS, PA, CCEMT-P, Physician Assistant, director at the Erie County Medical Center. Dr. Army National Guard, Afghanistan Myers is an active member of the Specialized Medical Deborah Kufs, MS, RN, EMT-P, Interim Director, Assistance Response Team, western New York’s Paramedic Program, Hudson Valley Community physician response team, which is called upon to College, Troy, New York augment local EMS during MCIs, and special situations, Jeffrey Thompson, MD, Attending Physician, for example patient entrapment and providing Professional Emergency Services and Clinical tactical medical support. He is the assistant medical Instructor of Emergency Medicine, State University director for Rural Metro Medical Services of Western of New York at Buffalo, Buffalo, New York New York, based out of Buffalo, New York. Dr. Myers Brett Williams, MD, Florida Emergency Physicians, has several publications in peer-reviewed journals Orlando, Florida and is an author for Delmar Cengage Learning, writing Automated Defi brillation for Professional For the development of the art program in this and Lay Rescuers and Principles of Pathophysiology volume—the countless hours spent in preparation, and Emergency Care. He also produced and directed set up, and shooting of the photography appearing the Techniques in Airway Management DVD series. in this book, as well as the extensive research, Dr. Myers has spoken at several regional and national persistence, and acquisition of those “hard to fi nd” conferences on a variety of topics. For more photos and graphics—we express our gratitude to information on topics or to provide feedback on the the following individuals: textbook, please check out Dr. Myers’ website at Jon Behrens, AAS, EMT-P, Paramedic Instructor, http://ems-ed.photoemsdoc.com. State University of New York at Cobleskill Chris Lenaghan, Photographer, CML Media Services Abigail Reip, Photo Acquisition and Permission Acknowledgments Coordinator As with all of our projects, the Professional Para- Liana Dypka, Art Manuscript Development medic Series would not have been possible without the support, guidance, and participation of the con- tributors, reviewers, and advisory board members. Reviewers We owe these individuals our sincere thanks. To the reviewers, who provided an honest evaluation of the content in the book and continual guidance throughout development of this volume, we express Contributors our appreciation: During the development of Volume I: Foundations Melissa Alexander-Shook, Director of EMS Academy, of Paramedic Care, we were honored to have the University of New Mexico, New Mexico following contributors participate in researching, Steve Kanarian, Paramedic Instructor, Rockland writing, editing, and reviewing materials to Community College, New York ensure a comprehensive and accurate Paramedic Mike McLaughlin, Director of Health Occupations, guide: Kirkwood Community College, Iowa xxvi Preface Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. M. Jane Pollock, Extension Education Training From the |
Authors Specialist, Emergency Medicine, East Carolina Beebe University, North Carolina Don Royder, Emergency Medical Services Program First, I would like to acknowledge my friends Coordinator, Texas Engineering Extension Service, and family, and particularly my wife Laura, whose Emergency Services Training Institute, Texas support has sustained me over the 10 years that it took to write this book. Thank you for your love. EMS Advisory Board I would also like to thank the professionals at Delmar/Cengage Learning who have helped support We offer special thanks to our Advisory Board this idea from its onset and continue to encourage Members, who take time out of their schedules to me to greater accomplishments. I would like to advise us on our training materials, the status of the thank Sandy, Benj, Erin, and particularly Jennifer, EMS fi eld, and to work with us as partners in striving the backbone of this excellent team. to meet the needs of the students and instructors of Finally, I would like to thank my students who, each today—and those of the future: and every year, challenge me to be the best Paramedic Scott Bourn, National Director of Clinical Programs, and educator that I can be and who, even to this day, National Resource Center, American Medical continue to inspire me. In the 30-plus years I have been Response, Colorado involved in EMS and EMS education, I have truly seen Deb Cason, Associate Professor, University of Texas EMS in general—and Paramedics in particular—evolve Southwestern Medical Center, Texas into a caring profession that we all can be proud of. Don Collins, Captain, Massport Fire-Rescue, Logan International Airport, Boston Myers Stephen Dean, Director, Corporate Training, Thanks and love to my family. This textbook (and Paramedic Plus, Oklahoma all my life’s projects) would not be possible without Joe Grafft, President, Customized Safety Training their support. Art Hsieh, Chief Executive Offi cer and Director of Education, San Francisco Paramedic Association, Delmar/Cengage Learning Team California For the team that always fi nds a way, every day, Mike Kennamer, Director of Workforce Develop- to turn an idea into a reality, we thank these ment, Northeast Alabama Community College, extraordinary people for their hard work, dedication, Alabama support, and creativity: Guy Piefer, Paramedic Program Coordinator, Borough of Manhattan Community College, City Janet Maker, Product Development Manager of Yonkers Fire Department, New York Jennifer Starr, Senior Product Manager Ed Racht, Vice President of Medical Affairs and Amy Wetsel, Editorial Assistant Chief Medical Offi cer, Piedmont Newnan Hospital, Jennifer Hanley, Senior Content Project Manager Georgia Erin Coffi n, Senior Marketing Manager Karla Rickards, EMS Training Coordinator, Unifi ed Shanna Gibbs, Marketing Coordinator Fire Authority, Salt Lake County John Rinard, Training Coordinator, TEEX, Texas Closing Thoughts A&M University In this time when the importance of quality John Sinclair, Fire Chief, Kittitas Valley Fire improvement is understood and appreciated, Rescue Emergency Manager, City of Ellensburg, we encourage students and instructors alike to Washington; Immediate Past Chair and communicate with us. Via these conversations, International Director, International Association all parties can improve their understandings. We of Fire Chiefs, Emergency Medical Services are all enriched through this communication. Section Mike Ward, Director of Emergency Health Services, Richard W.O. Beebe Jeffrey W. Myers George Washington Medical Center, Washington, Bassettmedic@gmail.com h ttp://ems-ed. DC photoemsdoc.com Preface xxvii Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. A ll things must be built on a solid foundation, and the practice of EMS is no different. What does a Paramedic do, why do they do it, and how did the fi eld develop? How are EMS systems put together and why? How do we remain safe at what we do? What is research, how do I read it and why is it important during my daily practice in the street? The four chapters in this section answer these questions and examine these subjects in depth. As the fi eld of paramedicine becomes more evidence based, understanding research and how it applies to our practice becomes more important. • Chapter 1: Roles and Responsibilities of the Professional Paramedic • Chapter 2: Introduction to Emergency Medical Service Systems • Chapter 3: Workforce Safety and Wellness • Chapter 4: Research and EMS 1 Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. KEY CONCEPTS: Upon completion of this chapter, it is expected that the reader will understand these following concepts: • The profession of paramedicine combines aspects of public health, public safety, and health care • Standards and scope of practice defi ne the Paramedic’s knowledge, skills, and attitudes • The Paramedic’s role is as a healer, clinician, and teacher • Quality assurance, Quality improvement, and continuing education enhance both the Paramedic’s individual practice and that of the profession as a whole • The Paramedic is a physician extender through stewardship, leadership, and followership Case Study: Traffi c was slowed around the accident site. As the two teens drove slowly by, each looked at the Paramedics who were providing and directing care of the victims. The fi rst teen stated, “They sure looked like they knew what they were doing.” The second teen added, “I wonder what else they do.” 2 Foundations of Paramedic Care Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. Roles and Responsibilities of the Professional Paramedic 3 Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. OVERVIEW Although paramedicine is a relatively young profession compared to many others, it has found its footing as a unique part of the healthcare system. The Paramedic’s role has evolved from simply responding to emergencies to now practicing an expanded scope of practice as a physician extender. In this way, the Paramedic has proved to be a vital part of the public health and safety team. This chapter not only examines the origins of paramedicine but also how national education standards and accreditation of educational programs coupled with professional organizations have helped to validate paramedicine as a profession. The chapter also examines the Paramedic’s core values and his or her role as healer, clinician, and teacher. As the Paramedic’s scope of practice and community responsibilities continue to develop, quality assurance, quality improvement, and continuing educational programs need to be established. The Paramedic’s independent and interdependent role as a physician extender relies on leadership and stewardship. What Is Paramedicine? examinations and become licensed to practice paramedicine. All Paramedics understand the importance and the necessity Paramedicine is a special subset of medicine that Paramedics of giving back to their profession through teaching Paramedic provide in the out-of-hospital setting. Paramedics, as allied students. healthcare professionals, practice paramedicine under often The practice of paramedicine, like the practice of medi- austere conditions and with a minimum of equipment. cine, is constantly evolving. Professional Paramedics incor- Paramedic practice is both independent as well as interdepen- porate and apply new information and technologies in their dent. The universe of independent Paramedic practice includes practice. Through programs of competency assurance and pro- disaster planning, response readiness, scene management, and fessional development, offered in continuing education pro- emergency vehicle operations. Collaboratively, Paramedics grams, the Paramedic stays current with the profession. work interdependently with emergency physicians to bring The Paramedic’s professional identity revolves around the the highest level of medical care outside of the hospital. voluntary assumption of certain roles and responsibilities and While Paramedics traditionally have provided emergency a code of ethics. Once Paramedic status is attained, that person care as part of the emergency response system, Paramedics is a Paramedic and, regardless of other roles the person may also provide care during transportation between medical have in a lifetime, will always see himself as a Paramedic. facilities. Interfacility patient care often involves a high level of medical complexity and requires education above that of The practice of medicine is an art, not a trade; a the entry-level Paramedic. calling, not a business; a calling in which your heart Paramedicine is positioned at the intersection of health will be exercised equally with your head. care, public health, and public safety. Owing its existence to each, the Paramedic is cross-trained in each of these areas. As — William Osler, MD a result, a synergy occurs among the knowledge from these three areas and the result is paramedicine, a unique body of The professional Paramedic has many roles, the fi rst knowledge which is exclusive of its origins. of which is as a healer. Healing is an attempt to mollify the More than a vocation, paramedicine involves exten- effects of disease. In many instances the Paramedic is unable sive educational preparation, typically at a collegiate level, to effect a cure and strives instead to relieve pain and suffer- to attain the specialized knowledge necessary to become a ing. Healing is a process of helping people physically, men- Paramedic. Paramedic education is usually attained in an edu- tally, and spiritually endure their illness. As one of the healing cational program that is accredited by a body which includes professions, when the practicing Paramedic demonstrates professional Paramedics. empathy, respect, and a genuine interest in the patient, the Paramedicine is also an applied science. To attain profi - Paramedic is seen as a compassionate caregiver—a healer. ciency at patient care skills and apply the knowledge gained This ability to help the patient in distress to heal while provid- to care of patients, Paramedic students learn and work under ing medical care could be seen as the art of paramedicine. the watchful eye of preceptors. Upon completion of a pro- While Paramedics rarely cure a disease, the practice gram of study, Paramedics complete professional certifi cation of paramedicine is also based, in part, on the science of 4 Foundations of Paramedic Care Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. medicine.1,2 The science of medicine focuses on cure and Table 1-1 Qualities of a Profession medical research is continually improving the treatment of • Extensive educational preparation patients with diseases. In turn, the medical treatments that • Accreditation of educational programs Paramedics provide are based, to the extent possible, on med- ical research. A professional Paramedic always keeps abreast • Mentoring of the medical science which has an impact on the practice. |
• Certifi cation Paramedics are also stewards. As a shared practice that • Licensing originates in medicine, Paramedics are responsible for main- • Professional development taining the ideals of medicine and to practice in a manner • Professional societies that would bring honor to themselves and their physician • Code of ethics—professional boundaries colleagues. The right to practice paramedicine is given to Paramedics by physicians who understand the importance of collaborative practice. of education is typically provided in a college or university As members of the healthcare team Paramedics are also environment in accredited educational programs. During leaders. Paramedics are not leaders by virtue of their posi- their education, Paramedic students would need professional tion but by their ability to affect the behavior of other mem- models, or mentors to guide them along in their educational bers of the team to accomplish the goal of patient care. As a development. Upon successful completion of the original leader, the Paramedic may have to take on the role of teacher education, the Paramedic’s rite of passage into the profes- or patient advocate, but in every instance the patient’s welfare is foremost in the Paramedic’s mind.3 sion would be certifi cation and licensure. Once in the fi eld, the practicing professional Paramedics would be expected As the leader, the Paramedic also understands the impor- to maintain their education through competency assurance tance of followership. A Paramedic’s adherence to the phy- and professional development.5 Paramedics would also be sician’s orders, as well as those of other authority fi gures, expected to contribute to the profession through active par- is an example of followership. Followership is not offered ticipation with fellow Paramedics in an association or soci- begrudgingly but instead willingly, with an understanding of ety. Central to these professional associations or societies is a the importance of teamwork for patient care. code of ethics which helps defi ne the profession. Many quali- ties are common in all professions (Table 1-1). Currently Paramedics are required to obtain extensive Professional Paramedic educational preparation to acquire a unique body of knowl- edge. An increasing number of Paramedic programs are being offered in accredited programs provided at postsec- The role of patient advocate encompasses all of the ondary schools where Paramedic students also learn from Paramedic’s other roles and responsibilities. experienced preceptors during an internship. Plus, there is a growing trend toward licensing Paramedics. These efforts, and others, will help to shape and develop the Paramedic profession. Hallmarks of a Profession In the past, Paramedics were considered auxiliary healthcare providers, unlicensed care providers who received the major- Cultural / Regional differences ity of their training “on the job” (OJT) and were not con- sidered to be healthcare professionals. Classic examples of No national exam serves as a culminating point for healthcare professionals are physicians, nurses, and physician assistants. These groups are considered professional because entry into the profession of paramedicine as does they meet certain criteria to be considered a profession. the NCLEX for professional nursing. A tapestry of Paramedics have not yet met those criteria. However, the fi eld county, regional, and state requirements often create of paramedicine is in the process of professionalization. Some of the criteria for consideration as a healthcare diffi culties in transferring from one geographical area professional were discussed in the fourth report of the Pew to another. Health Professions Commission entitled, “Recreating Health Professional Practice for a New Century.”4 The section entitled, “Professional Characteristics of Allied Healthcare To assist current and aspiring healthcare professionals, Providers” describes what is needed for a group to be consid- the Pew Health Commission listed what were felt to be the 21 ered an allied healthcare provider. competencies that healthcare professionals needed to aspire To be considered an allied healthcare provider, Paramedics to in the twenty-fi rst century. Some of these are especially would fi rst need extensive educational preparation. This type germane to Paramedics (Table 1-2). Roles and Responsibilities of the Professional Paramedic 5 Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. Table 1-2 Partial List of the 21 Competencies National Registry of Emergency for Healthcare Professionals for the Twenty-First Medical Technicians Century from the Pew Health Commission The culmination of a Paramedic education should be certifi - • Embrace a personal ethic of social responsibility and service cation. A certifi cation is a formal process in which an outside • Exhibit ethical behavior in all professional activities organization, often an organization that represents the profes- • Provide evidence-based clinically competent care sion or the professional association, verifi es through written • Integrate population-based care in services into practice and/or practical examination the competency of an individ- • Improve access to healthcare for those with unmet health needs ual who wishes to enter the profession. This process seeks • Provide culturally sensitive care to a diverse society to ensure that the individual possesses the minimum level of • Use communication and information technology effectively and knowledge and skill required to practice that profession. appropriately The National Registry of Emergency Medical • Work in an interdisciplinary team Technicians (NREMT) presently provides a certifi cation process of practical testing and written examinations for the • Practice leadership certifi cation of Paramedics. Successful completion of the • Contribute to continuous improvement of the healthcare National Registry testing demonstrates that the Paramedic system has demonstrated a minimally acceptable level of profi ciency • Continue to learn and help others learn in the core elements. The National Registry was initiated by recommendation of the American Medical Association’s (AMA) Committee Education Systems on Highway Traffi c Safety, chaired by Dr. Oscar Hampton Jr. The committee included notable EMS authorities such as Key to a profession is the educational preparation required to Dr. J.D. “Deke” Farrington, author of the infl uential article enter that profession. In the past, the DOT National Standard “Death in the Ditch.” The National Registry of EMT was Curriculum has served as the basis for EMS education. Since formed in June 1970 and—under the leadership of its fi rst the creation and adoption of the fi rst EMT-A National Standard executive director, Rocco V. Morando—proceeded to meet its Curriculum (NSC) in 1969, the DOT NSC has served as both mission “to certify and register EMS professionals through- curriculum and a scope of practice in that EMS lacked any out their careers by a valid and uniform process to assess the other unifying documents. The document which will replace knowledge and skills for competent practice.” the NSC is the National EMS Education Standards. The stan- dards, together with the national core content and national scope of practice, identify the Paramedic’s knowledge, skills, National Association of Emergency and attitudes. Medical Technicians The National EMS Education Standards (NEMSES) pro- vide the foundation for that fi nal terminal objective of every The EMS profession is relatively young compared to other EMS education program—the graduation of a competent healthcare professions. While EMS has roots in the past, the entry-level Paramedic.6 emergence of EMS as a profession has occurred in less than four decades. Nevertheless, EMS has strived to meet its ide- Commission on Accreditation als and become recognized as a profession. of Allied Health One of the other attributes of a profession is a profes- sional organization or society that speaks on behalf of the Education Programs members. The National Association of EMT (NAEMT) is To ensure that Paramedic education programs adhere to these a professional organization, founded in 1975, whose mission educational standards, the Commission on the Accreditation is to represent the views and opinions of all prehospital care of Allied Health Education Programs (CAAHEP) charges the providers. As the voice of the profession, it has been lead- Committee on Accreditation of Educational Programs for the ing efforts to help professionalize EMS. Through its leader- EMS Professions (CoAEMSP) to investigate and report to ship, the NAEMT has been infl uential with the advancement CAAHEP. of EMS as an allied healthcare profession. The NAEMT has Accreditation of a Paramedic program is evidence of a liaisons with at least 28 federal agencies and professional satisfactory report from the CoAEMSP having been furnished organizations with interests in EMS. That list of collaborating to CAAHEP. At present, CAAHEP accredits over 2,000 edu- organizations includes the American College of Emergency cational programs in 19 healthcare professions. Physicians (ACEP), the National Association of EMS Beginning in 2012, the National Registry of Emergency Physicians (NAEMSP), the Advocates for EMS, the National Medical Technicians will only permit those individuals who Registry of EMT (NREMT), the International Association have completed their education in an accredited Paramedic of Firefi ghters (IAFF), the International Association of Fire education program to seat for the Paramedic national certifi - Chiefs (IAFC), the Emergency Nurses Association (ENA), cation examination. the American Red Cross (ARC), EMS for Children (EMSC), 6 Foundations of Paramedic Care Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. the Federal Emergency Management Agency (FEMA), expressed when the provider recognizes the presence of the National Rural Health Association (NRHA), and the strong emotion and then responds to the patient in a support- Commission on the Accreditation of Ambulance Services ive manner. To be supportive, all the Paramedic need do is (CAAS), to name a few. imagine the feeling the patient is experiencing, be it anger or fear or hopelessness, and then acknowledge those feelings to National Institute of Medicine Report the patient in a simple statement such as, “This must be dif- The landmark National Institute of Medicine Reports entitled fi cult for you.” This simple offer of respect and support will “EMS at the Crossroads” and “Hospital Based Emergency be appreciated by the patient. Care: At the Breaking Point,” released in 2006, spoke of the Sympathy is the quality of suffering with the patient. While dysfunctional and fragmented emergency services in the United empathy is a quality to be practiced, sympathy can interfere States.7 These reports encouraged standardization of emergency with the patient–provider relationship. Sympathy is lending an services through processes such as national accreditation of emotional quality to the relationship that is neither wholesome the Paramedic programs, national certifi cation of Paramedics, nor professional and which can lead to burnout. The Paramedic and organized efforts at improving the delivery of patient care should strive to understand the patient’s feelings (empathize) through cooperation with other healthcare professions. but not take on the patient’s feelings (sympathy). Caring implies emotional vulnerability on the part of Core Values both the patient, who confi des in the Paramedic, and the Paramedic, who is trying his best to provide care, often under The clinical care provided by Paramedics, guided by evidence- trying circumstances. To be truly caring, the Paramedic must based science, is dictated by protocols, guidelines, and algo- be willing to also share his mistakes with the patient and rithms. But the human side of paramedicine—that aspect apologize if necessary. of EMS which makes it part of the patient care realm—is While the thought of apologizing for an error may seem dictated by another set of rules, the core values of a Paramedic abrasive or unwise to some, physicians and Paramedics are professional. Paramedics must possess these core values, increasingly accepting of the need to apologize. Simply stated, which complement and enhance their clinical skills and no matter how skillful or knowledgeable the Paramedic, mis- medical knowledge. Otherwise, Paramedics will be ineffec- takes will be made. The Institute of Medicine (IOM) 1999 tual as patient care providers. report estimated that between 44,000 and 98,000 patients will The key professional attribute and the fi rst core value of a die while in the hospital |
