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C O G N I T I V E T H E R A P Y O F S U B S T A N C E A B U S E -•̂ .̂ '̂ ySi:'yf̂ '̂ ''->->*' 'r. ^'i-'Mt