from mistakes.8 Mistakes are a part Paramedic is caring. Caring is an expression of concern toward the of the practice of paramedicine and each mistake represents patient by the Paramedic and is foundational to the Paramedic– an opportunity for improvement. The Paramedic’s accep- patient relationship. To practice caring, some Paramedics tance of the mistakes and willingness to apologize will be have been taught to use the PEARLS model advanced by the important to the patient’s satisfaction with care.9 Whenever a American Academy on Physician and Patient. The letters in the professional standard of care is breached, or the outcome is PEARLS mnemonic stand for partnership, empathy, apology, unwanted or unexpected, a caring Paramedic admits the error respect, legitimization, and support. These are the qualities that and demonstrates caring when he apologizes. provide for a strong Paramedic–patient relationship. The fi rst step whenever an error is encountered is to inves- While in the past most patients willingly accepted a tigate why the error occurred. If there is no immediate expla- physician’s advice without question, patients today are less nation forthcoming, then the Paramedic should explain to the tolerant of this paternalistic approach. Patients now want to patient that an error occurred and, if appropriate, explain that be knowledgeable about their choices and to be involved in “I will fi nd out why” and get back to the patient later with their healthcare decisions. They want to partner with their an answer. healthcare provider. Paramedics who involve patients in If the decision is made to apologize, the Paramedic should their own care, in a partnership, are demonstrating an accep- choose an appropriate time and place—perhaps after patient tance of the patient’s wishes to be involved and in control. care has been turned over at the emergency department—and Paramedics who involve patients in decisions about their own explain the situation, stating that an error has been made. A care empower the patients to take more responsibility for skillful Paramedic listens to the family’s response and answers their own health. This Paramedic–patient cooperation tends their questions thoughtfully and after a moment’s refl ection. to improve the patient’s overall satisfaction with the care pro- Fundamental to the Paramedic–patient relationship is vided by the Paramedic. respect for the patient. Respect is based upon a nonjudgmen- Another key to quality patient care is empathy. Empathy is tal attitude toward the patient, regardless of the personal cir- an emotional understanding of the patient’s feelings; to be able cumstances. While many Paramedics are aware of prejudices to understand what it is like to walk in the other person’s shoes. about race or religion, the problem of economic prejudice Some refer to empathy as a good bedside manner. Paramedics is less recognized. Regardless of the social status or eco- can demonstrate their empathy through both action and words. nomic position that a patient holds at any one moment, the Like the teachable moment—that point in time when Paramedic should respect the patient as a person in need of the student is most susceptible to learning—empathy is best help and worthy of care. Roles and Responsibilities of the Professional Paramedic 7 Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. On occasion some Paramedics have diffi culty under- the Paramedic, as a healer, supports the patient, both physi- standing the patient’s concerns, and may even cite “9-1-1 cally and spiritually, through an illness or injury. abuse” when speaking about these patients. Regardless of The role of the healer revolves around showing compas- the Paramedic’s attitude, these patients have a concern that sion. Dr. Bernard Lown, noted cardiologist and Nobel Peace prompted them to call for emergency medical services. The Prize winner, states in his book The Lost Art of Healing that caring Paramedic listens and seeks to understand the patient healing involves two aspects: preserving the personhood of and the patient’s concern, regardless of how seemingly insig- an individual and providing comfort measures. nifi cant the problem. This process of legitimization supports By its nature, illness is an attack upon an individual’s the patient and demonstrates caring. A patient who is put at sense of person, the individual’s personhood. Illness threat- ease is more cooperative with care and has a more positive ens the patient’s quality of life and perhaps even the patient’s regard for the Paramedic. life itself. Moreover, illness is something that the patient has Finally, the Paramedic demonstrates caring and compas- limited ability to prevent and little control over once it occurs. sion by offering the patient support and acting as a patient As a result of illness, the patient may feel helpless. This sense advocate. Being a patient advocate is important in a chaotic of helplessness leads to suffering. world where people are “lost in the process” and “treated like To help reduce suffering, the Paramedic need only show a number.” compassion. Compassion is an awareness of another’s suffer- ing. In some cases it only takes the Paramedic’s concerned The secret of the care of the patient is in caring for the presence (presencing) to help alleviate the suffering. The patient. importance of presencing is exemplifi ed by the common feel- ing often voiced by others that no one wants to die alone. By —Dr. Francis Weld Peabody— merely being there and showing compassion, the Paramedic Harvard Medical School—1925 helps to support the patient and, specifi cally, helps the patient validate himself and his sense of personhood. Another key to quality patient care is the attribute of Illness also brings pain. The Paramedic, as healer, can integrity. Professional integrity, described in more detail provide a range of comfort measures to the bedside. In some in Chapter 5 on ethics, involves an unabashed truthfulness cases that comfort measure is in the form of pharmaceutical with the patient which serves as a foundation for the patient– pain management. But in almost every case the Paramedic’s provider relationship. therapeutic use of touch helps to relieve the patient’s pain and Inherent within interpersonal communications is the con- provides comfort. Therapeutic touch has long been recognized cept of diplomacy. A thoughtful consideration of the words by nursing as an effective treatment for pain. Therapeutic spoken, to ensure that the message spoken does not have an touch involves one-on-one attention and human touch. unintended meaning, improves interpersonal understanding and, ultimately, patient care. Clinician While the science of emergency medical care can be A clinic is a place dedicated to the diagnosis and care of a learned from a book, the art of emergency medical service— patient. A clinician is the person who works in that place. combining the previously stated qualities in an effective It could be said that the Paramedic’s clinic is the back of an manner—is best learned by practice in the fi eld with a master ambulance, a place where the Paramedic assesses and diag- Paramedic. A professional mentor can help with the process noses a patient’s ailment. of socialization needed to create a professional Paramedic. A Paramedic’s diagnosis is a broad diagnosis made after A novice Paramedic subjected to intense socialization at the an assessment. During the assessment the Paramedic ascer- hands of seasoned professionals within a healthy EMS c ulture tains a symptom complex. This symptom complex is simply can quickly mature into a professional Paramedic. a list of abnormal conditions found by the Paramedic during the history of the present illness and the physical examina- Roles of a Paramedic tion. The Paramedic then, in turn, takes the symptom com- A Paramedic assumes many roles during the course of a plex, compares it to his knowledge of disease, and matches career. The primary roles are those of healer, clinician, and it to a known symptom pattern associated with a disease to patient advocate. As the Paramedic’s practice evolves, the arrive at a diagnosis. Paramedic may become involved as a researcher or a teacher. With only crude medical instruments and a limited time These changing roles keep a Paramedic engaged with the for history taking, the Paramedic’s diagnosis, sometimes profession and continuously striving to improve his practice. called a fi eld diagnosis, must be broad and comprehensive. Typically a Paramedic makes a diagnosis of a syndrome, Healer a group of signs and symptoms that signifi es a specifi c disease, or of a primary disorder of homeostasis, such as The Paramedic’s primary role is that of healer. A healer is hypoxia. a person who supports another during illness. From the old As a clinician, the Paramedic’s fi rst responsibility is to English “Haelan” meaning to make whole, sound, and well, treat disorders of homeostasis which threaten the patient’s 8 Foundations of Paramedic Care Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. survival. The brain’s survival is paramount. The three essen- In some other circumstances, such as rural communities, tial conditions for the brain’s survival are adequate oxygen, or under special conditions such as an epidemic, it may be glucose, and perfusion. If the brain lacks any of these three appropriate to give Paramedics an expanded scope of prac- conditions, then the patient has a fundamental disorder of tice to supplement existing healthcare resources.11 cerebral function and manifests an altered mental status. The American College of Emergency Physicians, in a The approach to the assessment and treatment of these position paper on expanded scope of practice, specifi es sev- disorders is exemplifi ed by the mnemonic ABC. The patient eral conditions that must be met before Paramedics can per- is assessed for hypoxia, hypoperfusion, and hypoglycemia. form an expanded scope of practice.12 ACEP maintains that While this description is technically accurate, it is a gross all expanded scope of practice must be closely monitored, simplifi cation of a process which is expanded upon and dis- with intimate physician involvement and a rigorous quality cussed throughout this series. assurance process that has standards and mechanisms for The Paramedic, as clinician, keeps one invaluable rule remediation. ACEP, in its position paper, further states that foremost in the mind when treating the patient. That rule, such expanded scope of practice must fulfi ll a community simply stated, is “do no harm.” While some harm will always need, usually based on an assessment and plan of action, and come from a treatment or drug (e.g., the pain of a needle), the that the practice is legally permissible. harm is outweighed by the benefi t that the treatment or drug will have for the patient. The rule “do no harm” is intended Self-Evaluation and Continuous to cause Paramedics to pause and consider every treatment Quality Improvement intervention before proceeding. The Paramedic, as clinician, is always trying to improve the The decision to treat in the fi eld is multifactorial. In some practice of paramedicine. This is best accomplished by criti- instances it is more prudent to withhold certain treatments cal self-evaluation and planned action. For example, an often until arrival at the hospital where more experienced physi- quoted goal of EMS is the patient’s satisfaction. Patient sat- cians can make the judgment about which treatments to ini- isfaction may result from many factors including the provi- tiate. At other times, delaying treatment in the fi eld can be sion of high-quality emergency medical care, timeliness of detrimental to the patient. The concept of “do no harm” is response, or respect for the patient’s rights. An EMS system further discussed in Chapter 5 on ethics. objective would be an eight-minute response in 90% of calls The Paramedic, as clinician, understands that medicine is for EMS. It might also be in response to a patient demand a practice, meaning the science of medicine must |
be matched for a timely response. If that objective is met then, to some to the patient to try to obtain a maximum benefi t for the extent, patient satisfaction with EMS should be higher. patient. In some instances that match is not perfect. Learning While an EMS system may periodically look at certain the right time to perform specifi c procedures or administer practice parameters, a superior EMS system is always in a particular medication is often a function of trial and error. It process of review and re-engineering, trying to refi ne the pro- takes practice. cess and improve the delivery of EMS. This approach is called The Paramedic, as clinician, understands that the prac- continuous quality improvement (CQI) and involves a pro- tice of medicine is fi rst and foremost about the patient. The cess that can be summarized as plan-do-check-act (PDCA). Paramedic understands that while the technology to treat This PDCA cycle is different than simply verifying compli- the patient is becoming truly amazing, the priority remains ance with established standards, or quality assurance (QA), to treat the patient as a person. The Paramedic under- because it has an action component. stands that the love of technology and the science of medi- Any system of self-analysis, whether it is QA/CQI or cine (philotechnia) comes second to caring for the person others, is dependent on the data collected. These information (philanthropia). systems can be real-time (i.e., direct observation of skills or Expanded Scope of Practice performances in the fi eld), but are often done retrospectively, after the fact, by a chart audit. For a chart audit to be reliable The traditional role of a Paramedic has been in the out-of- and dependable, it is important that Paramedics accurately hospital setting responding to medical emergencies. But as and completely describe the care given. As the saying goes, necessity has required, the Paramedic’s role has expanded in “If it wasn’t written down then it didn’t happen.” some limited situations and the Paramedic’s scope of practice has expanded as well. Driven by the increasing specialization of hospitals (i.e., Continuing Medical Education trauma centers), interventional cardiology centers, stroke Another responsibility of a professional Paramedic as clini- centers, children’s hospitals, and so on, and accelerated by the cian is to stay current with the state of the art. This is best nursing shortage, more Paramedics are becoming involved accomplished through continuing medical education which in specialty care transport (SCT). Paramedics who perform culminates in periodic recertifi cation. Paramedics also have SCT have training above that of the typical Paramedic. The a responsibility to re-register every two or three years. The fl ight medic is an example of a specially trained Paramedic re-registration is intended to ensure the public that the Paramedics who performs SCT.10 that serve them have remained competent as Paramedics. Roles and Responsibilities of the Professional Paramedic 9 Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. to a great deal of concern regarding the effectiveness of EMS by some. To counter these claims, Paramedics have turned to an evidence-based approach to the practice. Changes in prac- tice are now driven by research and the practice is becoming more reliable and valid in the process. Professional Paramedic The professional Paramedic is interested in research because it offers the opportunity to improve the effi ciency of paramedicine. Figure 1-1 EMS journals are a means to obtain information about the state of the art. Teacher However, the Paramedic understands the necessity of not Paramedics, in an effort to reduce injury and illness, have only maintaining minimal skills and an adequate knowledge started to educate the public. These opportunities to educate base, or competency assurance, but the need to continue the public sometimes occur during an emergency call, on a to remain current with the state of the art. Paramedics are one-to-one basis, or in public education programs. expected to keep abreast of new developments in the fi eld To be effective, this education must occur when the per- of medicine as they pertain to EMS through involvement in son, or the public, is ready to learn. This is called the teach- professional development. able moment. For example, a campaign to wear seat belts Attendance at state and national EMS conferences as may have more impact immediately following a fatal motor well as attending regional workshops help ensure that the vehicle collision involving teenaged drivers. At that moment Paramedic is continuing to develop and provide high-quality the public is sensitive to preventable death from motor vehi- emergency medical care. Alternatively, Paramedics often turn cle collisions. to their medical directors for guidance and education on new technologies. Another way to keep up with the profession is reading EMS trade journals (Figure 1-1). The best EMS trade journals have research that is peer-reviewed or articles that Professional Paramedic are refereed. Whenever research has been peer reviewed, that means A newer role for the Paramedic is that of health the article or research was critically appraised by experts in the educator. fi eld for validity. To be valid, the research has to objectively support its conclusion. In other words, the research must not be personal opinion, contain exaggerated statements, or make unjustifi able claims. Public Education However, articles are not peer reviewed per se but rather Public education is one means of garnering public support are refereed. Typically an editor will distribute an article to while simultaneously providing the public with the informa- a panel of expert Paramedics, in this case, and these expert tion they need about injury and illness prevention. A model Paramedics offer input. They edit the article and act as refer- public education system called PIER was developed by the ees. Then the article is returned to the author and the author National Highway Traffi c Safety Administration (NHTSA).13 is allowed to revise the article before re-submission. Often PIER stands for public information, education, and relations, the comments offered by these referees cite current research and incorporates the three aspects of public education. or best practices. The fi rst aspect, public information, pertains to infor- The commitment made by all Paramedics when they mation regarding people and events that the media tradition- attain that fi rst certifi cation is to remain current with the pro- ally communicates to the public. Many EMS agencies have fession through life-long learning. a public information offi cer (PIO) whose responsibility is to interface with the news media and to provide public Researcher information. The PIO must be cautious about not reveal- EMS practice in years past was based upon either in-hospital ing restricted personal health information (PHI), a violation practice, which sometimes did not fi t into the prehospital of the Health Insurance Portability and Accountability Act environment, or anecdotal experience. This approach has led (HIPAA) regulations, while simultaneously providing the 10 Foundations of Paramedic Care Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. Table 1-3 Public Education Activities Stewardship Public Information Because Paramedics work under the physician’s license, • Press conferences paramedicine is a shared practice with physicians. However, often a physician is not present when the Paramedic is taking • Newspaper announcements about weekly EMS activity care of the patient. Nevertheless the Paramedic is still repre- • Annual reports to government boards or councils senting the physician and the responsibilities of medicine. Public Education Therefore, in the absence of the physician, the Paramedic • CPR classes shares the physician’s responsibilities, including veracity, • Life-saving classes fi delity, benefi cence, avoidance of malfeasance, and jus- • Pediatric drowning education tice. These concepts are discussed in Chapter 5 on ethics. • Elderly fall prevention classes Whenever a Paramedic upholds noble traditions of medicine the Paramedic is acting in the role of a steward. Stewardship Public Relations is a weighty responsibility for the Paramedic. A Paramedic’s • Open house failure to properly conduct himself, as a physician would, • Blood pressure clinics often leads to confl ict between the Paramedic and physician and loss of medical privileges. news media the information that it is entitled to due to the Leadership freedom of the press. As the highest level of out-of-hospital EMS provider, The second aspect of PIER is public education. All edu- Paramedics are often thrust into the leadership role by virtue cation is an attempt to change behaviors. Public education, of their education. This traditional form of top-down man- from an EMS perspective, is an attempt to change the public’s agement (vertical leadership) was common in the immediate behavior toward medical emergencies. Examples of public post-World War II business world. It can be visualized as a education programs include CPR classes for citizens or pub- pyramid with a distinctive chain of command. lic access defi brillation (PAD) for school offi cials. However, enlightened Paramedics as leaders seek to The fi nal aspect of PIER is public relations. Public rela- “fl atten the pyramid” and work toward linking, or network- tions is less an effort to educate the public (though there can be ing, with the members of a public safety team. This horizon- overlap) as it is to garner the public’s support of Paramedics. tal leadership style demonstrates that the Paramedic values The public’s opinion of Paramedics can be directly translated the contributions of every team member. Horizontal leader- to support for new programs or support of public funding. ship emphasizes an “out and back” line of communication The Paramedic is involved in a number of public education instead of an “up and down” line of communication and can activities (Table 1-3). be visualized more like a wagon wheel. Patient Advocate In an information intensive era, horizontal leader- ship is an effective technique for knowledge management. Finally, the professional Paramedic is a patient advocate. Nevertheless, there still needs to be a nexus for control. Being a patient advocate means that the Paramedic defends Traditionally the Paramedic assumes that role, offering com- and supports the patient’s rights to health care. Whenever a mon direction and a strong vision to fellow EMS team mem- Paramedic acts to help a patient obtain needed health care bers as well as other public safety partners. he is acting in the advocacy role. A Paramedic is also acting The Paramedic, as leader, needs to have a sense of direc- in an advocacy role when she supports, through constructive tion and a strong personal vision of paramedicine. He must argument, the need for equipment that will improve patient also constantly refl ect upon the values common to a profes- care. Some would see reporting child abuse as a Paramedic sional Paramedic (ethics) and work to incorporate those val- acting in an advocacy role as well. ues into daily practice. Besides being a model of ethical behavior, the Paramedic Paramedics as Physician Extenders as a leader is also a coach. As coach the Paramedic teaches While physicians are educated in medical schools, it is the others, or trains the team, to work together to reach a com- state, through licensing legislation, that authorizes the physi- mon goal. cians to practice medicine. Most states have state statutes, The qualities of a good leader can be summed up in called a medical practice act, that defi ne medical practice. the 5 “C’s”: competence, command presence, choreogra- Many of these medical practice acts have a reference to phy, communications, and confl ict resolution. Competence physician extenders, allied health professionals who work goes beyond merely being technically profi cient at skills and under the license granted to the physician. Paramedics, as instead means having operational competence. Operational physician extenders, are among those allied healthcare pro- |
competence includes knowing how the various team mem- fessionals who are permitted to perform limited medical pro- bers interact, knowing an organization’s policies and proce- cedures while under the supervision of a licensed physician. dures, and possessing situational awareness. Roles and Responsibilities of the Professional Paramedic 11 Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. The Paramedic, as leader, has situational awareness. He It is inevitable that disputes about patient care will can read the scene and can detect both opportunity and threat. occur among team members. Without the authority given These opportunities include teaching moments, times for the in a traditional chain of command, the Paramedic must be team members to learn, without risk to either the team’s or masterful at confl ict resolution in order to maintain order the patient’s safety. This skill cannot be easily learned from and control. In high stress situations (i.e., those with a high books but rather is a result of witnessing master medics func- life hazard), it may be necessary for the Paramedic to assert tion in the fi eld. authority, issue a command, and offer to review the call Another quality of a good leader is command presence. later with the team. In those cases it is important for the Command presence can be defi ned as that ability to present Paramedic to institute an “after action review” and allow oneself as the person of authority. The Paramedic’s authority all parties to express their viewpoints and vent their emo- fl ows, in part, from the respect that the team has for the medi- tions. But if time permits, and it is not disruptive to patient cal director and the Paramedic’s role as the medical director’s care, the Paramedic may elect to listen to the suggestions of steward. other team members offered in civil discourse. During these Outwardly, the Paramedic’s appearance can demonstrate teachable moments learning can occur for all involved, confi dence, a key command trait. A clean pressed uniform including the Paramedic leader. and the “tools of the trade,” such as a stethoscope, give the Paramedic the appearance of a medical professional. A pro- Followership fessional appearance, along with a professional attitude, can Consistent with the concept of leadership is followership. substantially improve one’s command presence. Followership is a willingness to follow a leader’s direction Confi dence can also be manifest in one’s behaviors. The and to support the mission, putting aside personal ambitions. confi dent Paramedic walks purposefully toward the patient Every leader is a follower at some level. Inherent in the defi - with an eye toward the patient as well as the surrounding envi- nition of paramedicine is the willing submission to medical ronmental, i.e., situational awareness. Confi dence is further command. But followership is more than submission. demonstrated in purposeful speech with a low tone. Instead A Paramedic, as follower, understands the mission of yelling into the scene, instructions are pointedly given to (patient care) and is dedicated to that mission. The Paramedic, individuals by looking toward that individual and speaking an as follower, understands the team’s need for compliance (team unambiguous message in a directive manner. play) in order to achieve the team’s common goals. The good The next quality of a Paramedic leader is the ability to follower puts the needs of the team and the patient above organize the team’s efforts in order to deliver appropriate one’s own needs. interventions in a timely manner. This skill could be described A Paramedic, as follower, makes timely recommenda- as choreography. While algorithms are helpful with orga- tions to the leader. That includes respectfully disagreeing nizing patient care, acting almost like a pre-plan, on-scene with the leader when need be, if that is what is in the best conditions and other variables make it imperative that the interests of the team and/or the patient. Paramedic take an active role in leading the team down the A Paramedic, as follower, sets the example for others by treatment pathway. understanding the leader, anticipating the orders of the leader, To be truly effective, the Paramedic, as leader, must also and complying with those orders. Perhaps more importantly be a strong communicator. A key to success in teamwork is the Paramedic, as follower, knows when to take appropriate possessing excellent communication skills. The Paramedic action when no orders are forthcoming. must be articulate with both patients and family, speaking to Finally, the Paramedic, as follower, keeps the informa- them in terms that they understand while still being able to be tion fl owing to the leader and does not horde vital informa- conversant with fellow healthcare professionals, most notably tion. Through clear communications, all members of the team the emergency physician, in terms that they will understand. can provide the highest quality of care. 12 Foundations of Paramedic Care Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. Paramedicine is a pattern of thinking and behaviors, that outward manifestation of thinking, that is consistently applied in varying situations until a practice has been achieved. The art of paramedicine is the ability to apply that practice while maintaining focus, using one’s wits and creative abilities. Key Points: • Paramedic practice is both independent, • Roles and responsibilities describe a Paramedic’s encompassing specialized prehospital practices, and scope of practice. interdependent, through a working relationship with emergency physicians. • A superior EMS system is always in a process of review and re-engineering through continuous quality • The Paramedic is cross-trained in health care, improvement (CQI) and quality assurance (QA). public health, and public safety. • Involvement in professional development provides • The National EMS Education Standards, together the Paramedic with competence assurance, and with the national core content and national scope of allows the Paramedic to remain current with the practice, identify a paramedic’s knowledge, skills, state of the art as a life-long learner. and attitudes. • Changes in EMS are now driven by research, and the • Professional organizations or societies, such as process has become more reliable and valid to the the National Association of EMT (NAEMT), provide Paramedic practice. a voice for the profession and have been leading efforts to professionalize EMS. • In an effort to reduce injury and illness, the Paramedic has become a health educator. • The landmark National Institute of Medicine Reports entitled “EMS at the Crossroads,” and “Hospital • The professional Paramedic is also a patient Based Emergency Care: At the Breaking Point,” advocate. released in 2006, encouraged changes in the • As a physician extender, the Paramedic is delivery of patient care. authorized to practice under the license granted to • Caring is an expression of concern toward the the physician. patient and is foundational to the Paramedic— • The Paramedic serves as a model of ethical patient relationship. behavior. • A Paramedic may assume the role of healer, • A Paramedic leader is a strong communicator and clinician, and patient advocate. has the ability to organize a team’s efforts to • During the assessment, the Paramedic ascertains a deliver appropriate intervention in a timely manner. symptom complex. • The Paramedic, as a follower, is willing to follow a • The Paramedic, as clinician, keeps one rule in mind leader’s direction and support the mission. when treating the patient: do no harm. Roles and Responsibilities of the Professional Paramedic 13 Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. Review Questions: 1. How has the Paramedic’s role changed since 6. Describe how a Paramedic develops a the inception of the profession? Paramedic fi eld diagnosis. 2. What professional organizations or societies 7. How do continuous quality improvement serve as a voice for the Paramedic profession? (CQI), quality assurance (QA), and research How have they helped to advance EMS? improve the practice of paramedicine 3. Using the mnemonic PEARLS, explain how 8. What is the relationship between stewardship caring is the Paramedic’s fi rst core value. and the Paramedic as a physician extender? 4. Why is it important for the Paramedic to take 9. What leadership qualities should the Paramedic part in continuing education? exhibit? 5. How does the rule “do no harm” relate to a 10. How is being a good follower as important as Paramedic’s scope of practice? being a good leader? Case Study Questions: Please refer to the Case Study at the beginning of the 3. Discuss the importance of a science and chapter and answer the questions below: mathematics curriculum as the basis for 1. How would you counsel high school students Paramedic study. who are interested in EMS? 2. What could you say to someone who says, “I want to be a Paramedic but I only want to take care of trauma patients”? References: 1. Fan E, MacDonald RD, Adhikari NK, Scales DC, Wax RS, 5. Bartlett WD. Paramedic education and the development of Stewart TE, et al. Outcomes of interfacility critical care adult professional status: a prognosis. Paramed Int. 1979;4(1): patient transport: a systematic review. Crit Care. 2006;10(1):R6. 36–39. 2. Svenson JE, O’Connor JE, Lindsay MB. Is air transport 6. http://www.nemses.org faster? A comparison of air versus ground transport times for 7. National Academies Press. Hospital-Based Emergency Care: interfacility transfers in a regional referral system. Air Med J. At the Breaking Point (Future of Emergency Care). Washington, 2006;25(4):170–172. DC: National Academies Press; 2007. 3. American Academy of Pediatrics. Committee on Pediatric 8. Leape LL. Institute of Medicine medical error fi gures are not Emergency Medicine. American College of Critical Care exaggerated. Jama. 2000;284(1):95–97. Medicine. Society of Critical Care Medicine. 9. Brennan TA, Leape LL, Laird NM, Hebert L, Localio AR, 4. Minarik PA. A vision for health professions regulation in the new Lawthers AG, et al. Incidence of adverse events and negligence millennium: recommendations from the Pew Health Professions in hospitalized patients. Results of the Harvard Medical Practice Commission. Clin Nurse Spec. 1999;13(6):306–309. Study I. N Engl J Med. 1991;324(6):370–376. 14 Foundations of Paramedic Care Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. 10. Gryniuk J. The role of the certifi ed fl ight Paramedic (CFP) as a 12. American College of Emergency Physicians. Expanded roles of critical care provider and the required education. Prehosp Emerg EMS Personnel. Revised April 2008. Available at: http://www Care. 2001;5(3):290–292. .acep.org/practres.aspx?id29444. Accessed May 4, 2009. 11. Hatley T, Ma OJ, Weaver N, Strong D. Flight Paramedic 13. Thoma T, Vaca F. National Highway Traffi c Safety Administration scope of practice: current level and breadth. J Emerg Med. (NHTSA) notes. PIER: public information, education, and 1998;16(5):731–735. relations for EMS injury prevention modules. Ann Emerg Med. 2004;43(4):521–524. Roles and Responsibilities of the Professional Paramedic 15 Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially |
affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. KEY CONCEPTS: Upon completion of this chapter, it is expected that the reader will understand these following concepts: • The paradigm in EMS has shifted from ambulance transport to advanced prehospital care • Emergency Medical Services are incorporated into all levels of public life: local, state, and national • The EMS Agenda for the Future has redefi ned both the scope of practice and educational standards Case Study: The Paramedics were at the squad building and the group of them stared at the invitation. The local Emergency Physician’s Advocacy Group had invited a Paramedic to their next meeting to speak on the history of paramedicine, its scope of practice, its educational requirements, and its role in the local healthcare system. Who would go and represent them to their physician colleagues and what would they say, everyone asked. One thing was for sure, they wanted to put their best foot forward. 16 Foundations of Paramedic Care Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. Introduction to Emergency Medical Service Systems 17 Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. OVERVIEW What started out as the simple idea of transporting the sick or wounded to medical care has evolved into an integral component of our healthcare system in the United States. Its development—one that originated out of necessity—now plays a vital role in an ever-expanding system of health care. This chapter will not only outline the history and progression of EMS but also identify what defi nes EMS practices. The evolution of EMS in the healthcare system prompted the development of an EMS Agenda for the Future that establishes a clear vision for the future of EMS. This vision has been implemented by means of national core content, a defi ned scope of practice, and educational standards. With knowledge of how the EMS system is constructed and an understanding of the origin of its various components, a Paramedic can better appreciate the responsibility and function they have in the healthcare system. The Evolution of EMS overcrowding in inadequate housing and almost nonexistent sanitation systems.4,5 While medicine has been in existence since the beginning of recorded time, Emergency Medical Services (EMS) is a rel- Revolution in the Laboratory ative newcomer to the fi eld of medicine. Modern EMS, with During the early and mid-1900s, discoveries in the laborato- its specially trained EMS providers and a systems approach, ries brought about a revolution in medicine. Scientists used is generally considered to have started in the late 1960s and microscopes to identify the sources of many infectious dis- early 1970s.1–3 From these early beginnings EMS, and spe- eases and developed crude but effective treatments—using cifi cally Paramedics, have rapidly developed into one of the the scientifi c method—to treat these diseases. Word of these newest allied healthcare professions. medical breakthroughs was widely disseminated via journals A constant throughout the development of EMS is the such as the New England Journal of Medicine. The fi eld of close working relationship of EMS with other parts of the medicine began to change. healthcare system, particularly the emergency department. Almost overnight, county and state medical societies Therefore, to understand the evolution of EMS it is important were created and physicians gathered to discuss new devel- to fi rst review the history of American health care. opments in medicine in a climate of openness that fostered more medical research and established the beginning of mod- Historical Evolution ern medicine. of American Health Care Before the 1800s, health care was largely delivered by phy- Public Health Care Emerges sicians who traveled by mule to the homes of the sick and As great strides were being made against infectious disease, injured. In its day that level of health care was satisfactory for the delivery of health care also changed. For example, in 1906 the fl edgling republic. St. Luke’s Hospital in New York City opened its fi rst private As cities grew during the 1800s, largely due to a dra- pavilion. This change marked the beginning of a healthcare matic infl ux of European and Asian immigrants, the demand system.6,7 for more public healthcare facilities escalated. Forward think- Prior to that time there was no perceived advantage to ing physicians helped develop large urban hospitals to meet having patients cared for in the hospital setting rather than that demand. These hospitals (e.g., Massachusetts General in in the home where patients could receive equally good care. Boston and Bellevue in New York City) could care for hun- However, after the turn of the century—with the advent of dreds of patients, and allowed economies of scale (savings hospital laboratories equipped with powerful microscopes made from bulk purchases), which in turn made health care as well as expansive pharmacies fi lled with new cures— affordable to vast legions of poor and underserved persons. the hospital setting provided distinct advantages. These The physician in the 1800s, armed with only limited resources empowered the physicians to encourage patients experience and even more limited education—or no formal to be admitted into the hospital. Soon hospital admission for education at all—dealt largely with infectious diseases. Many illness, predominantly infectious diseases, became a public of these infectious disease outbreaks occurred because of expectation. 18 Foundations of Paramedic Care Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. Evolution of Medicine Following World War II and the successful introduction of modern antibiotics, the incidence of infectious diseases was waning. For example, smallpox was being eradicated due to the use of a new vaccine. Soon chronic diseases, such as cancer, stroke, and heart disease, were replacing infection as the leading killers. As a result, medicine began to concentrate less on infectious diseases and more on chronic diseases. Also during this time the development of medical sciences (biology, pharmacy, etc.) blossomed and the biotechnology industry—the marriage of medical science and technology— emerged in the health care industry. At the same time, the growth of widespread employer- provided health insurance permitted an increasing segment of the U.S. population to afford medical care. With the wide- spread availability of health insurance the healthcare industry was then fi rmly established. Also beginning in the 1980s, medicine began to integrate information technologies such as computers, and other bio- medical devices, into healthcare. The advancement of phar- maceutical research had also taken on revolutionary new directions, including the development of new bioengineered drugs. Partially as a result of the signifi cant advances in medi- cal science, healthcare costs have skyrocketed. For this rea- son the federal government, in part because of Medicaid Figure 2-1 Lillian Wald, RN, a pioneer in public and Medicare health programs, has taken a greater role in health. (Photo courtesy of American Nurses Association) healthcare policymaking in an effort to curb rising health- Street Settlement in New York City, a social services shelter, care costs. in 1793 and coining the term “Public Health Nurse.”10 Public Health Movement Public Health Service Paralleling the advances in medicine, and the development The federal Public Health Service actually evolved out of of healthcare systems, was the public health movement. The the need for health care for the maritime fl eet. The Public public health movement started in the early 1800s as a result Health Service roots can be traced to the creation of the of the smallpox, yellow fever, and cholera epidemics that rav- Marine Hospital Service in 1798. At that time, sailors paid aged the larger cities.8,9 20 cents a month to fund the Marine Hospital Service. The ser- During that time, quarantines and in-house confi ne- vice provided them with medical care if they should get sick ment were the only effective means of preventing the further away from home and while in a distant port of call. As the spread of disease. As a result of widespread illness, business public health movement grew, and pressure mounted on the and the manufacturing industries suffered and productivity federal government to provide service to the poor, the Marine was affected. Hospital Service became the federal Public Health Service. In order to temper the effect of illness and sick call outs The federal Public Health Service is a key portion on business a few wealthy patrons hired graduate nurses to of the Department of Health and Human Services today. care for the sick and the poor in Boston, Cincinnati, and With 5,700 commissioned health services offi cers and Washington, DC. These nurses, referred to as community 51,000 civilian employees, all led by the Surgeon General, nurses, worked tirelessly in the ghettos and tenements of the current United States Public Health Service provides major cities trying to improve sanitation and decrease mor- support to county and state Public Health Departments as bidity and mortality as a result of infectious disease. well as health care to medically underserved areas. Similar to modern-day Paramedics, these public health The United States Public Health Service (PHS) consists nurses would leave the safety of the hospital to go to workers’ of eight agencies, including the National Institute for Health homes and worksites. Some community nurses established (NIH), the Food and Drug Administration (FDA), the Agency clinics to advance sanitary practices in the home and improve for Toxic Substances and Disease Registry (ATSDR), and the maternal–child health, as infant mortality was particularly Centers for Disease Control and Prevention (CDCP). high in the inner cities. Lillian Wald, RN (Figure 2-1), an Current challenges to public health, including Lyme early social work pioneer, is credited with starting the Henry disease, West Nile virus, SARS, Avian fl u, and swine fl u, to Introduction to Emergency Medical Service Systems 19 Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. name a few, have placed a renewed emphasis on public health However, credit for the concept of the modern ambulance medicine. is generally given to Dominique-Jean Larrey of Baudean, The mission of EMS is now seen as being more in step France. A surgeon, Larrey got a great deal of his training with the Public Health Service than previously thought. treating victims of the French Revolution during his stay at Relationships between Paramedics and the Public Health the Hotel Dieu, the premier French hospital in Paris. Larrey, Service’s physicians, nurses, scientists, and sanitarians are pressed into military service by the Prussians, was disturbed growing and evolving; especially in light of the threats of by the then-common practice of waiting for the battle to end pandemic fl u and natural disasters. before rescuing the wounded. Larrey went about creating a light carriage that could swoop into a battle, scoop up the wounded, and then rapidly transport them to the waiting sur- The History of Emergency geons at the “ambulance.” Those light two-wheeled carriages Medical Service that carried an attendant as well as a |
driver were called les ambulance volantes, or fl ying ambulances. The transportation of the sick and injured has seen many The American Civil War utilized what could be described developments over the past millennium. The earliest exam- as weapons of mass destruction, such as rapid fi re or repeating ples may be seen in the Roman Empire. Romans would use rifl es and devastatingly accurate cannon fi re. These improved chariots to move battle-injured soldiers from the battle fi eld in weapons caused greater casualties and put greater demands the time of Caesar (100 A.D.). This innovation was followed on battle surgeons. While casualties were greater, medical by the fi rst hammock-wagon, a wagon designed specifi cally attention to these combat casualties improved and resulted for transporting the sick and injured, and a forerunner of the in many advances in fi eld care of wounded soldiers. And to modern ambulance, but the hammock-wagon was not created respond to the mass casualties sustained during these military until about 900 A.D. In their day these crude carriages and engagements, army surgeon Major Jonathan Letterman com- horse litters would carry one invalid patient to medical care pletely reorganized the military fi eld medical service, called at a distant physician, at a monastery, for example, but the long the Letterman plan, into what was to be the forerunner of the transfer over rough roads often proved to be more dangerous modern trauma system. to the wounded patient than the original battlefi eld wound. The Letterman plan called for “an act to establish a During the Spanish crusade of Ferdinand and Isabella uniform system of ambulances in the Armies of the United against the Moors in the late fi fteenth century, the use of States,” and was ratifi ed by the United States Congress in ambulancias, or mobile military hospitals, came into being. 1864. The act declared that ambulances were a special corp. These facilities, which were located closer to the battlefront, that needed personnel, in distinctive special uniforms, who helped provide more immediate care to the wounded. As a drove specially marked wagons, and answered to the head of result, this more timely medical intervention improved the the medical department of the army, a physician, and not the chances for a soldier’s survival from battle wounds. battlefi eld commander (Figure 2-2). Figure 2-2 Civil War ambulance accepting patients. (Courtesy of the Library of Congress, Selected Civil War Photographs, Photo No. LC-B8171-7636) 20 Foundations of Paramedic Care Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. As a result of the shear number of casualties and the hor- York City provided ambulances staffed with an ambulance rible carnage of war there was a public outcry to control war- driver and a surgeon in accordance with a plan advanced by fare. In 1864, a convention was held in Geneva, Switzerland, Dr. Dalton. These ambulances responded to medical emer- to “civilize” warfare. The result was the Geneva Treaty. gencies throughout the City of New York. Among its many precepts, the Geneva Treaty established The practice of prehospital care rapidly advanced as the neutrality of all ambulance workers who wore the “Red new technologies were created to deal with the unique envi- Cross”—an icon created by the reversed colors of the Swiss ronment encountered in the civilian world as well as on the fl ag created in honor of the Swiss, who hosted the conven- battlefi eld. For example, the outbreak of World War I and the tion. In 1882 the United States Congress ratifi ed the Geneva invention of the motorized ambulance coincided, improving Convention accords. both the quality and the speed of ambulance transportation. In keeping with the accords of the Geneva Treaty, and Another example is the splint created by Sir Hugh Owen- with the help of Clara Barton (Figure 2-3), the American Red Thomas. Dr. Thomas invented an external fi xation and trac- Cross was formed and chartered by the Congress in 1881 “to tion splint, called the Thomas half-ring, which reduced the provide volunteer aid in time of war to the sick and wounded number of fatalities resulting from a traumatic fractured of the armed forces.”11,12 femur from roughly 80% to less than 20%. The American Red Cross differs from its European coun- The combination of advances such as the Thomas half- terparts because it was active during peacetime as well as ring splint, rudimentary fi rst aid treatments to stop bleeding, during war, responding during peacetime with disaster relief and the introduction of motorized ambulances substantially and humanitarian aid. Since the American Red Cross is not a reduced battlefi eld mortality during World War I. These bat- government agency, it offers neutral humanitarian service to tlefi eld advances, which were also adopted for the civilian victims of war. population, led to improved survival from trauma in general Around the same time as the appearance of the American during the same time. Red Cross, hospital-based civilian ambulance services started to appear in the United States. The fi rst hospital-based Emergence of Civilian EMS ambulance, the ambulance of the Commercial Hospital After World War I, citizens started to see the importance of of Cincinnati (later Cincinnati General), was started in an organized emergency medical service and subsequently 1865, followed by Bellevue Hospital ambulance in 1869. the fi rst volunteer rescue squad was formed in Roanoke, By 1891 Bellevue Hospital’s ambulance had responded to Virginia. The Roanoke Rescue Squad, lead by Stanley Wise 4,392 calls. Shortly thereafter, hospitals throughout New (Figure 2-4), started to provide emergency medical service to the citizens of Roanoke in 1921. After early successes with this model, community-based rescue squads began to spring up across the country. Many of these “independent” rescue squads (i.e., not hospital-based or commercial ambulance services) sprang from local volunteer fi re departments and heralded an era of volunteer ambulances. Changing Paradigms Before World War II, the ambulance was chiefl y seen as an expedient means to get a patient to a hospital. Following the successes of army “para-medical” personnel during World War II and the advent of a new treatment for cardiac arrest called “cardiopulmonary resuscitation” or CPR, it became apparent that the ambulance driver might be able to provide more than just a fast ride. In 1958, Dr. Peter Safar demonstrated the safety and effi ciency of mouth-to-mouth ventilation, using trained Baltimore fi refi ghters, on anesthetized medical residents. This idea of non-medical personnel performing medical pro- cedures was revolutionary in its day. The introduction of the lifesaving CPR technique quickly intrigued the public.13–16 The “can do” attitude in America led organizations such as the American Red Cross and the American Heart Figure 2-3 Clara Barton, founder of the American Association to conduct mass CPR and fi rst aid training for Red Cross. (Courtesy of the National Archives, the public in fi rehouses and rescue squad buildings across the Photo No. 111-B-4246, Brady Collection) country. By 1960, fi refi ghters in major cities like Columbus, Introduction to Emergency Medical Service Systems 21 Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. From 1965 to 1966, two reports on highway safety were produced. One, by the National Academy of Sciences, enti- tled “Accidental Death and Disability: The Neglected Disease of Modern Society,” discussed shortfalls in the nation’s EMS system.18–20 The other, the report of the President’s Commission on Highway Safety, entitled “Health, Medical Care and Transportation of the Injured,” also echoed the prob- lems EMS was experiencing.21 In 1966, President Lyndon B. Johnson signed into law the National Highway Safety Act. This act provided for fed- eral funds as well as other improvements in highway safety.22 The Highway Safety Act, among its many provisions, created an EMS program within the Department of Transportation (DOT) and is seen as the fi rst federal commitment to EMS. Following the passage of the Highway Safety Act there was a fl urry of activity in emergency medicine. For example, The American College of Emergency Physicians was formed in 1968, a group consisting of physicians who specialized in emergency medicine. These early physicians, pioneers in emergency medicine, provided medical oversight and control to the growing EMS community. In support of the EMS community the federal DOT pro- duced the fi rst Emergency Medical Technician-Ambulance curriculum in 1969, a national standard curriculum for the training of ambulance drivers/attendants in new skills and life-saving techniques. Figure 2-4 Julian Stanley Wise, founder of the While the EMT curriculum was developed to deal with fi rst volunteer rescue squad. (Courtesy of the Julian vehicular trauma, cardiologists were dealing with another Stanley Wise Foundation) threat to Americans: the heart attack. Physicians, like Dr. Barnard Lown, noted that when certain drugs, such as lidocaine, were given during a heart attack there was a Los Angeles, Seattle, and Miami, to name a few, were trained decrease in the incidence of sudden cardiac death (SCD). to provide CPR. Another cardiologist, Dr. Paul M. Zoll (Figure 2-5), also Also in 1960, Asmund S. Laerdal, a Norwegian dollmaker, theorized that an electrical current passed through the heart created the fi rst “resusci-annie,” a manikin for CPR practice. could terminate the lethal dysrhythmia called ventricular With an acceptable simulator/manikin, the American Red fi brillation. And in 1956 Dr. Zoll delivered the fi rst external, Cross and the American Heart Association began to train the 750-volt, alternating current countershock to a fi brillating public in vast numbers. CPR training, along with American heart, which effectively stopped the dysrhythmia. Shortly Red Cross advanced fi rst aid training, became the standard thereafter defi brillators, now battery-powered direct current for ambulance drivers. (DC) defi brillators, were placed in service in many hospitals The White Paper and emergency departments. As America prospered, and medical care improved, it was Prehospital Coronary Care becoming increasingly apparent that prehospital care, par- Dr. J. “Frank” Pantridge, of Belfast, Ireland, noted that 90% of ticularly for motor vehicle trauma, was not keeping pace with young or middle-aged men who died from heart attacks did so the medical community. In 1960 President John F. Kennedy made the statement that “Traffi c accidents constitute one of the greatest, perhaps the greatest, of the nation’s public health Street Smart problems.”17 At that time, the majority of ambulance service was provided by a variety of tow truck operators, hospital sup- The defi brillators, some weighing over 100 pounds, ply companies, and funeral homes. To illustrate the point, in were placed on top of mobile carts which had a the 1950s and 1960s over 50% of ambulances in the United tendency to roll over, or “crash,” when pushed States were owned and operated by some 12,000 morticians. Funeral hearses were often used as ambulances as they were through the halls of the hospital; hence the term the only public conveyance that could transport a patient “crash carts.”23—25 horizontally on a stretcher. 22 Foundations of Paramedic Care Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. Image not available due to copyright restrictions Figure 2-6 Emergency Paramedics Jon Gage and Roy DeSoto. (Courtesy of Everett Collection, Inc.) his success with creating the television show Adam-12, Mr. Cindar approached then Captain James Page of the Los Angeles Fire Department and asked him if he would be the |
technical advisor for a new “reality” television program to be called Emergency. The show was to be loosely based on the new Paramedic program. Subsequently, the crew of the tele- vision Squad 51 of the L.A. County Fire Department began to roll. These fi re department Paramedics, or fi re-medics, responded to all variety of emergencies, from fi res to special and technical rescue to every imaginable medical emergency, always rendering expert medical care in the fi eld. An entire generation of future Paramedics was raised watching the emergency medical care provided by Firefi ghter/Paramedics due to ventricular fi brillation. These deaths usually occurred Gage and DeSoto (Figure 2-6). within one hour of onset of initial symptoms. Realizing the potential of rapid defi brillation in the fi eld to reverse sudden EMS Act of 1973 cardiac death, Dr. Pantridge placed the “heart-shockers” into In 1973 Congress passed the EMS Act, Public Law 93-154, ambulances and staffed those ambulances with trained coro- an amendment to the Public Health Service Act of 1944, nary care nurses. which offered technical assistance to regions and municipali- The patient survival rates from sudden cardiac death ties.27 The EMS Act of 1973 delineated the 15 aspects of an were remarkable and Dr. Pantridge reported his success in the EMS system that needed improvement including education British medical journal Lancet in 1967. After reading of his (both public as well as provider), improved communications success with prehospital defi brillation, the American College (including public access), and system evaluation but offered of Cardiology invited Dr. Pantridge to speak at its annual con- little money to help make those improvements. vention the following year.26 After learning of Dr. Pantridge’s success, physicians Federal EMS Efforts in the 1980s at Ohio State University started their own version of the The 1981 Omnibus Budget Reconciliation Act took mon- mobile coronary care unit which they dubbed the “heartmo- ies previously earmarked for EMS and placed them under a bile.” The heartmobile continued to operate through Ohio broader rubric of preventive health money. The federal gov- State University until July 1971 until it became a part of the ernment provided the states with large “block” grants to fund Columbus Division of Fire as Squad 52. various programs including EMS. While the intention was to continue to fund EMS, the effect was to turn control of EMS Emergency Hits TV Screens funding over to the states. The states then choose how to spend Robert A. Cindar was interested in emergency medical ser- the allocated monies. Some states did not support funding for vices, and particularly the advent of the Paramedic. Following EMS to the same level as the federal government had. Introduction to Emergency Medical Service Systems 23 Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. 1500 B.C. Roman Wars 1950–1970 Korean and Vietnam Wars • Evidence of fi rst treatment protocols. • Mobile Army Surgical Hospitals (MASH) were developed during the • Romans and Greeks used chariots to remove wounded from the Korean and Vietnam confl icts in an attempt to save the most seriously battlefi eld. injured patients through a transportation-dependent method of triaging. 1797 The Napoleonic Wars • Transportation of wounded soldiers by helicopter to medical units, • Baron Dominique-Jean Larrey, Napoleon Bonaparte’s chief surgeon, used fi rst during the Korean War, was the genesis of modern constructed a horse-drawn carriage called the ambulance volante or aeromedical transportation. “fl ying ambulance.” • The HU-1 (Huey) helicopter used during the Vietnam War had a large 1860s The U.S. Civil War patient compartment to allow emergency care to begin while in • The fi rst ambulance service in the United States was developed by U.S. fl ight. Army surgeon Jonathan Letterman, who reorganized the Army Medical 1960s Development of an EMS System Corp to include ambulances, similar to Baron Dominique-Jean Larrey’s fl ying ambulances. • (1966) The National Academy of Sciences produced a white paper, “Accidental Death and Disability: The Neglected Disease of Modern • Clara Barton was a volunteer on the Civil War battlefi elds and saw the Society” for President Kennedy. It stated that, to that date, more mayhem fi rst hand. Returning from the Franco–Prussian War, where Americans had died on American Highways than in all of the she witnessed the good work of the Red Cross on the battlefi eld, she U.S. wars. founded the American Red Cross. • (1966) The National Highway Safety Act of 1966 encouraged states to 1865–1950 U.S. Ambulance Service begin organized EMS programs. • (1865) Cincinnati established the fi rst civilian ambulance service. • (1967–1968) The fi rst paramedic services were established in Miami, • (1869) New York City established an ambulance service with hospital Florida, using telemetry units designed by Dr. Eugene Nagel and interns riding in horse-drawn carriages designed specifi cally for the Dr. John Hirchmann. sick and injured. • (1968) St. Vincent’s Hospital in New York City established the • (1901) At the Pan American Expo in Buffalo, NY, the fi rst electric- fi rst coronary care unit in the United States, and Columbus, Ohio powered ambulance was demonstrated and used to transport people established mobile coronary units staffed with cardiology fellows from to the on-site hospital. OSU. Both soon replace physicians with advanced • (1910) One of the fi rst ambulances, called the “Invalid’s Car,” ran out trained EMTs. of Iowa Methodist Hospital, Des Moines, Iowa, staffed with a nurse • (1969) The fi rst nationally recognized EMT course was held in and resident from the hospital. Wausau, Wisconsin. Dr. J. “Deke” Farrington was the course • (1928) The Roanoke Life Saving and First Aid Squad was the fi rst medical director. volunteer rescue squad in the United States. • (1969) Dr. Leonard Cobb, Harborview Medical Center, and Seattle 1910–1940s The World Wars Fire Department established the Medic One paramedic program. • An unmodifi ed French fi ghter aircraft was used for air medical 1970s The Star of Life and Voice of EMS transport during the retreat of the Serbian army from Albania. • (1970) The National Registry of EMTs (NREMT), a national EMS • “Combat medics” cared for the wounded in the fi eld with advanced certifi cation organization that maintains a registry of certifi cations, procedures including intravenous solutions, crude antibiotics, and was established. intraosseous (bone) needles. • (1971) “Emergency!” debuted on television, putting a public face on • Improved systems for trauma care were established including fi eld EMTs and Paramedics providing expert medical care on the scene of hospitals and forward fi rst-aid stations. an accident. The show increased public awareness of EMS and possibly infl uenced government funding of EMS. • Mechanized ambulances with the characteristic Red Cross emblem on the side were used and the era of the ambulance driver had arrived. • (1973) Star of Life was adopted as the national EMS symbol, representing the six points of the complete EMS system: detection, 1950s Out of Hospital Medical Advances reporting, response, on-scene care, care in transit, and transfer to • American Red Cross took the lead in providing basic medical training, defi nitive care. The central staff with a serpent wrapped around it making classes such as Standard and Advanced First Aid the standard represents medicine and healing. of care for rescue squad members. • (1973) U.S. Congress passed the Emergency Medical Services Systems • Cardiopulmonary resuscitation (CPR) was taught to civilians for the Act (PL93-144), which identifi ed 15 essential components of an EMS fi rst time in the late 1950s and early 1960s. system and allocated federal funding for individual EMS regions to • (1958) Mouth-to-mouth ventilation was demonstrated by Dr. Peter address these components. Safar using volunteers from the Baltimore Fire Department, who • (1975) National Association of EMTs (NAEMT) was formed agreed to be paralyzed. to represent the needs of all EMTs to the public and • (1958) Dr. Joseph K. “Deke” Farrington, known as the Father of EMS, government. and Dr. Sam Banks started a trauma training course for the Chicago • (1979) American Ambulance Association (AAA), a representative Fire Department in what was to become the prototype of the EMT- organization for the ambulance service industry and legislation Ambulance course. affecting EMS, was founded. Figure 2-7 EMS Timeline. 24 Foundations of Paramedic Care Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. 1970s–Present Iraq War • (1986) The Comprehensive Omnibus Budget Reconciliation Act • With an advanced skill set, the 68W healthcare specialist (a.k.a. (COBRA) prevented patient “dumping,” or transferring patients Army medic) is prepared to treat combat casualties as well as incapable of paying for services. civilian combatants. • (1988) The National Highway Traffi c Safety Administration initiated • Development and deployment of special blood-stopping dressings, the Statewide EMS Technical Assessment program based on ten key one-handed tourniquets, and special surgical procedures for extremity components of EMS systems. injuries and burns. • (1990) The Trauma Care Systems and Development Act of 1980s–2000 Agenda for the Future—Education 1990 provided funding to states for trauma system planning, and Federal Funding implementation and evaluation, encouraging development of inclusive trauma systems. • (1981) The Omnibus Budget Reconciliation Act of 1981 consolidated EMS funding into state preventative health and health services block • (1993) The Institute of Medicine published “Emergency Medical grants. Funding under the EMSS Act is eliminated. Services for Children,” pointing out defi ciencies in the healthcare system’s ability to address the emergency medical needs of pediatric • (1984) Medical Priority Dispatching began in Salt Lake City, Utah. patients. • (1984) EMS for Children (EMS-C) program, under the Public Health • (1996) “The EMS Agenda for the Future” was released, outlining Act, was established, providing funds for enhancing the EMS system 14 essential attributes for future EMS development. to better serve pediatric patients. • (2006) The controversial report, “The Future of Emergency Care: • (1985) The National Research Council published “Injury in America: Emergency Medical Services at the Crossroads” was released by A Continuing Public Health Problem,” describing defi ciencies in the the Institute of Medicine. progress in addressing the problems of accidental death and disability. Figure 2-7 (continued) EMS Agenda for the Future Table 2-1 Statement from the EMS Agenda for the Future As shown in Figure 2-7, EMS has developed out of a long and rich history. In 1995, the National Association of State Emergency Medical Services (EMS) of the future will be community- Emergency Medical Services Directors (NAEMSD) and based health management that is fully integrated with the overall the National Association of EMS Physicians (NAEMSP), healthcare system. It will have the ability to identify and modify illness and injury risks, provide acute illness and injury care and follow-up, with assistance from the National Highway Traffic Safety and contribute to the treatment of chronic conditions and community Administration (NHTSA), met to reflect upon the previ- health monitoring. This new entity will be developed from redistribution ous 25 years of EMS practice experience and to establish of existing healthcare resources and will be integrated with other their vision for the future of EMS. Their intention was to healthcare providers and public health and public safety agencies. It will guide EMS toward its own destiny. The product of those improve community health and result in more appropriate use of acute meetings was called the EMS Agenda for the Future healthcare resources. EMS will remain the public’s emergency medical safety net.28 (Table 2-1). The EMS Agenda for the Future suggests that EMS will be more intimately intertwined with public health, as well as EMS agencies should also strive to improve their opera- public safety, and continue to |
evolve along with health care. tional preparedness. Proactive EMS agencies will look to The EMS Agenda suggested that public expectations and the leaders in the EMS industry and use their operational demands of EMS will remain high. These expectations will practices as benchmarks. These benchmarks will rapidly be fueled in part by increasing media attention by the press, become the standard of care and public offi cials will mea- television, and Internet as well as consumer demand. sure their EMS systems operations against the EMS stan- To meet those expectations, Paramedics and emergency dard of care. physicians are going to need to make better decisions regard- To survive in a world of ever tightening fi scal constraints, ing what care provides the best patient outcomes in the most and in order to remain the public’s “safety net,” EMS will cost effective manner. The standard of care that was formerly have to demonstrate its effi ciency and effectiveness and its provided may not be the best care that can be offered. In that willingness to adapt to improved medical technology. case, the public is going to demand performance improve- The EMS Agenda for the Future describes the attributes ment and cost effi ciency. of an effective and effi cient EMS system. The EMS Agenda In other words, EMS practice is going to have to become for the Future was reviewed by 500 EMS organizations and more evidence-based (i.e., supported by the medical research). individuals, who came to consensus about EMS excellence. In situations where the evidence is lacking, EMS should The panel that created the EMS Agenda for the Future listed review their experience and refl ect upon those practices that 14 attributes of EMS (Table 2-2) and noted that EMS needs have led to the most desirable outcomes and strive to replicate to continue to develop those 14 attributes if it is to reach its them. These practices are the so-called best practices. greatest potential. Introduction to Emergency Medical Service Systems 25 Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. Table 2-2 Attributes of an EMS System National EMS According to the EMS Agenda for the Future Core Content 1. Integration of Health Services 2. EMS Research National EMS 3. Legislation and Regulation Scope of Practice Model 4. System Finance 5. Human Resources 6. Medical Direction National EMS 7. Education Systems Education Standards 8. Public Education 9. Prevention National EMS National EMS 10. Public Access Certification Education Program 11. Communication Systems Accreditation 12 Clinical Care Figure 2-8 The fi ve essential elements of the 13. Information Systems EMS educational system. (Courtesy of National Highway 14. Evaluation Traffi c Safety Administration) National EMS Education Agenda One advantage of a national SOP is that there is a stan- dardization of EMS providers of four levels. The four levels for the Future of EMS providers described in the NEMSSOP include the In 1996 the National Highway Traffi c Safety Administration emergency medical responder (formerly the certifi ed fi rst convened a meeting of over 30 EMS organizations with the responder), the emergency medical technician (formerly the intent of implementing the educational portions of the EMS emergency medical technician–basic), the advanced emer- Agenda for the Future. The results of that meeting became gency medical technician (formerly the advanced emergency known as the national EMS Education Agenda for the medical technician–intermediate), and the Paramedic (for- Future.29 The Education Agenda set out to describe how merly the emergency medical technician–Paramedic). all EMS providers, including Paramedics, would be pre- The emergency medical responder (EMR) is an EMS pared for service in EMS by following a systems approach. provider who is expected to render lifesaving care with mini- The National EMS Education Agenda, a systems approach, mal equipment. This person may be the lone provider on scene established fi ve components that incorporated the essential for an extended period of time. For example, a member of the elements of an educational system and how these elements emergency response team at a plant or a security offi cer at a interacted in a system (Figure 2-8). shopping mall, would be an emergency medical responder. The fi rst component was the National EMS Core The emergency medical technician (EMT)–Basic is Content. The core content defi nes the entire universe of part of a team that responds to the emergency scene, typically disorders, diseases, syndromes, and skills that an EMS pro- aboard an ambulance, and is trained to provide initial care on vider might encounter and for which he would be expected to scene as well as medical care to the patient while in transit to provide emergency care (i.e., the domain of EMS practice). the hospital. Naturally, EMS physicians had a lead role in defi ning the The advanced emergency medical technician (AEMT) domain of EMS practice. To the extent possible, the core con- is an EMT with additional skills. These additional skills are tent tried to include those practices that had strong evidence skills or medications that have been shown to positively to support them or those that appeared in the 2004 practice impact patient survival (i.e., evidence-based practices). These analysis conducted by the National Registry of EMT. skills include the administration of a limited number of drugs The second component of the EMS Education Agenda as well as, among other things, supraglottic airway devices. for the Future was the National EMS Scope of Practice The highest level of EMS provider is the Paramedic. The (NEMSSOP) model.30 The scope of practice defi nes and Paramedic’s medical education includes advanced assessment divides EMS into four groupings. The National EMS Scope and diagnosis of syndromes and disorders and the treatment of Practice, created under the leadership of the National thereof. In many states a Paramedic can obtain an associate’s Association of State EMS Offi cials (NASEMSO), formerly degree or higher. known as the National Association of EMS State Directors Each level of EMS provider has knowledge and skills (NAEMSD), clearly defi nes four levels of EMS provid- that are clearly delineated. If an EMS provider was to per- ers. More importantly, it identifi es the knowledge and skills form a procedure that was not within one’s scope of practice required for each level (i.e., what is the scope of practice for then that individual could be accused of practicing medicine that level within the domain of EMS practice). without a license. 26 Foundations of Paramedic Care Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. Education Standards exclusive rights to perform a function or profession it is a In the past, the scope of practice for many EMS providers license. The use of the term “certifi cation” in this regard is was defi ned by the National Standard Curriculum (NSC) a semantic difference. The National Registry of EMT has a well written legal opinion on the matter on its website.33, 34 for EMS. A seminal document, created with the assistance of the NHTSA in the 1970s, the NSC quickly became the only In a growing number of states the certifi cation of the available source of information about the domain of prehos- National Registry of Emergency Medical Technicians pital emergency care (i.e., the scope of practice).31,32 (NREMT) is accepted as proof positive that the individual With a defi nition of both the core content of EMS and the being licensed is minimally competent to provide that level of scope of practice of EMS establishing the domain of EMS, care. Presently, the majority of states accept National Registry the National Association of EMS Educators (NAEMSE) certifi cation for licensure. set out to replace the NSC with the broader National EMS Education Standards. These National EMS Education Standards serve as the basis for EMS instruction and provide Street Smart direction for EMS educators regarding both the core content and the scope of practice. The original designation EMT-A (the A was for Accreditation ambulance) was changed to EMT-B (B for basic) National EMS Education Program Accreditation, like to emphasize that EMTs operate in many varied other educational program accreditations, assures students environments other than the ambulance. Currently, who enter an EMS education program that the education the letter B has been eliminated altogether. they are about to receive meets national standards. Perhaps more importantly, accreditation helps assure the public, who depends on the graduates of those educational programs, that the graduates will be competent providers. Mission of the EMS System Presently the Commission on Accreditation of Allied The fundamental mission of EMS has been to respond to a Health Education Programs (CAAHEP) accredits Paramedic medical emergency, provide on-scene care, and transport education programs. CAAHEP grants accreditation after patients to the closest appropriate medical facility. This mis- receiving a favorable report from the Committee on sion is exemplifi ed in the star of life, the symbol of EMS as Accreditation of Educational Programs for EMS Professions represented by the six points; detection, reporting, response, (CoAEMSP). CoAEMSP site visitors visit the program and on-scene care, care in transit, and transfer to defi nitive care.35 review the facilities, faculty, and courses of a Paramedic pro- To be effective, the EMS system must provide a coor- gram to determine if they meet the national accreditation dinated response of health and safety resources in a timely standards and then issue their report either recommending manner and be successful in mitigating the effects of illness for or against accreditation. For most healthcare profes- and injury. To attain this goal, EMS must have both horizon- sions, graduation from an accredited school or program is a tal linkage with other public safety agencies and vertical link- minimum requirement for entry to certifi cation examina- age with the rest of the healthcare system. tions. Eventually this will become the standard for Paramedic Through complementary relationships (i.e., horizontal education as well. linkage) with other emergency services, such as law enforce- ment and/or the fi re service, EMS can realize effi ciencies Licensure and Certifi cation through rapid response and treatment. All states, as a matter of state rights, license individuals for Take, for example, a citizen who experiences a cardiac practice in that state. Licensure permits an individual to prac- arrest. If a law enforcement offi cer (LEO) in a quick response tice a trade or a profession. Generally that license is issued system (QRS) were to arrive on-scene within minutes of the after demonstration of satisfactory completion of a course cardiac arrest, the offi cer could apply an automated external of education, usually called a certifi cation. By defi nition, a defi brillator (AED). Following the instructions of the AED, license precludes other non-licensed individuals from prac- and the lessons learned during CPR training, lifesaving care ticing in the profession or trade. If a non-licensed person was could be initiated. (LEO is used to categorize that large group to practice, then that person could be accused of “practicing of professionals that are involved in law enforcement, includ- without a license,” which might involve criminal and/or civil ing but not limited to constables, Sheriff ’s deputies, police penalties. offi cers, state troopers, border patrol offi cers, agents and In some cases the state not only licenses but also cer- investigators from the Federal Bureau of Investigation, Drug tifi es those individuals, through written and practical test- Enforcement Agency, and so on.) Immediately afterward a ing, before they are licensed. This has been cause for some basic life support (BLS) engine company from the fi re ser- confusion about the difference between licensure and certi- vice would arrive to support the LEO effort and provide addi- fi cation. Simply stated, any time |
a state gives an individual tional skills and equipment, such as suction and oxygen. An Introduction to Emergency Medical Service Systems 27 Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. advanced life support (ALS) ambulance would then arrive. computer-assisted dispatch (CAD) technology identifi es the The Paramedic would assume care of the patient, provide caller’s location as well. additional skills and equipment (such as intubation and venti- With the growing number of mobile cellular telephones lation), and transport the patient to the emergency department which cannot utilize the 9-1-1 technology, the early advan- for stabilization. Once stabilized in the emergency depart- tages of 9-1-1 location identifi cation may have been lost. The ment, the patient would be transferred to a coronary care unit Federal Communications Commission (FCC) is now working (CCU) for further treatment and evaluation by a team of car- with the telecommunications industry and has undertaken a diologists. The patient’s entry into this critical care pathway is special wireless project that permits identifi cation of a cellular an example of horizontal linkage between EMS and the rest telephone’s location within 125 meters. Telecommunications of the healthcare team. professionals, represented by the National Emergency This ideal system illustrates one example of the effec- Number Association, have been working to improve the pub- tiveness that can be realized from an integrated approach to lic’s access to EMS. emergency response by all public safety agencies. Communication Systems Legislation and Regulation A typical EMS communication starts at the public safety EMS at its core is a public service. As such, the public has access point (PSAP) when the professional telecommunicator, certain expectations of performance. To ensure that EMS is or dispatcher, answers the call and starts the emergency medi- available, states have enacted legislation that provides for the cal dispatch process. It ends when the Paramedic presents the existence of EMS and regulates its functions.36–38 patient over the radio to the medical control physician. In many states this enabling legislation describes the An overview of emergency communications under- various levels of providers and, more importantly, links the scores its importance. The emergency communications cen- practice of those providers with the state medical practice act ters alert the public of impending natural disasters or terrorist and physician oversight. Furthermore, these statutes typically attacks. From the simple color-coded terrorist alert used in the empower either the state health department or the state depart- Homeland Security Advisory System to the Emergency Alert ment of state with responsibility for EMS system oversight. System (EAS) that predates the Homeland Security Advisory At a larger, macro level, local, state, and federal govern- System, emergency communications professionals have been ment have an interest in EMS. EMS responds to and miti- alerting the public to potential danger for years. Keeping up the gates the consequences of a disaster as part of the larger tradition of watchfulness over our communities, telecommu- government response. For that purpose, government often nicators can now alert drivers of a child abduction, via Amber funds EMS disaster preparedness through grants and other alert, or dangerous persons with a special “be on the lookout mechanisms. (BOLO)” alerts via public signs and television announcements A further discussion of other medical–legal responsibili- using the Emergency Notifi cation System (ENS). ties is contained in Chapter 6 on the law and EMS. As technology improves, emergency communications takes advantage of these advances and incorporates them into Public Access the emergency communications system. There is a further discussion of emergency communications, both process and When a citizen is suddenly confronted with a potentially life- technology, in Chapter 18 on communications. threatening emergency, the person turns to EMS for help. To get that help, the citizen can use a variety of telecommunica- Architecture of EMS Systems tions devices but by far the most common means is to call on a telephone. The wide variety of EMS system confi gurations speaks to Previously the citizen had to memorize a seven-digit the ingenuity of EMS offi cials and system administrators number for that jurisdiction. This often led to confusion and whose planning refl ects the community’s capability to pro- mistakes, some that were fatal. The obvious answer was to vide EMS. have a universal number for emergencies. Britain has had a Contemporary EMS depends on a number of confi gu- universal number, 9-9-9, since 1937. However, the United rations of emergency responders—some fi re-based, some States did not see a universal number, 9-1-1, until 1967.39–42 municipal, some volunteer, some proprietary, and some When that famous 9-1-1 call was made from Haleyville, a combination of these—to ensure EMS is provided to the Alabama, in 1967, the era of modern telecommunications community. was ushered in. Early 9-1-1 service provided the public immediate access System Confi gurations to the local public safety access point (PSAP), as well as The predominant means of delivering EMS in the United automatic number identifi cation (ANI), so that a “call-back” States is via fi re-based EMS.43,44 The combination of trained could be performed if necessary. Since that time, basic 9-1-1 personnel, lifesaving equipment, emergency vehicles, and has been improved. Enhanced 9-1-1 is now in use. Not only strategically located stations make the fi re service an ideal does it provide rapid access to emergency services, but platform for the delivery of EMS. 28 Foundations of Paramedic Care Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. The fi re service has a long tradition of rescue and fi rst In still other cases, groups of physicians established aid. During World War II, in a time before self-contained ambulance services, such as the Physicians and Surgeons breathing apparatus, many early fi re services carried heavy Ambulance Service (P&S) of Columbia University. E&J or Emerson Resuscitators for use in reviving fi refi ghters Commercial ambulance services, or for-profi t EMS, and fi re victims overcome by smoke and fumes. Eventually, have long provided interfacility medical transportation as the fi re service started getting requests for “resuscitator” well as emergency medical services to patients. Many of runs. Despite the availability of this equipment, medical calls these commercial ambulance services originated from the remained infrequent until a few visionary physicians saw the funeral homes that previously provided the service. potential of fi re-based EMS. Today, commercial ambulance services provide EMS to Leaders in fi re-based EMS—such as Dr. “Deke” vast areas. Some companies (e.g., Rural-Metro and American Farrington of Chicago, Dr. Nagal of Miami, and Dr. Cobb of Medical Response) are so large that the company’s stock is Seattle—saw the advantages in fi re-based EMS and encour- sold in the market on the stock exchange. aged the fi re service to get involved in EMS. Today, many Following the example of the Roanoke Volunteer Rescue major cities operate fi re-based EMS services. For example, Squad in 1920, rescue squads sprang up across America. the Fire Department of New York (FDNY) operates the larg- These community-based EMS squads were independent est fi re-based EMS service in the United States and had of local fi re departments and largely staffed with volun- 1.2 million ambulance “jobs” or trips in 2007. teers. Pressured by a lack of volunteers today, many of these The International Association of Fire Chiefs (IAFC) and community-based ambulances have turned to paid crews. the International Association of Fire Fighters (IAFF) has However, the fact that these community-based ambulance supported the development of fi re-based EMS and has made services remain not-for-profi t differentiates them from com- EMS a major priority for the Fire Service (Figure 2-9). mercial ambulance services. Hospital-based EMS is another common EMS sys- Some citizens believe that the government should provide tem design. When the large urban hospitals—such as the EMS as part of its responsibilities for public safety. In those Commercial Hospital in Cincinnati or Bellevue in New York communities, a municipal EMS service was established as City—were started it became clear that these hospitals needed the third of three public safety departments (the other two ambulance service to bring invalid patients to the hospital. public safety services being law enforcement and the fi re ser- In some cases proprietors of local livery stables dedicated a vice). In some cases small cities and villages would cross- specially outfi tted carriage for the hospital to provide special train police offi cers as Paramedics to provide service and transportation. That tradition continues today in many large effi ciency. cities. New York City, for example, still has a large number of The military is decidedly the largest provider of emer- ambulances that respond from the “voluntary” hospitals. gency medical care (i.e., military emergency medicine) and Figure 2-9 A fi re service-based ambulance stands ready for an EMS call. (Image copyright 2009, Jenny Woodworth. Used under license from Shutterstock) Introduction to Emergency Medical Service Systems 29 Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. has been providing EMS for a longer period of time than any or rotor aircraft from scenes or other facilities to defi ni- other EMS system. The healthcare specialist and corpsmen of tive care. Upon completion of advanced EMS education, today’s military care for some 1.37 million active service men with emphasis on critical care medicine and fl ight medi- and women alone. cine, fl ight Paramedics may test to become certifi ed fl ight Modern EMS in the armed forces can be traced back to Paramedics. surgeon Jonathan Letterman’s efforts to establish a system Frontier/rural Paramedics and woodlands search and of ambulances in 1864. In many respects the lessons that the rescue teams are tasked with providing patient care in wil- military has learned while providing emergency medical care derness areas. The Wilderness EMT (WEMT) has special on the battlefi eld have been translated to emergency medical training that fosters critical thinking as well as creativity in care in the civilian sector. an environment where supplies may be limited and patient transport to defi nitive care prolonged. Resource Management Paramedics who provide EMS in a rural setting often Resource management involves placing vehicles and person- have different circumstances and more diffi cult obstacles to nel in a position to provide the most expeditious response to overcome than their counterparts in the city. To prepare for an emergency. Some communities require, through contract these emergencies many Paramedics take the FarMedic® or regulation, a minimal response time. While there is not course, which is specifi cally directed to the farm emergency. a national standard response time, many EMS services have The FarMedic® course teaches how to care for a patient under accepted a 6- to 10-minute response time. This time is consis- an overturned tractor (Figure 2-10) and a number of other tent with cardiac arrest studies that indicate the greatest like- rural emergencies. lihood of return of spontaneous circulation (ROSC) is within Another area of EMS specialization is medical support 6 to 10 minutes of cardiac arrest.45–50 for special weapons and tactics (SWAT) teams. Despite care- Traditionally EMS was stationed in standing facilities ful planning and preparation, casualties do occur in these and many EMS services still utilize this fi xed-post staff- highly charged operations. Tactical EMS (TEMS) provid- ing method of resource distribution. Using squad buildings, ers are trained on how to provide care to the |
wounded while ambulance bays, or fi re stations, ambulances respond from in hostile surroundings as well as maintain the health of the these centrally located stations to calls for emergency medi- SWAT team members on prolonged operations. cal service. Some EMS services have gone to a dynamic posting Information Systems method called system status management (SSM) or event- In the age of computers EMS began to incorporate informa- driven deployment. Instead of posting in fi xed locations, tion systems into patient care. From electronic patient care such as a fi re house, the ambulances or emergency response reports that are capable of being transmitted prior to the vehicles are “on-the-road” moving to new locations, or posts, arrival of the ambulance to integrated information systems that optimize response times. The decision of where to post that permit inter and intra-agency communications, EMS these resources is typically made after an analysis of histori- systems are embracing information technology. cal data of call volume and knowledge of geography and traf- Some new challenges have also been presented with this fi c conditions. new technology. Patient confi dentiality, a fundamental tenet Still other systems, trying to combine fi xed-post staffi ng of patient care, is at greater risk for inadvertent disclosure. with system status management, provide peak-load staffi ng. Recent federal legislation, the Health Insurance Portability During predictable hours of high demand, additional ambu- and Accountability Act (HIPAA), has placed conditions lances are placed in-service at strategic locations. upon all healthcare providers that protect patient privacy dur- ing claims processing, data analysis, utilization review, qual- Specialization ity assurance, and practice management.54–59 There is further discussion of information systems in Unique environments, certain occupations, and special cir- Chapter 19 on documentation. cumstances require specially trained Paramedics. Over a dozen subspecialties have been created in EMS. The following are short descriptions of some of the notable subspecialties. Integration of Health Services A growing subspecialty in EMS is the area of Specialty EMS does not operate independently but is a link between Care Transport (SCT). Called to transport sick and injured the public and the rest of the healthcare continuum. EMS can patients from outlying clinics and critical access hospitals be seen as one of the doors to health care, a system within a to tertiary care centers, such as trauma centers and cardiac system. The seamless transition of care from the streets to the centers, for example, these Paramedics perform critical care hospital ensures the continuation of quality medical care. interfacility transportation. A number of healthcare “stakeholders” depend on Many consider the fl ight Paramedic as the most highly EMS. Social service workers depend on the assistance of trained level of EMS provider.51–53 Flight Paramedics trans- Paramedics to report child abuse, domestic violence, and port critically ill patients in either fi xed-wing aircraft elder abuse. Trauma surgeons depend on Paramedics to 30 Foundations of Paramedic Care Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. Figure 2-10 Disentangling a patient under an Figure 2-11 Radio communications permit the overturned tractor. (Courtesy of Chris Randall/Michigan physician to have direct access and control of the Rural Rescue, Inc.) Paramedic in the fi eld. expeditiously transport trauma patients to defi nitive care at Finance Systems the trauma center. Cardiologists have an interest in the pro- The means of fi nancing EMS systems is typically driven vision of advanced life support and stabilization of cardiac by community capabilities. For example, a fi re-based EMS patients in the fi eld, including the identifi cation of high-risk patients using 12-lead ECG.60–63 system may be supported, in part or in whole, from property taxes, whereas a volunteer EMS rescue squad may receive its funds from taxes collected in a special district similar to a Medical Direction fi re district. Other volunteer ambulances or fi re districts may In 1989, the American College of Emergency Physicians depend on community generosity by seeking donations. (ACEP) published a position paper, “The Principles of EMS The majority of EMS—be it commercial, hospital-based, Systems,” which called for strong physician involvement in or any other confi guration—is funded by billing a fee-for- prehospital medicine as well as the active participation of service. In a fee-for-service system, the patient is billed physicians in EMS.64 a charge that is customary for such a service in the area. Terms such as medical oversight and medical com- Payment for ambulance service may come from the patient mand illustrate the direct control that a physician has over a but is usually paid by the patient’s health insurance. Paramedic’s practice. One of the largest payers for EMS is Medicare. Medicare Medical oversight is present whenever a physician is reimbursement is paid according to a schedule established involved in the quality assurance/quality improvement pro- by the Centers for Medicaid and Medicare Services (CMS) cess and provides direction, either in the form of protocols which is part of the federal Department of Health and Human or education, to Paramedics. This medical oversight is often Services. retrospective and may be remedial in nature. Grants for special projects or research are also available Medical command implies a more immediate and direct to EMS services from government agencies or groups (e.g., involvement in patient care. The physician’s authority can the Centers for Disease Control and Prevention (CDC), the be exercised either on-scene or over-the-air at the time of an Maternal and Child Health Bureau, or the EMS for Children emergency, referred to as on-line medical control. Physicians program). can give medical direction via the base radio and exercise One of the diffi culties facing EMS is the inconsistency medical command (Figure 2-11). in funding. Driven by patient transportation, as opposed to More commonly, the physician’s authority is exerted the emergency medical care provided, payments have been through a written set of instructions, called protocols. The erratic and undependable. The CMS has attempted to modify protocols can be used by the Paramedic in specifi c situations the federal Medicare rules to account for not just transporta- in the absence of the physician.65–67 These preauthorized med- tion but emergency medical care as well. ical orders, or standing orders, are often given to Paramedics Some health insurance organizations have tried to elimi- in a fl owchart format called an algorithm. An algorithm is a nate payments by limiting the defi nition of a medical emer- logic tree that simply states: if this, then do that; if not this, gency to these conditions, listed in a discharge diagnosis, that then do this other thing. Algorithms can be useful during an without immediate care and treatment would result in harm to emergency when time is of the essence. the patient’s health. Any medical condition that does not fall Introduction to Emergency Medical Service Systems 31 Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. under this defi nition and could have been treated later and at or governmental sources, such as state-run Medicaid or fed- less expense to the insurance company is thus not a covered eral Medicare programs. condition. This limited retrospective view of an emergency These insurers then gather groups of healthcare fails to take into account the patient’s fears and anxiety when providers—physicians as well as allied healthcare suddenly faced with an unknown illness or injury. providers—and obtain a reduced rate in exchange for a Many health insurance carriers have adopted a more guaranteed client base. These savings could only be pos- fl exible and a reasonable approach to defi ning an emergency. sible because of the economies of scale. The managed These organizations use the prudent layperson standard to healthcare insurance plan then mandates that patients seek establish medical necessity. The prudent layperson standard treatment from this preferred medical group, in essence simply places the proverbial “average person” in the situation managing the care that the patient will receive by provid- and asks if that average person would reasonably think, under ing medical care for the lowest price. those conditions, that this problem was an emergency.68–72 A multiplicity of managed care arrangements exist. This approach allows for the inclusion of human factors such However, generally managed care can be broken down into as fear and anxiety. three basic confi gurations. The fi rst and earliest system is the health maintenance National Healthcare Systems organization (HMO). The HMO provides payments to healthcare providers at a negotiated annual per capita rate. Medical care in the majority of the world is a government- These rates are based on practice history of the insured operated enterprise, a social welfare system of sorts which patients and helps to prevent fl uctuations in payments, thus ensures the health and well-being of the citizens within its making expenses, costs, and budgets more predictable. borders. The next confi guration is the preferred provider orga- Health care in the United States is more of a medley of nization (PPO), a modifi ed fee-for-service schedule, that private payment and public funds, private physicians, and permits patients to choose their healthcare provider from government-run treatment centers. This unique blend of dif- amongst a roster. Although there is increased fl exibility for ferent approaches to healthcare delivery has resulted in a the patient with the PPO, some limitations still exist in terms healthcare system that provides numerous opportunities, as of the patient’s choice of provider if not on the roster. well as remarkable ineffi ciencies. The last confi guration is called point of service (POS). Previously the majority of health care was provided on a POS has qualities of both an HMO and a PPO. In a POS pro- fee for service basis, or pay as you go, with a certain amount gram the patient is allowed to choose a healthcare provider of medical care provided gratis to the poor or uninsured. from amongst a list of preferred care providers (PCP) but However, the pressures of modern economics have generally may elect to see another “out of system” provider, without a encouraged all healthcare providers to embrace the concept referral, at a substantially higher copayment and/or deduct- of managed health care. ible, similar to a fee-for-service arrangement. The employer, Managed health care is a system where there is a pur- in turn, gets the advantages of cost savings whenever the chaser of services, such as a large corporation or the govern- patient/employee participates in the managed care program. ment. The purchaser in turn obtains health insurance for its The POS is gaining increasing popularity with patients and workers via private sources, such as Blue Cross/Blue Shield, employers alike. 32 Foundations of Paramedic Care Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. From its early beginnings, when hearses were used as ambulances and the patient might be lucky enough to have an ambulance driver with basic fi rst aid training, EMS has evolved into a highly complex system of emergency responders who provide the public with an emergency medical safety net and who work as part of the larger healthcare system. Key Points: • Emergency Medical Services (EMS) became created to provide aid in a time of war to the sick recognized as part of the public health services in and wounded of the armed forces. the late 1960s. • Hospital-based civilian ambulance services began to • The historical evolution of |
American health care appear in the United States during the 1860s. began with physicians making house calls to treat the sick and injured. • The emergence of civilian EMS came from the fi rst volunteer rescue squad in Virginia, 1921. Many • Following World War II, medicine began to of these “independent,” or non-hospital-based concentrate less on infectious diseases and more on services, developed from local volunteer fi re chronic diseases, such as cancer, stroke, and heart departments. disease. • A paradigm shift occurred as ambulances were seen • Health insurance made it more affordable to receive as more than just fast rides but rather as a way to health care. However, technology has signifi cantly deliver faster medical care to the patient. increased costs. To curb rising costs, the federal government has taken a greater role in healthcare • The White Paper addressed public health concerns policymaking. regarding traffi c accidents and led to the development of stronger educational programs for • Public health was advanced by nurses who sought emergency care providers. to improve sanitation and decrease morbidity and mortality as a result of infectious diseases. • New drug therapies and defi brillators developed as a result of research in sudden cardiac death. • The Public Health Service is a key portion of the Department of Health and Human Services overseen • Television helped demonstrate the role of by the Surgeon General. emergency services to the public. • Deriving from once crude horse-drawn carriages • The EMS Act of 1973 amended the Public used as far back as Roman times, the concept Health Service Act of 1944 and outlined needed of the ambulance developed from the trials of improvements in the EMS system. several wars. • The National EMS Education Agenda for the Future • While the tools of war became more devastating, established a core content, scope of practice, the fi eld care of soldiers improved. During the educational standards, accreditation, and American Civil War the military fi eld medical service certifi cation. was reorganized and became the forerunner of the • National EMS Core Content listed the knowledge and modern trauma system. skills necessary for the provision of emergency care. • Stemming from the Geneva Convention in 1864 the • The National EMS Scope of Practice delineated the American Red Cross, founded by Clara Barton, was four levels of EMS providers. Introduction to Emergency Medical Service Systems 33 Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. • Replacing the National Standard Curriculum, the • Subspecialties exist in EMS. Some include training as National EMS Education Standards serve as the basis a Specialty Care Transport (SCT), Flight Paramedic, for EMS instruction and provide direction for EMS Wilderness EMT, or Tactical EMS. educators. • EMS systems use information technology to • EMS Education Program Accreditation assures students incorporate information systems into patient care. that their education meets national standards. • A key component to an EMS system is medical • A license is issued by a state, giving the license oversight and command performed by emergency holder the right to perform a function. physicians. • Completion of a specifi c educational program leads • In a fee-for-service billing system, the patient is to certifi cation. billed for service but the cost is usually covered by • the patient’s health insurance. Most EMS systems The EMS system provides a coordinated response are funded this way with Medicare being the largest of resources with other public safety agencies. The payer. EMS system also constitutes a vital link with the rest of the healthcare system by providing rapid • A health maintenance organization (HMO) provides response and emergency treatment. payment to a specifi ed group of healthcare • providers at a negotiated annual rate in turn for Expectations of performance for each provider are health care for employees. maintained through the state medical practice act and physician oversight. • The preferred provider organization (PPO) is similar • to a HMO but permits patients to choose their The 9-1-1 system created a public safety access healthcare provider from among a roster. point (PSAP) to provide immediate public assistance. • • A point of service (POS) confi guration contains A wide variety of EMS system confi gurations provide qualities of both an HMO and PPO by allowing EMS to communities ranging from urban to rural. patients to choose a healthcare provider or see • Resource management involves placing vehicles another “out of system” provider without referral. and personnel in a position to provide the most expeditious response to an emergency. Review Questions: 1. Name the key developments in the evolution of 5. Who was Clara Barton? What agency was American health care. derived from her interventions? 2. What effect do wars have on the advancement 6. Describe the paradigm shift from ambulances of public health? as transportation to ambulances delivering fast 3. What is the role of the public health nurse? medical care. 4. What departments in government are overseen 7. In what way did the White Papers address public by the U.S. Surgeon General? health concerns? 34 Foundations of Paramedic Care Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. 8. What is the EMS Agenda for the Future? 10. Explain the importance of educational 9. How does the National EMS Scope of Practice standards and accreditation. model defi ne the different practice levels of 11. What is medical oversight of the Paramedic? EMS providers? 12. How do protocols assist the Paramedic? Case Study Questions: Please refer to the Case Study at the beginning of the 3. In what ways is EMS meeting the goals set out by chapter and answer the questions below: the EMS Agenda for the Future? 1. Respond to the statement: The role of EMS is still 4. What opportunities exist to strengthen the to transport the sick or injured to medical care. relationship between EMS and physicians? 2. After your presentation, a physician asks for clarifi cation of the role of ER physicians in local prehospital care. How would you respond? References: 1. Bencze B. From the history of ambulance and rescue squad director of Henry Street Visiting Nurse Service. Home Healthc services. Orv Hetil. 1976;117(42):2557–2559. Nurse. 2007;25(4):235–239. 2. Donchin Y. On the history of the ambulance. Harefuah. 11. The American Red Cross charter section 2, paragraph 1. 2001;140(7):658–660. 12. Evans GD. Clara Barton: teacher, nurse, Civil War heroine, 3. Pal E. The history of ambulance services. Orv Hetil. founder of the American Red Cross. Int Hist Nurs J. 1978;119(13):802–805. 2003;7(3):75–82. 4. English PC. Diphtheria and theories of infectious disease: 13. Berry D. The history of cardiopulmonary resuscitation. centennial appreciation of the critical role of diphtheria in the Circulation. 2007;115(5):f20. history of medicine. Pediatrics. 1985;76(1):1–9. 14. Cooper JA, Cooper JD, et al. Cardiopulmonary resuscitation: 5. Kass EH. A brief perspective on the early history of history, current practice, and future direction. Circulation. American infectious disease epidemiology. Yale J Biol Med. 2006;114(25):2839–2849. 1987;60(4):341–348. 15. DeBard ML. The history of cardiopulmonary resuscitation. Ann 6. Jahiel RI. Healthcare system of the United States and its Emerg Med. 1980;9(5):273–275. priorities: history and implications for other countries. Croat Med 16. Vrtis MC. Cost/benefi t analysis of cardiopulmonary resuscitation: J. 1998;39(3):316–331. a history of CPR—Part I. Nurs Manage. 1992;23(4):50–54. 7. Kearney PR, Engh CA. History of the American healthcare 17. http://www.jfklink.com/speeches/jfk/publicpapers/1961/ system: its cost control programs and incremental reform. jfk338_61.html Orthopedics. 1997;20(3):236–247; quiz 248–249. 18. National Academy of Sciences. Accidental death and disability: 8. Lloyd S. The Ottawa typhoid epidemics of 1911 and 1912: a case the neglected disease of modern society. National Academy study of disease as a catalyst for urban reform. Urban Hist Rev. Press; 1966. 1979;8(1):66–89. 19. Howard JM. Historical background to accidental death and 9. White CR. Yellow fever; history of the disease in the eighteenth disability: the neglected disease of modern society. Prehosp and nineteenth century. J Kans Med Soc. 1959;60(8):298–302 Emerg Care. 2000:4(4):285–289. passim. 20. Gaston SR. Accidental death and disability: the neglected 10. Reed AS. Looking back. A tribute to my great aunt, Marguerite disease of modern society. A progress report. J Trauma. Wales: author, leader, consultant, public health nurse, and 1971;11(3):195–206. Introduction to Emergency Medical Service Systems 35 Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. 21. National Highway Traffi c Safety Administration. The National 44. Davis J. Fire-based EMS. Emerg Med Serv. 2000;29(1):12, 14, EMS Scope of Practice Model. Washington, DC: U.S. 16; author reply 93, 101. Department of Transportation/National Highway Traffi c Safety 45. Krep H, Bottiger BW, et al. Time course of circulatory and Administration; 2005. metabolic recovery of cat brain after cardiac arrest assessed by 22. Guide to Federal Records in the National Archives of the United perfusion- and diffusion-weighted imaging and MR-spectroscopy. States. Compiled by Robert B. Matchette et al. (September Resuscitation. 2003;58(3):337–348. 9, 1966). Washington, DC: National Archives and Records 46. Matot I, Shleifer A, et al. In-hospital cardiac arrest: is outcome Administration (80 Stat. 718 and 80 Stat. 731). related to the time of arrest? Resuscitation. 2006;71(1):56–64. 23. Benhamou-Jantelet G, Heron L, et al. Emergency crash cart and 47. Morley PT. Improved cardiac arrest outcomes: as time goes by? its use in an academic medical center. Soins. April 2007;(714):35. Crit Care. 2007;11(3):130. 24. Clarke RH, Phillips OC, et al. Hospital designs crash cart for 48. Ornato JP, Gonzalez ER, et al. Arterial pH in out-of-hospital each nursing station. Mod Hosp. March 1965;104:126. cardiac arrest: response time as a determinant of acidosis. Am J 25. Nussbaum GB, Fisher JG. A crash cart that works. Am J Nurs. Emerg Med. 1985;3(6):498–502. 1978;78(1):45–48. 49. Schoerkhuber W, Kittler H, et al. Time course of serum neuron- 26. Pantridge JF, Geddes JS. Cardiac arrest after myocardial specifi c enolase. A predictor of neurological outcome in patients infarction. Lancet. 1966;1(7441):807–808. resuscitated from cardiac arrest. Stroke. 1999;30(8):1598–1603. 27. Public Law 93-154–Nov. 16, 1973. Title XII–Emergency Medical 50. Vukmir RB. Survival from prehospital cardiac arrest is critically Services Systems. 58 Stat. 682; 86 Stat. 137. dependent upon response time. Resuscitation. 2006;69(2): 28. National Highway Transportation Safety Administration. EMS 229–334. agenda for the future. 1996. Available from: http://www.nhtsa 51. NFPA. The role of the fl ight paramedic in the prehospital .gov/people/injury/ems/agenda/emsman.html environment. NFPA (National Flight Paramedics Association) 29. National Highway Transportation Safety Administration. EMS position paper. Air Med J. 1993;12(6):203–204. education agenda for the future: a systems approach. 2000. 52. Gryniuk J. The role of the certifi ed fl ight paramedic (CFP) as a Available from: http://www.nhtsa.gov/people/injury/ems/ critical care provider and the required education. Prehosp Emerg FinalEducationAgenda.pdf Care. 2001;5(3):290–292. 30. http://www.nasemsd.org/documents/FINALEMSSept2006_ 53. Hatley T, Ma OJ, et al. Flight Paramedic scope of practice: PMS314.pdf current level and breadth. J Emerg Med. 1998;16(5):731–735. 31. http://www.health.state.ny.us/nysdoh/ems/original/intro/ 54. Bacon GV. Legislative activity: HIPAA and recommendations to intro.pdf protect individual privacy. J Law Med Ethics. 1997;25(4):316–319. 32. Salzman JG, Page DI, et al. Paramedic student adherence to the 55. Burkhartsmeier G. HIPAA: where are we now? MLO Med Lab national standard curriculum recommendations. Prehosp Emerg Obs. 2007;39(6):28. Care. 2007;11(4):448–452. 56. Gaines R. HIPAA: privacy and public good. Update. 33. http://www.nremt.org/nremt/about/Legal_Opinion.asp 2003;18(4):9–13. 34. Cannon GM, Jr., Menegazzi JJ, et al. A comparison of paramedic 57. Hansen, E. HIPAA (Health Insurance Portability and didactic training hours and NREMT-P examination |
performance. Accountability Act) rules: federal and state enforcement. Med Prehosp Emerg Care. 1998;2(2):141–144. Interface. 1997;10(8):96–98, 101–102. 35. Alberts ME. The star of life. J Iowa Med Soc. 1972;62(8):431. 58. Kumekawa J. HIPAA: how our healthcare world has changed. 36. Doyle OJ. Federal EMS legislation. JEMS. 1997; Online J Issues Nurs. 2005;10(2):1. 22(9):26–27, 30. 59. Schoppmann MJ, Sanders DL. HIPAA compliance: the law, 37. Lipsky J. The need for EMS legislation. J Iowa Med Soc. reality, and recommendations. J Am Coll Radiol. 2004;1(10): 1978;68(3):85–86. 728–733. 38. McKenna W. Understanding EMS legislation. Emerg Med Serv. 60. Collins D. The prehospital 12-lead EKG: starting outside the 1988;17(5):52–55. emergency department. J Emerg Nurs. 1997;23(1):48–50. 39. Davenport J. Anatomy of a 911 call. Northwest Dent. 61. Cummins RO, Eisenberg MS. From pain to reperfusion: 2005;84(4):37–38. what role for the prehospital 12-lead ECG? Ann Emerg Med. 40. Isler C. Dial 911 for the coronary ambulance. RN. 1990;19(11):1343–1346. 1969;32(8):48–51. 62. Davis DP, Graydon C, et al. The positive predictive value of 41. Kimball KF. 911—the emergency number. Nebr State Med J. paramedic versus emergency physician interpretation of the 1971;56(2):68–70. prehospital 12-lead electrocardiogram. Prehosp Emerg Care. 42. McSwain NE, Jr. The effectiveness of 911. Ann Emerg Med. 2007;11(4):399–402. 1992;21(10):1242–1243. 63. Greiff SJ. Taking it to the street: advanced monitoring and 43. Greiff SJ. Fire-based EMS: the trend of the future? Emerg Med 12-lead EKGs in prehospital care. Emerg Med Serv. Serv. 1999;28(6):43, 45–46, 48 passim. 1998;27(9):47–48, 54–55. 36 Foundations of Paramedic Care Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. 64. John A, Brennan E. Principles of EMS Systems (3rd ed.). 69. Kucera WR. Narrow defi nition of “emergency” can spell American College of Emergency Physicians; Boston, MA: Jones “litigation.” Hosp Med Staff. 1978;7(9):21–27. and Bartlett, 2005. 70. Li J, Galvin HK, et al. The “prudent layperson” defi nition of an 65. Myers MB, Norwood SH. Standing orders for trauma care. J emergency medical condition. Am J Emerg Med. 2002;20(1): Emerg Nurs. 1994;20(2):111–117. 10–13. 66. O’Connor R. Paramedic standing orders. Del Med J. 71. Mitchell TA. Nonurgent emergency department visits—whose 1993;65(7):465–466. defi nition? Ann Emerg Med. 1994;24(5):961–963. 67. Schedler P. Standing trauma orders should also be cost-effective. 72. Schneider SM, Hamilton GC, et al. Defi nition of emergency J Emerg Nurs. 1994;20(5):346–347. medicine. Acad Emerg Med. 1998;5(4):348–351. 68. American College of Emergency Physicians. Defi nition of emergency medicine. Ann Emerg Med. 1994;24(3):553–554. Introduction to Emergency Medical Service Systems 37 Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. KEY CONCEPTS: Upon completion of this chapter, it is expected that the reader will understand these following concepts: • Paramedic wellness defi ned as more than absence of disease • The body’s responses to both positive and negative stresses • Stress management techniques for managing acute stress and chronic stress • Safety tips and stress management prevention strategies Case Study: “I can’t believe that I pulled my back on that last call,” said the young Paramedic. “Now what am I supposed to do? We’re expecting our fi rst baby and I’ve got the house payment and car payment. I can’t be out of work and I need the overtime!” 38 Foundations of Paramedic Care Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. Workforce Safety and Wellness 39 Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. OVERVIEW The health and wellness of the Paramedic goes beyond simply avoiding illness. It involves the social, spiritual, intellectual, emotional, and physical well-being as a part of a well-balanced lifestyle. The Paramedic encounters stress each day. This stress can have a harmful physiological effect on the body. It is important for the Paramedic to have built-in mechanisms for stress management and be familiar with the methods of crisis intervention to help prevent stress related illness. The Paramedic has many responsibilities, but perhaps the most important is personal safety. Focusing on the Paramedic’s response to emergencies and scene hazards, awareness is what can keep the Paramedic, his team, and the public safe. Safety is more than body substance isolation. Wellness Benefi ts of Wellness The concept of wellness could be thought of as merely the The benefi ts of wellness include a heightened sense of pur- absence of illness. However, this simplistic approach fails pose, an inner tranquility, as well as a physical being capable to take into account the complexity of human existence. of greater feats. Physical health is the most outward sign of Wellness is a multidimensional concept which includes wellness. Physically, the healthy body is more resistant to all aspects of a person—social, spiritual, intellectual, and injury (such as back injuries), as well as to illness. The body, emotional—as well as physical well-being (Figure 3-1). as a machine, functions better with a lower resting heart rate One defi nition of wellness, advanced by DePaul and blood pressure, more respiratory reserve, and generally University, is that wellness is an active process of becoming has a better cardiovascular capacity when it is healthy. Risk aware of, and making choices toward, a more successful exis- factors for all of the major diseases—cardiovascular disease, tence. This defi nition, intrinsically, implies that wellness is diabetes, and cancer—are reduced in healthy people. more than an absence of illness, which could be thought of as the lowest level of wellness. Paramedics who are aware of the Methods Used to Achieve Wellness practice of wellness are more likely to not experience illness Nutrition and to lead more productive lives. The components of physical health include a proper diet, one that provides the necessary nutrients, in the quantities suf- fi cient for life. A balanced intake of carbohydrates for quick energy, fats and proteins for body maintenance, as well as essential vitamins and minerals, can help the body main- Social tain optimal functionality. These nutrients can be obtained from the major food groups illustrated in the Department of Agriculture’s Food Pyramid (Figure 3-2). Foods, taken in the quantities indicated, can sustain a body and provide it with the materials and resources it needs to withstand the stresses Spiritual Physical encountered in emergency services. Food should always be eaten in moderation, with atten- Wellness tion paid to the type of foods being eaten. Excess amounts of fatty foods, for example, or excessive intake can lead to obesity. Obesity is a growing health crisis, second only to cigarette smoking as the leading cause of preventable death.1,2 Obesity can lead to a host of associated complications includ- ing diabetes and cardiovascular disease.3–6 Intellectual Emotional Medically speaking, a person is obese when his body mass index is 30 or greater.7 A common layperson defi nition of morbid obesity is 100 pounds over ideal weight. Over 60% of American men are obese by defi nition and therefore have Figure 3-1 The interconnectedness of wellness. an increased chance of illness, injury, and premature death. 40 Foundations of Paramedic Care Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. PEACHES Grains Vegetables Fruit Milk Meat & Beans Figure 3-2 United States Department of Agriculture’s Food Pyramid with a new emphasis on exercise. (Courtesy of United States Department of Agriculture) Figure 3-3 Physical fi tness is essential to longevity in EMS. Street Smart health. Whether using free-weights (isometric) or resistance exercises (isotonic), strength training can lead to increased Specialized bariatric equipment is available to help muscle strength and fl exibility (Figure 3-3). This in turn transport patients with obesity. The Paramedic should can help reduce the incidence or the severity of on-the-job injuries, particularly back injuries. know how to obtain this equipment and use it to prevent personal injury. Stress Stress is a function of daily living, a result of the interaction between the person and the environment. During the course of a day, the human body is constantly being bombarded Exercise by stimuli. The body reacts to this stimuli accordingly. The Exercise is also essential to physical health. A combina- amount of stimulation results in a certain level of stress in tion of aerobic exercise (e.g., walking or jogging), as well the body. If the stress is manageable (i.e., tolerable within as strength training is considered optimal for maintaining the limits of a person’s physical, psychological, emotional/ spiritual, and intellectual capacity to respond to the stimuli), then it is a positive form of stress or eustress. Eustress can Professional Paramedic lead to improved health as well as a sense of fulfi llment or accomplishment. Alternatively, overwhelming stimuli can lead to unhealthy Some Paramedic employers contract with stress, which in turn can have a negative impact on the per- chiropractors, personal trainers, or health educators son. This is called distress. Distress is the result of the body’s with a specialty in injury prevention to conduct maladaptive reaction to stress. The stimulus causes the body to react in a self-protective manner. This “survival instinct,” assessments and teaching sessions in an effort to awareness of and the ability to respond to one’s surroundings, reduce back injuries. is immediate and uncontrollable. Workforce Safety and Wellness 41 Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. When distress occurs, the body undergoes a reaction con- the vagus nerve. These functions are summarized as “feed trolled by the autonomic nervous system. The autonomic ner- and breed.” vous system can affect organ function throughout the body. The other autonomic nervous system responses are the Walter Cannon coined the term “fi ght or fl ight” to describe result of the sympathetic nervous system. Normally the sym- the generally adaptive response of the autonomic nervous pathetic nervous system includes those emergency responses system to stress. “Fight or fl ight” describes the body’s instinc- that are at “stand-by,” ready to provide the person with the tive response to a potential life threat. This primitive stress ability to fl ee (fl ight) or fi ght. Under normal conditions, the response may have been critical to the survival of primeval parasympathetic nervous system takes dominance, through man, but can be unhealthy today. vagal tone, and maintains homeostasis. However, under Modern man faces a host of new behavioral and emo- emergency conditions in which there is suffi cient stimulus, tional stressors beyond the mere physiologic stressors faced the epinephrine-based sympathetic nervous system assumes by early man. Modern |
stressors include psychosocial pres- more dominant control of the organs’ functions.11,12 sures from family, coworkers complaints, and supervisors’ The sympathetic nervous system is greatly infl uenced demands. In addition, intellectual pressures to perform to by the brain’s cognition, that ability to comprehend stimulus, perhaps unrealistic expectations, as well as new physiologi- and thought, the ability to comprehend a stimulus’s meaning. cal stressors that include noise pollution from sirens wailing, When repeatedly overstimulated, perhaps by constant bom- can lead to distress. Distress can be caused by any stimulus bardment by stress-inducing stimuli, the body begins to show that creates a maladaptive response from the autonomic ner- the fatigue, a prelude to illness in many cases, in a condition vous system. called strain. Hans Selye, an endocrinologist, observing the impact The chief neurotransmitter in the sympathetic nervous of stress upon physiology, advanced his theory of the “gen- system is epinephrine. Epinephrine has organ-specifi c effects eral adaptation syndrome.” In his theory he suggested that that alter that organ’s function. For example, epinephrine all human experience creates stress, but it is how the per- attaches to beta-receptors in the heart to make it contract son responds to that stress that determines if it is eustress or more forcefully (inotropy) and more quickly (chronotrophy). distress.8–10 Selye believed that the power of the body to resist Simultaneously, epinephrine also attaches to alpha-receptors distress, over a prolonged period of time, was limited and that in the peripheral vasculature, leading to increased peripheral the body would eventually become exhausted and typically vascular resistance (PVR). manifest in mental or physical illness. The stimulation of both receptors, alpha and beta, by epi- nephrine released during a stimulus response causes the heart to beat faster and harder against a greater resistance (PVR). Symptoms of Stress The heart’s increased workload leads to cardiovascular The manifestations of a Paramedic’s pending exhaustion from complications if the stress is prolonged. stress can be divided into psychological, cognitive, behav- Stress can also cause abnormal contraction of skeletal ioral, and physiological signs and symptoms. muscles, contractions beyond their functional needs, lead- For some people, the psychological signs of distress include ing to muscle spasms, spinal column misalignment and an unreasonable irritability at seemingly minor annoyances, resultant backache, contraction of facial muscles leading to uncharacteristic angry outbursts, open or covert hostility, and headache, jaw clenching, nocturnal teeth-grinding (brux- a general restlessness. For other people, distress is manifested ism), and neck pain. Internally, the immune system, set on by depression, withdrawal, self-deprecation, as well as reduced high alert for potential bacterial invasion, eventually fatigues. self-esteem. The Paramedic may also manifest stress by hav- T-lymphocyte counts drop, resulting in immunosuppression ing uncharacteristic bouts of forgetfulness, reduced creativity, and, paradoxically, more infections. The signs and symptoms shortened attention span, and disorganized thought. of overstress, or distress, include persistent tachycardia, pal- The person under extreme stress may demonstrate pitations, hypertension, chest pressure, and chronic pain. uncharacteristic changes in behavior such as increased smok- Physical disorders associated with chronic high stress ing, aggressive behavior (e.g., road rage), increased alcohol include, from head to toe, migraine and tension headaches, or drug use, over-eating, and a general carelessness about and cardiovascular disorders, respiratory disease, ulcers, and coli- withdrawal from activities of daily living. All of these may be tis, as well as hypertension and cancer. signs of impending stress-induced crisis. Emotional and behavioral disorders are also associated Walter Cannon referred to the symptoms of stress as a with stress. These include anxiety, with associated panic “fi ght or fl ight syndrome” and all of the manifestations of attacks, depression, alcoholism, and conduct disorders. These stress, system by system, are all attributable to a heightened emotions, behaviors, and somatic complaints should alert fel- autonomic nervous system state. The autonomic nervous low Paramedics that the person is under stress and may or system’s function can be roughly divided into two portions. may not be coping well emotionally.13 The fi rst portion, the parasympathetic nervous system, is The human psyche is not immune to the effects of chronic responsible for the involuntary vegetative functions includ- stress either. The psychological defense mechanisms against ing digestion, heart rate, and the like, largely controlled by stress include projection, denial, and conversion, among 42 Foundations of Paramedic Care Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. many others. When the individual’s coping mechanisms fail the individual can take action to eliminate the source of the to provide the relief needed, the individual may resort to mal- stress. This activity would constitute stress reduction. A job adaptative coping mechanisms. Examples of these maladapta- change or even divorce can be examples of stress reduction. tive coping mechanisms include substance abuse, alcoholism, If the source of the stress cannot be eliminated, then some smoking, and the use of other addictive substances. action must be taken to reframe the brain’s interpretation of the stimulus so that it is non-threatening. This technique, The Crisis Process called cognitive restructuring, provides hope for recovery A person is in crisis when he has experienced a threatening for some people with fatigue, strain, or stress. event but no longer has the capacity to respond, due to mental To understand the benefi ts of stress management, and/or physical exhaustion. The crisis process is somewhat Paramedics need to fi rst learn to recognize the early warning analogous to the transition from compensated to decompen- signs of stress, both immediate and long-term. Examples of sated shock. Anxiety, panic, and, in some cases, terror sets in the effects of long-term stress include recurrent headaches and the patient may become profoundly depressed or start to and unremitting fatigue. Part of managing stress is recogniz- manifest frank psychiatric symptoms. ing events that trigger stress and attempt to either eliminate Like the shock syndrome, the crisis process is reversible, them or respond to them differently. provided a crisis intervention is provided in time. The goals There are several effective models for stress manage- of crisis intervention start with stopping the acute process. ment, both short-term and long-term. For short-term stress Depending on the situation, this may be accomplished simply some EMS responders use controlled breathing or isotonic by removing the person from the source of the stimulus. Once exercise. Long-term methods of stress management are dis- removed, the downward spiral of emotions must be stopped cussed shortly. In every case, Paramedics need to become and the person’s thoughts and/or feelings can stabilize. In aware of their warning signs of impending stress and plan other cases it will take psychotropic medications and/or acute how they are going to respond to those stressors. crisis intervention to stop the crisis. With the acute symptoms While stress management is focused on the individual, managed, the goal of crisis management is to return the per- in this case the Paramedic, there are organizational benefi ts son back to independent functioning. to stress management training. In a cost–benefi t analysis, the One example of a crisis intervention approach used loss of time in stress management training is outweighed by for emergency services personnel is the SAFE-R model loss in sick leave, worker’s compensation, associated medical (Table 3-1). The letters in the SAFE-R model each stand for a costs, and employee turnover. Paramedics who learn how to step in the process. Stimulation reduction (S) is the fi rst goal manage their stress tend to have increased morale, decreased of crisis intervention using the SAFE-R model. Next, the confl ict with fellow workers and supervisors, reduced errors, facilitator would then acknowledge (A) the crisis and, using and enhanced performance while on-the-job. carefully chosen probing questions, facilitate (F) an under- Paramedics can learn a number of stress management standing of the situation. techniques that will help mitigate the long-term effects of After gaining the person’s attention, using empathy and stress.14–17 The majority of these techniques can be done therapeutic communications, the facilitator would explain (E) quietly, on-the-job, and without additional equipment. One the basic concepts of stress. The universality of stress would technique, autogenic training, stems from the practice of be emphasized and the facilitator would offer some plans autohypnosis fi rst advanced by Vogt in 1900. A form of for coping with the current situation. Finally, the facilitator “self-regulation” akin to biofeedback, autogenic training was would discuss a plan to return or restore (R) the person back developed in 1932 by Johannes Schultz as a means to train to independent function. the autonomic nervous system. Other stress management While the SAFE-R technique appears easy, as the say- techniques that emphasize the power of the mind–body con- ing goes, the devil lies in the details. Crisis interventions nection include progressive muscle relaxation and diaphrag- are best left to personnel trained in critical incident stress matic breathing. Some Paramedics have been trained in the management. use of mental imaging, which is useful for immediate stress relief, as well as meditation. Meditation has long been known Stress Management as a technique for stress reduction. Stress management is a process of coping with chronic stress in an effort to recover from its effects. In some instances, Specifi c Stressful Situations Acute Traumatic Stress Table 3-1 SAFE-R Model Witnessing horrifi c and disturbing events can generate intense S Stimulation reduction fear and a sense of helplessness in Paramedics. Unchecked, A Acknowledge the crisis these feelings can lead to acute traumatic stress. Acute F Facilitate E Explain traumatic stress is an unexpected and sudden stressful event R Return or restore which is unlike the stress of day-to-day EMS and understand- ably requires a different approach. Workforce Safety and Wellness 43 Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. reports,” should be used to emphasize the successes on-scene. Professional Paramedic Disagreements regarding specifi c aspects of scene develop- ment should be reserved until later. During a debriefi ng, fi rst- line responders should be monitored, possibly including an Like medicine, the most effective critical stress exit physical examination. These post-event physicals can management is prevention-oriented. Planning for reveal signs of stress including sustained tachycardia, persis- the ability to provide humane relief during a major tent headaches, and hypertension. After a major incident all responders should be encour- incident provides the best opportunity to reduce aged to get rest, moderate their intake of alcohol, and reduce acute stress. their caffeine intake. Responders should also be encouraged to engage in self-affi rming activities such as spending time with family and friends or getting involved in a favorite When possible, a predeployment briefi ng that explains sport. the situation, and potential stressors that the Paramedic is about to encounter, can go far toward decreasing the shock Defusings and subsequent acute traumatic stress. For example, search On occasion, and because of the nature of the incident or and rescue predeployment briefi ngs should include a discus- based upon an observation of emergency services respond- sion of the possibility of the operation changing from one ers, it may necessary to order a defusing. A defusing is an of rescue to a recovery operation. Tempering the hopes of immediate intervention intended to avert acute stress reac- concerned rescuers can help to reduce the impact of a poor tions among the responders. Usually initiated within eight outcome, thereby protecting rescuers, without diminishing hours, a critical-incident response team (CIRT) is called the prospect of a rescue. in to meet with the affected personnel, typically front-line Clear delegation of authority and the assignment of responders. specifi c tasks can help to eliminate some of the confusion The purpose of a defusing is to quickly explore the event and helplessness that Paramedics will experience when and then educate |
responders about the effects of stress. The confronted with a horrifi c situation. With proper guidance, lesson includes a discussion of signs and symptoms of acute command, and control, Paramedics can persevere against stress reaction as well as means of managing stress. If done incredible adversity. correctly, a defusing can either eliminate the need for further Incident command also needs to consider the mental critical incident stress debriefi ngs or enhance the productiv- and physical limitations of the emergency service respond- ity of future critical incident stress debriefi ngs. Crew leaders, ers under their command. Rotations to out-of-service in educated in debriefi ng techniques, can support their fellow order to take a rest break, eat some food, drink fl uids, and crew members (Figure 3-4). use lavatories, all part of rehabilitation, can help respond- Several criteria can establish the need for a critical inci- ers handle stress more effectively. It is also useful to have dent stress debriefi ng (CISD).18–20 Perhaps the most com- trained counselors who are observing for signs of stress and mon reason for a CISD is an extraordinary event-related can provide immediate interventions in the case of an acute occurrence. Examples of responder-related extraordinarily stress reaction. stressful events include a line-of-duty death, serious injury of a coworker while on-the-job, and post-event suicide of a fellow responder. Examples of event-related extraordinarily Street Smart stressful events include the traumatic death of a child or chil- dren; prolonged rescues, especially those that turn into a body recovery operation; and prolonged hostage situations.21–24 Whenever possible, the media should be restricted Dr. Jeffrey Mitchell, a leader in critical incident stress from the rehabilitation area. Reporters tend to use management, has identifi ed 10 critical incidents with high infl ammatory or untactful language in their questions potential for stress (Table 3-2).25 A CISD can be triggered by a request for CISD, often in order to achieve a desired effect or to prompt a from either an affected responder or an enlightened incident response. Unfortunately, ill-chosen or less than tactful commander. It can also be triggered by indirect personnel, words can have devastating effects upon emergency such as family members, who observe behavioral changes in services responders. the responder. Concerned coworkers, who are still witnessing signals of distress, such as constant ruminating after three weeks, can also request a CISD. A CISD is a private meeting, where only the CIRT and Demobilization is another opportunity to mitigate the responders are invited. Typically, rank holds no privilege effects of the acute stressors and to decrease the incidence of and conditions are established from the outset. This encour- acute traumatic stress reactions. Debriefi ngs, or “after action ages open dialogue among the CISD’s participants. With all 44 Foundations of Paramedic Care Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. Figure 3-4 Defusing session led by a Paramedic. Table 3-2 High Potential Critical Incidents Following a CISD, a member of the CIRT may have identifi ed a responder manifesting symptomology consistent 1. Line of duty death with acute stress reaction who might benefi t from profes- 2. Suicide of a colleague sional psychiatric services. These psychiatric interventions, 3. Serious work-related injury provided immediately after the event, can potentially prevent 4. Multi-casualty incident long-term disability such as post-traumatic stress disorder. 5. High threat incident (terrorism) Post-Traumatic Stress Disorder 6. Severe traumatic injury to children 7. Close relationship with victim If symptoms of acute stress disorder do not resolve within a four-week period, then post-traumatic stress disorder 8. Excessive media exposure (PTSD) must be considered.26,27 The essential feature in 9. Prolonged operations post-traumatic stress disorder, per the American Psychiatric 10. Overwhelming events (disasters) Association’s (APA) Diagnostic and Statistical Manual, fourth edition (DSM-IV), is the development of “character- istic symptoms following exposure to an extreme traumatic stress involving direct personal experience of an event that responders and the CIRT assembled in one room, the CIRT involves actual or threatened death or serious injury, or other leader begins by making introductions. A typical CIRT has a threat to one’s physical integrity; or witnessing an event that mental health practitioner as well as emergency responders involves death, injury or a threat to the physical integrity of who are trained in critical incident stress debriefi ngs. Once another person.” the introductions are completed, the leader starts the process Symptoms of PTSD include persistent intrusive recol- of divining the facts, asking for thoughts and reactions, all in lections of the event and fl ashbacks. Chronic absenteeism a nonconfrontational atmosphere. may represent the Paramedic’s attempts to avoid anything Timing is important to a CISD. If responders are still associated with the psychological trauma. Paramedics who experiencing acute stress they will have a limited number of have experienced a violation of a key psychological assump- communication channels to handle incoming information. tion, such as safe return from duty, might have tendencies They will not be able to tolerate the ambiguity that may occur toward PTSD. during the discussion. The objective of every CISD, and the next step in the process, is education. Responders are fi rst taught about typi- Personal Injury Prevention cal or “normal” reactions to stress, asked to refl ect upon these Many individuals get involved with emergency services symptoms, then taught about means to manage the stress that because of the excitement and danger of a rescue, never really naturally accompanies any incident. thinking that they themselves might actually get hurt. To the Workforce Safety and Wellness 45 Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. Paramedic, nothing may be more stressful than personal Risk Management injury. Despite their best efforts to mitigate hazards, injuries Progressive EMS agencies have developed a plan for risk do occur. In many situations, these injuries could have been management, a plan that emphasizes safety and whose goal lessened, or eliminated altogether, with proper preplanning is to reduce Paramedic injury in an effort to promote a culture and a safety-conscious attitude on the part of Paramedics. of safety in their organization. The problem of emergency responder death and injury In those agencies, either a risk manager or a safety may have been brought to the forefront by a 1973 publica- committee identifi es known hazards and then tries to mitigate tion entitled America Burning. America Burning, a presiden- those hazards. These activities are consistent with require- tial white paper, brought to light the indifference to safety ments under the general duty clause contained within the in the fi re service.28 Subsequently, all emergency responders Occupational Safety and Health Administration’s (OSHA) have experienced an increased emphasis on safety, primar- regulations. ily through increased regulations and standards (Table 3-3). Through a study of the frequency of injury, the severity of Paramedics, both in and out of the fi re service, must be aware injuries, and the economic impact of those injuries (including of the standards and regulations that affect them. workers’ compensation claims), the risk management team Regulations are mandatory and carry the weight of law, identifi es trends and implements change (e.g., new regula- whereas guidelines and standards are voluntary and only tions, procedures, or protocols). The risk management team offer directions for safe practice. Other recognized sources of would then perform an audit and reassess the success of the standards include the American National Standards Institute change. This plan-do-check-act approach, the PDCA cycle, (ANSI) and the American Society of Testing and Materials is a form of continuous quality improvement and is the same (ASTM). However, when specifi c injuries increase in certain model used in business. areas lawmakers frequently turn to standards and guidelines for direction. Safety Back Injury The saying goes “safety starts at home.” Every Paramedic has The prevalence of back injury among Paramedics is high and a responsibility to help maintain the safety of both the station potentially preventable.29–31 A reduction in the incidence of and the emergency response vehicle (ERV). back injury can be realized if Paramedics adhere to a few Of immediate concern in the station is the problem of fi re basic back safety rules. In many cases, back injury occurs and life safety. EMS stations should serve as models of a safe because of improper lifting and carrying. building for the community. Sprinklers should be placed in A Paramedic should lift only those loads that can be car- all living areas and fi re extinguishers, as well as fi re alarms, ried safely. Many EMS agencies have guidelines regarding safe should be readily available. In addition, fi re escape routes lifting, often tied to a functional job description, and mandate should be posted and clearly visible and fi re drills should be that additional rescuers be called for heavy lifting. When lift- routinely practiced. ing any object—stretchers to jump kits—Paramedics should Another concern is falls that occur while on the prem- bend their knees, stoop down, and lift with their legs. Keeping ises. Wet fl oors and snow-covered walkways present a clear the object close to the body and in-line helps to reduce the and present danger. Precautions should be taken to eliminate chance of a back injury. Part of back safety is back health. or mitigate the danger if possible. Exercise, discussed earlier, helps to maintain the strength and Vehicle Safety fl exibility of the back and reduces the chance of injury. Paramedics depend on their emergency response vehicle (ERV) for protection during an emergency response. A Table 3-3 Sample of Safety Regulations combination of lights, refl ective surfaces, and sirens help and Standards Applicable to Paramedics to increase the visibility of EMS while on-scene. Therefore, • Safety Regulations within the Code of Federal Regulations (CFR) these safety devices should be regularly checked to be sure • Confi ned Space Rescue 29 CFR 1910.146 they are in working order. However, a greater danger may • Hazardous Materials Response 29 CFR 1910.120 exist from mechanical failure. High speed driving, sudden stopping, and multiple drivers driving in all kinds of condi- • Bloodborne Pathogens 29 CFR 1910.1030 tions combine to put an extraordinary stress on ERVs. • National Fire Protection Association Standards To prevent mechanical failure, and ensure a timely • Fire Department Infection Control NFPA 1581 response, EMS agencies should have a program of preven- • Hazardous Materials Awareness Competencies NFPA 472 tative maintenance (PM) for their ERV. As opposed to a • Centers for Disease Control and Prevention (CDC) traditional “wait until it breaks then fi x it” approach, a pre- • Guidelines for Exposure to Tuberculosis ventative maintenance program forestalls the incidence of • Guidelines for Hepatitis B Exposure failure, thereby decreasing the incidence of injury and poten- tial litigation. 46 Foundations of Paramedic Care Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. Emergency Response If the emergency responder is the fi rst emergency vehicle Paramedics are at greatest risk of personal injury during the on-scene then the vehicle should be placed in such a manner initial response to the scene of an emergency. Despite safe so as to protect the patient and the responders. Typically, the vehicle operation, collisions with other vehicles on the road ERV is staggered, out-of-line, from the vehicle ahead so that do occur. Every emergency vehicle operator (EVO) should a safety zone is created. practice caution when advancing |
upon intersections. Many The ERV is now acting as a warning device, with its EMS agencies require all ERV to come to a complete stop, lights fl ashing, and as a physical barrier. To improve its func- when opposed by the red light, before proceeding. tionality as a barrier, the tires should be turned sharply, away When passing other vehicles, while running lights and from the pathway to the vehicle ahead. sirens, the EVO should expect the unexpected and be pre- If the scene is already protected by another emergency pared to drive evasively in order to avoid collision. Most responder, then most EMS agencies have a policy of parking states require emergency vehicles to pass on the left. Passing beyond the scene, parking in the direction of the most likely on the right runs the risk of having confused drivers suddenly destination hospital, and toward the route of intended exodus. turn into the path of the ERV. Parking in front of the scene helps reduce the exposure of the Paramedics should be on a heightened state of alert when second emergency vehicle to collision. multiple emergency vehicles are on the road. Unsuspecting Before approaching an unknown vehicle, headlights motor vehicle operators, seeing one emergency vehicle pass, should be turned on high and any available takedown lights may pull out into the path of the next emergency vehicle. or spotlights aimed toward the vehicle ahead. This lighting Police escorts are discouraged in many EMS systems for this helps to illuminate the interior of the vehicle as well as create reason. a safe working zone. If more than one emergency vehicle is traveling the same Some EMS systems require that the Paramedic radio route it may be prudent to change siren modes. There is a the license plate of the vehicle before it is approached. If the better chance that the motorists will hear two distinctly dif- plate comes back on a stolen vehicle the Paramedic is to wait ferent sounds and recognize that there is a second emergency for the arrival of law enforcement. vehicle. While a safe following distance increases the safety After selecting only the minimal equipment required of the chase vehicle, the wisdom of having two ERV respond- for an initial response, the Paramedic would approach the ing lights and sirens must be questioned. If it is plausible, the rear of the vehicle. Carrying additional equipment, such as chase vehicle should turn off its lights and siren, allowing the ECG monitors and so forth, is unnecessary and presents an fi rst ERV to be the fi rst responder to arrive on-scene. additional burden if the Paramedic has to fl ee suddenly. The A defensive driving attitude, or due regard for others Paramedic should choose to either approach the vehicle from on the road, can help to limit the number of motor vehicle the passenger side or to go around the back of the ERV and collisions. A number of emergency vehicle operator courses approach the vehicle from the driver’s side. The Paramedic and accident reduction programs are available to Paramedics. should avoid walking in front of the ERV headlights, back- Some insurance companies offer a reduction in premiums lighting his position and announcing his presence to the (personal and corporate) for participation in these programs. driver. Surprise is an important safety technique. With fl ashlight in hand, and carried away from the body, the Paramedic would examine the inside of the vehicle for Scene Hazards weapons as well as for the number of patients and then posi- Personal safety is the primary concern of Paramedics upon tion him- or herself behind the B-post of the vehicle. From arrival on the scene of an emergency. The responsibility for this venue the Paramedic can continue to inspect the interior scene safety is both an individual responsibility as well as of the vehicle’s occupant compartment for evidence of dam- a collective responsibility of the team. At larger incidents a age as well as weapons before proceeding with patient care. safety offi cer may be assigned to maintain safety. However, A Paramedic approaches a house call much differently at a small incident (e.g., a typical call for an emergency), than a road call for a motor vehicle collision. While houses overall responsibility falls to the offi cer-in-charge. vary, from the apartment in a high-rise development to the When approaching the scene of a motor vehicle colli- bungalow on a beach, the basic safety principles remain the sion, the driver and the Paramedic should slow the vehicle same for all and need only be modifi ed to the conditions on- and take a moment to get a “windshield survey” of the scene. scene. A current controversy in EMS concerns the style of Obvious hazards, such as a patient lying in the roadway or uniforms. Some EMS agencies advocate the button-down smoke and fi re, should be reportedly immediately as part of style of uniform that presents a clean image and portrays a the “fi rst due” report. It is safe practice to call out, by radio, or military bearing to the wearer. Other Paramedics argue that note somewhere in the cab of the ERV the license plate num- these uniforms make Paramedics look like law enforcement bers of the vehicle being approached. Some EMS agencies offi cers, especially to the distorted eyesight of a confused are not allowed to approach vehicles that are reported stolen or intoxicated patient (Figure 3-5). Patients could respond until law enforcement offi cers arrive. inappropriately, even violently, to this misperception. Workforce Safety and Wellness 47 Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. Figure 3-5 Similarities between law enforce- Figure 3-6 Properly carrying equipment can ment offi cer uniforms and EMS uniforms. ensure the Paramedic’s safety. An alternative EMS appearance, dubbed the soft look, con- the Paramedic can take a moment to look and listen for evi- sists of polo-style shirts. These shirts, without the badges of dence of scene violence. authority, are argued to be safer. If there is no evidence of scene violence, the Paramedic The use of personal body armor while performing EMS should park the ERV either diagonal across the end of a drive- is another controversy in EMS. Some argue that body armor way, or backed into the scene. This position permits a hasty is necessary to protect Paramedics. Citing gun ownership sta- retreat if need be. tistics, body armor advocates believe that body armor is part Carrying only the minimum equipment needed, the of personal protective equipment (PPE). In opposition, other Paramedic should approach the house from an oblique angle Paramedics believe that wearing body armor will encour- if possible, cutting across the lawn if necessary. Potential age Paramedics to enter scenes that they would otherwise attackers assume the Paramedic will approach the house not have entered, under the false assumption that the body from the sidewalk or other walkways. If a fl ashlight is needed armor will protect them. Opponents of body armor argue that to illuminate the pathway, then it should be carried away Paramedics do not have a duty to enter into unsafe scenes. from the body and care should be taken to not backlight Like their approach to a motor vehicle collision, the Paramedic. Paramedics should slow their approach to a house call until Equipment bags should be slung over the shoulder, or both the driver and the Paramedic can get a windshield survey. carried by hand, where they can be slipped off and dropped Emergency lights should be extinguished well before arrival, in front of pursuers. If the equipment bag is slung over the so as to not alert the occupants of the impending approach of neck, attackers can grab the strap and drag the Paramedic to emergency responders. The ERV should be slowed to a near the ground. Paramedics must be sure to properly carry their stop at a 45-degree angle from the scene. From this vantage, equipment bag (Figure 3-6). 48 Foundations of Paramedic Care Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. If possible, the EVO should remain in the vehicle, with perform a scene size-up before proceeding. Some Paramedics, the ERV running and the mobile radio on, while the Paramedic once they are inside the door, immediately step to the side, approaches the house. This permits the EVO to contact LEO with their back to the wall, and start asking family members if assistance is needed and to more quickly depart the scene. simple questions. Taking advantage of the moment, these If the residence is an apartment complex or similar struc- Paramedics perform a quick sweep of the room for deadly ture with an elevator, then the Paramedic should consider weapons and dangerous instruments.32–35 using the fi re service functions. Upon arrival at the intended Domestic violence calls are some of the most dangerous fl oor, the elevator alarm should be silenced and the elevator calls for LEO and Paramedics alike. When arriving on the locked. One Paramedic should approach the apartment door scene with a potential for domestic violence, the Paramedic is while another Paramedic surveys the scene for stairwells, fi re well advised to wait for the arrival of LEO before entering. If escapes, and other emergency exits. Once safe entry is made Paramedics have inadvertently entered into the scene of prob- into the apartment, the elevator can be released for regular able domestic violence, they should consider the severity of service. the patient’s injuries versus their personal safety, keeping their The Paramedic should verify the address, then approach safety foremost in their minds. If the scene is unsafe, and the the door from the door handle side; this cuts down on the Paramedic can get the patient into the relative safety of the ERV, Paramedic’s angle of exposure. Using the door’s jam as a bar- they should attempt to do so. If the scene is unsafe, the Paramedic rier, the Paramedic would position himself perpendicular to should immediately withdraw and call for assistance. the wall and loudly announce his presence, using the butt of a If Paramedics are attacked or feel they are about to be fl ashlight or similar object to knock on the door while shout- attacked they should immediately withdraw from the scene. ing out, “Ambulance!” or “Fire department!” These terms are Some Paramedics will throw the clipboard into the hands of generally understood by most citizens and cannot be confused a potential attacker, to confuse the attacker and to allow them with “police” or other terms. more time to escape. Entering the residence, many Paramedics suspend the The fi rst goal for Paramedics during a hasty retreat is to get EMS equipment bag and carry it in front of them, provid- two or more objects called cover between themselves and their ing a barrier to attacking dogs and/or an obstacle to pursuers. would-be attackers. Cover is any object that cannot be pene- Paramedics should request that all dogs be locked in another trated by a projectile, from bullets to frying pans. Examples of room, regardless of pleas from the family or innocent appear- cover include telephone poles and even fi re hydrants. The tires ances. Even small, apparently harmless dogs can attack if and engine block of the ERV also make good cover; however, they sense that the Paramedic is hurting their master. Paramedics are reminded that a bullet tends to follow the plane Whenever possible, two responders should enter the scene of the ground after it ricochets and can travel under an ERV. together. One responder acts as the contact |
medic. The contact If cover is not immediately available then the Paramedic medic makes contact with the patient and begins patient care. will have to settle for concealment. Concealment is cre- This second responder acts in the role of the “cover medic.” ated by any object that blocks the pursuer’s vision of the The cover medic watches the scene for hazards. The cover Paramedic. However, concealment does not offer protection medic always keeps the “big picture” in mind, watching both and should be abandoned in favor of cover and retreat as soon the patient and the other people on scene. The cover medic as possible. should ensure that the doorway to the exit is never blocked. If possible, the cover medic should be stationed in the path to Special Operations the doorway, to ensure that it remains open. Often the cover Special operations, such as confi ned space rescue, vehicle medic carries the radio in case additional aid is needed. rescue, and water rescue, require special protective apparel The cover medic should also do a quick scan of the as well as training in its proper use. For example, a Paramedic scene to identify deadly weapons and dangerous instru- inside a vehicle should have, from head to toe, a helmet or ments. Deadly, or lethal, weapons are those objects that are, bump cap with strap, ear protection, eye protection, a fi re- by design, intended to infl ict death or disability (e.g., a pis- retardant turnout coat, leather or fi refi ghter-grade gloves, tol or a knife; Figure 3-7a). The defi nition of a dangerous overalls or bunker pants, and boots. instrument is more amorphous. A dangerous instrument is any object that could be used, under the right circumstances, to produce serious injury or even death. An example of a Infection Control dangerous instrument would be a box cutter or broken beer The ever-present danger on the scene of every EMS call is bottle (Figure 3-7b), both of which could produce serious infection. Paramedics have a good chance of preventing an lacerations. infection for themselves provided they have up-to-date immu- If a cover medic is not available then the Paramedic must nizations and use proper barrier protection. Immunizations perform a scene survey alone. The Paramedic should avoid considered standard in most EMS agencies include tetanus, tunnel-vision and, borrowing a term from the fi re service, diptheria, polio, and MMR (measles, mumps, and rubella). Workforce Safety and Wellness 49 Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. (a) (b) Figure 3-7 Deadly weapons versus dangerous instruments. Other common immunizations include the vaccination On-scene of a medical emergency, Paramedics utilize series for hepatitis B, offered free to Paramedics as part of a dress-up philosophy, meaning Paramedics add barrier the OSHA regulations regarding bloodborne pathogens, and devices for protection as the situation warrants. Practicing (in the future) smallpox vaccination. Many Paramedics also body substance isolation, Paramedics frequently don receive vaccination for infl uenza, not only to protect them- gloves before approaching the patient. In many cases, the selves, but to protect their infant and elderly patients who do patient’s chief complaint determines what additional barrier not recover as easily from these contagions. While, at pres- device is worn. Paramedics should be aware of commonly ent, there are no immunizations against tuberculosis (Tb) or used barrier protection for certain situations (Table 3-4). human immunodefi ciency virus (HIV), many Paramedics The list is not comprehensive nor should Paramedics limit obtain periodic testing, in order to obtain life-prolonging che- themselves to the listed devices if conditions warrant more motherapy in the event they are infected. protection. 50 Foundations of Paramedic Care Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. Table 3-4 Barrier Devices Used in Selected Activities Disposable Protective Task Gloves Gown Mask Eyewear Bleeding control Yes Yes Yes Yes Spurting blood Bleeding control Yes No No No Minimal blood Emergency childbirth Yes Yes Yes Yes Intravenous line insertion Yes No No No Endotracheal intubation Yes No Yes Yes Suctioning Yes No No No Measuring blood pressures No No No No Appropriate use of Body Substance Isolation (BSI) is recommended any time open skin or mucosa may be exposed to body fl uids.36–40 Source: This table is taken from the New York State Department of Health, Bureau of Emergency Medical Services, Recommendations for Body Substance Isolation. Infectious Disease Exposure Whenever blood or bodily fl uids from a patient are spilled, splashed, or dripped onto or injected into a Paramedic, an exposure to a potentially infectious material may have occurred. The prevention of exposure to blood and bodily fl uid is paramount and all efforts to provide equipment with built-in safety devices and for the proper disposal of sharps and other potentially infected materials should be given priority. Barrier devices, such as eye protection and gowns, should also be readily available and used in anticipation of a blood or bodily fl uid exposure (Figure 3-8). Whenever a potential exposure has occurred, the exposed area should be immediately blotted clear of visible blood or fl uids, then thoroughly washed with soap and water. If soap and water is not immediately available, the Paramedic should use a gelled alcohol cleanser, then (as soon as possible) use soap and water to cleanse the area. Blood or bodily fl uids inadvertently splashed into the eyes, nose, or mouth should be fl ushed away, using clean water. The Centers for Disease Control and Prevention (CDC) reports that there is no scientifi c evidence to support the prac- tice of applying antibiotics or squeezing fl uid from the wound to reduce or prevent the transmission of disease. Following agency guidelines, and after caring for the patient, the Paramedic should immediately report the expo- sure and seek medical treatment. Treatment may include Figure 3-8 Preparing for an intubation by fi rst obtaining a blood sample from both the Paramedic and the donning personal protective equipment. source patient, assuming the patient grants permission as well as post-exposure chemotherapy. fl uid contacts, and the chance of the Paramedic being infected Factors that combine to determine the risk of exposure to from a single blood contact with an infected patient. hepatitis B (HBV), hepatitis C (HCV), and human immuno- A great deal of concern is expressed about exposure to defi ciency virus (HIV) is a function of the number of infected HIV, but the CDC reports that the risk of HIV infection, even persons in the community, the type and number of blood or after needlestick with HIV-infected blood, is 0.3% (1 in 300). Workforce Safety and Wellness 51 Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. The risk for a splash of HIV-infected blood into the eye, nose, Using heavy-duty utility gloves, kitchen-type, the or mouth is less than 1 in 1,000.41–43 Paramedic should mix a 1:100 solution of bleach and water Following a call where potentially infectious material has (1/4 cup of bleach to a gallon of tap water) and wipe down been present, the equipment and the ERV should be decon- any contaminated surfaces. A ratio of 1:100 bleach is usable taminated. Decontamination of the emergency response for about 24 hours before it should be discarded. Many vehicle diminishes the potential for disease transmission EMS agencies prefer to mix a fresh solution before every and should be done as soon as practical. Moist blood should use. Soiled linens and the like, including soiled uniforms, be immediately blotted with a disposable towel at the time should be returned to laundry for proper cleaning and any of the spill, using a gloved hand. The towel should then be soiled dressing or other bloody materials disposed of in a red disposed of in a red biohazard waste container. More thor- biohazard waste container. ough cleaning should occur after the call. 52 Foundations of Paramedic Care Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. An enlightened attitude about health and wellness, as well as a “heads-up” attitude about safety, contribute to a Paramedic’s wellness and ability to continue practicing paramedicine. Key Points: • Wellness is more than an absence of illness • The Paramedic may handle acute traumatic and incorporates all aspects—social, spiritual, stress differently than the layperson; therefore, intellectual, emotional, and physical being—of management may require a different approach. a person. • Some incidents may require a defusing, or an • A healthy body is more resistant to both injury immediate intervention intended to avert acute and illness. stress reactions among responders. • A proper diet, one that provides the necessary • A typical CIRT (Critical Incident Response Team) nutrients in suffi cient quantities, is one of the most has a mental health practitioner as well as important components of physical health. emergency responders who are trained in critical incident stress debriefi ngs. • Exercise is essential to a Paramedic’s physical health. • In many situations, injury can be lessened, or eliminated altogether, with proper preplanning • Stimulation results in stress in the body. The and a safety-conscious attitude on the part of the positive form of stress is eustress while the Paramedic. maladaptive reaction to stress results in distress. • A Paramedic’s responsibility is to maintain the • Behavioral and emotional stressors can negatively safety of both the station and the emergency affect the Paramedic’s emotions, way of thinking, response vehicle (ERV). and behavior. • Paramedics are at greatest risk of personal injury • The dominance of the sympathetic nervous during the initial response to the scene of an system in a chronically elevated state can bring emergency. about physical, emotional, and behavioral • Scene safety is an individual responsibility as well disorders. as a collective responsibility of the team. • Maladaptive coping mechanisms include substance • Whenever possible, two responders should enter abuse, alcoholism, smoking, or the use of other the scene together. One responder acts as the addictive substances. contact medic, interacting with the patient and • Analogous to decompensated shock, people are in beginning patient care, while the second responder crisis when they experience a threatening event acts in the role of the “cover medic.” but no longer have the capacity to respond. • Domestic violence calls are some of the most dangerous calls for law enforcement offi cers and • Stress management is a process of coping Paramedics alike. with chronic stress in an effort to recover from its effects. • Paramedic safety should be kept foremost in mind. • Paramedics can learn a number of stress • If attacked, the Paramedic should withdraw management techniques that will help mitigate the immediately. long-term effects of stress. Workforce Safety and Wellness 53 Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. 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materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. • Immunizations and proper barrier protection offer • Any soiled dressing or other bloody materials Paramedics the best chance in preventing infection should be disposed of in a red biohazard waste for themselves. container. • The prevention of exposure to blood and bodily • Special operations, such as confi ned space rescue, fl uid is paramount. vehicle rescue, or water rescue, require special protective apparel as well as training in their • Contaminated surfaces should be wiped down with proper use. a cleaning agent. • Soiled linens or uniforms should be returned to laundry for proper cleaning. Review Questions: 1. What differentiates good stress from bad stress? 8. How does scene safety in the roadway of a 2. What are the signs and symptoms of stress? motor vehicle collision differ from the scene 3. Describe the physiological effects caused by stress. safety of a residential emergency? 4. How is the SAFE-R model used as a crisis 9. What is the responsibility of the cover medic? prevention tool? What should the Paramedic do when working 5. What are some stress management techniques alone? that are used by prehospital providers? 10. What steps should be taken by the Paramedic 6. How should a Paramedic lift a heavy load? prior to arrival that can help prevent exposure 7. How can the Paramedic reduce the risk of and/or infection? personal injury when responding to the scene of an emergency? Case Study Questions: Please refer to the Case Study at the beginning of 3. What stress management techniques could the the chapter and answer the questions below: Paramedic use? 1. What stress(es) is/are expressed by the young 4. In addition to back safety, what other illness Paramedic? and injury prevention techniques should the 2. Describe the body’s physiological responses to Paramedic employ? the stress(es). References: 1. Blackwell J. Identifi cation, evaluation, and treatment of 2. Beebe R. Size matters. Understanding morbid obesity & overweight and obese adults. J Am Acad Nurse Pract. its associated complications. Jems. 2002;27(1):22–28, 2002;14(5):196–198. 30–33. 54 Foundations of Paramedic Care Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. 3. Rashid MN, Fuentes F, et al. Obesity and the risk for mental health and emotional well-being. Br J Psychiatry. cardiovascular disease. Prev Cardiol. 2003;6(1):42–47. 2001;178(1):76–81. 4. Scaglione R, Argano C, et al. Obesity and cardiovascular risk: 24. Berger W, Figueira I, et al. Partial and full PTSD in Brazilian the new public health problem of worldwide proportions. Expert ambulance workers: prevalence and impact on health and on Rev Cardiovasc Ther. 2004;2(2):203–212. quality of life. J Trauma Stress. 2007;20(4):637–642. 5. Mensah GA, Mokdad AH, et al. Obesity, metabolic 25. http://www.sgsp.edu.pl/sos/mitchel/wyklady/stress.pdf syndrome, and type 2 diabetes: emerging epidemics and their Stress Management, Jeffrey T. Mitchell, PhD, CTS. cardiovascular implications. Cardiol Clin. 2004;22(4):485–504. 26. Foa EB. Psychosocial therapy for posttraumatic stress disorder. 6. Smith SC, Jr. Multiple risk factors for cardiovascular disease and J Clin Psychiatry. 2006;67 (Suppl 2):40–45. diabetes mellitus. Am J Med. 2007;120(3 Suppl 1):S3–S11. 27. Smith A, Roberts K. Interventions for post-traumatic 7. Bray GA, Bellanger T. Epidemiology, trends, and morbidities stress disorder and psychological distress in emergency of obesity and the metabolic syndrome. Endocrine. ambulance personnel: a review of the literature. Emerg Med J. 2006;29(1):109–117. 2003;20(1):75–78. 8. Selye H. Stress and distress. Compr Ther. 1975;1(8):9–13. 28. America Burning: Report of the National Commission on Fire 9. Seematter G, Binnert C, et al. Relationship between stress, Control. Chapel Hill: U.S. Government; 1973. infl ammation and metabolism. Curr Opin Clin Nutr Metab Care. 29. Mitterer D. Back injuries in EMS. Emerg Med Serv. 2004;7(2):169–173. 1999;28(3):41–48. 10. Selye H. The nature of stress. Basal Facts. 1985;7(1):3–11. 30. Powers DW, Wagner K. Getting back up from a back injury. 11. Arun CP. Fight or fl ight, forbearance and fortitude: the spectrum Emerg Med Serv. 2004;33(2):82–83. of actions of the catecholamines and their cousins. Ann N Y Acad 31. Terribilini C, Dernocoeur K. Save your back. Injury prevention Sci. 2004;1018:137–140. for EMS providers. Jems. 1989;14(10):34–35, 37–41. 12. Wortsman J. Role of epinephrine in acute stress. Endocrinol 32. Doyle TJ, Vissers RJ. An EMS approach to psychiatric Metab Clin North Am. 2002;31(1):79–106. emergencies. Emerg Med Serv. 1999;28(6):87, 90–93. 13. Crofford LJ. Violence, stress, and somatic syndromes. Trauma 33. Eckstein M, Cowen AR. Scene safety in the face of automatic Violence Abuse. 2007;8(3):299–313. weapons fi re: a new dilemma for EMS? Prehosp Emerg Care. 14. Verschuur M, Spinhoven P, et al. Making a bad thing worse: 1998;2(2):117–122. effects of communication of results of an epidemiological study 34. Dick T. Bar fi ght. A mental exercise in scene safety. Emerg Med after an aviation disaster. Soc Sci Med. 2007;65(7):1430–1441. Serv. 2003;32(3):38–39. 15. Hammer JS, Mathews JJ, et al. Occupational stress within the 35. Carlquist N. Five steps to scene safety. Emerg Med Serv. Paramedic profession: an initial report of stress levels compared 2007;36(2):82. to hospital employees. Ann Emerg Med. 1986;15(5):536–539. 36. Carrillo L, Fleming LE, et al. Bloodborne pathogens risk and 16. Stanzer M, Guarraci F, et al. Paramedic or EMT-basic partner? precautions among urban fi re-rescue workers. J Occup Environ Study evaluates preferred partner types & the effect of partners Med. 1996;38(9):920–924. on work-related stress levels. Jems. 2007;32(6):72–74. 37. DiGiacomo JC, Hoff WS, et al. Barrier precautions in trauma 17. Graham N. Done in, fed up, burned out—part 2: avoiding the resuscitation: real-time analysis utilizing videotape review. short career. Jems. 1981;6(2):25–31. Am J Emerg Med. 1997;15(1):34–39. 18. Caine RM, Ter-Bagdasarian L. Early identifi cation and 38. Madan AK, Rentz DE, et al. Noncompliance of health care management of critical incident stress. Crit Care Nurse. workers with universal precautions during trauma resuscitations. 2003;23(1):59–65. South Med J. 2001;94(3):277–280. 19. Bledsoe BE. Critical incident stress management (CISM): 39. Sadoh WE, Fawole AO, et al. Practice of universal precautions benefi t or risk for emergency services? Prehosp Emerg Care. among healthcare workers. J Natl Med Assoc. 2006;98(5): 2003;7(2):272–279. 722–726. 20. Neely KW, Spitzer WJ. A model for a statewide critical incident 40. Eustis TC, Wright SW, et al. Compliance with recommendations stress (CIS) debriefi ng program for emergency services for universal precautions among prehospital providers. Ann personnel. Prehosp Disaster Med. 1997;12(2):114–119. Emerg Med. 1995;25(4):512–515. 21. Sterud T, Ekeberg O, et al. Health status in the ambulance 41. http://www.cdc.gov services: a systematic review. BMC Health Serv Res. 2006;6:82. 42. Zanni GR, Wick JY. Preventing needlestick injuries. Consult 22. van der Ploeg E, Kleber RJ. Acute and chronic job stressors Pharm. 2007;22(5):400–402, 404–406, 409. among ambulance personnel: predictors of health symptoms. 43. Campos-Outcalt D. HIV postexposure prophylaxis: who should Occup Environ Med. 2003;60 (Suppl 1):i40–i46. get it? J Fam Pract. 2006;55(7):600–604. 23. Alexander DA, Klein S. Ambulance personnel and critical incidents: impact of accident and emergency work on Workforce Safety and Wellness 55 Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. KEY CONCEPTS: Upon completion of this chapter, it is expected that the reader will understand these following concepts: • Paramedics continually evaluate practices, protocols, and procedures • Connection between Paramedic practice and evidence-based practice • Different types of research appropriate for differing research questions • The research format and ability to identify errors • Ethical concerns associated with research • Types of research that can improve “the bottom line” Case Study: At a QA/QI meeting a Paramedic presents a case to her coworkers and medical director that introduces the need for medication- facilitated intubation (MFI). This developed after the Paramedic was presented with a patient who—due to the patient’s physical condition and medical emergency—could have been greatly aided by MFI. The Paramedic is charged with researching the topic and presenting her fi ndings at the next meeting. The Paramedic has been asked to examine the success or effectiveness of having MFI as an advanced airway skill at other agencies with MFI programs and to consult published research in an effort to support an evidence- based practice change. 56 Foundations of Paramedic Care Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. Research and EMS 57 Copyright 2010 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. OVERVIEW Hippocrates stated in his exposition “as to diseases, make a habit of two things—help or at least to do no harm” (Epidemics, Bk I, Section XI). Paramedics driven by the maxim “do no harm” often ask themselves if what they do truly helps, or if, at a minimum, no harm has been caused to the patient. Practice, Protocols, is defensible. A Paramedic practice is defendable if it estab- lishes evidence-based medical care is provided in specifi c and Procedures circumstances, such care can be independently evaluated by The question “does it help?” naturally leads to the question other Paramedics, it can be applied to a number of same or of where our practice, protocols, and procedures originated. similar circumstances, and it is the most effective means of Most current EMS practice parameters, protocols and proce- delivering desired patient outcomes. Such evidence-based dures, originated from anecdotal experience. These are the practice is more likely to weather the scrutiny of cautious result of apparently successful previous practices and of intu- public offi cials and alert community leaders. itiveness (i.e., this ought to work). In situations where science did not exist to support a Evidence-Based Practice practice, Paramedics and medical directors often used an Emergency medical service in general—and Paramedic prac- analogy to think through a situation (i.e., this worked for this tice in particular—are being attacked by some critics who say other problem in the past and the present situation is simi- that EMS is costly to the public and an ineffective means to lar). Experienced Paramedics call this “common sense” while delivering patient care. Paramedic educators refer to it as “pattern recognition” (i.e., To survive in the current cost-cutting environment comparison of similarities).1 Paramedics must prove that their practice is valuable. Unfortunately, some EMS practices have been driven by Paramedicine must prove that Paramedics can decrease correction of earlier misadventures. Practice improvement morbidity (e.g., through decreased hospital stays or length arrived at by conscious decision (i.e., by committee) is no of stays) and/or decrease mortality and should therefore be more reliable because it is simply the group’s combined anec- seen as valuable.5–7 dotal experience. To transform a practice to evidence-based practice, either As a result, Paramedic practice is often more likely to through updated protocols or continuing education, the fi rst be a function of what does not harm the patient. This form step is to look at the research that already exists. of practice can be ineffective and leads to the practice of While EMS research is still limited at this time, defensive medicine as well as the misdirected application of Paramedics can look to the research of other allied health resources. professions, such as medicine, nursing, respiratory care, and |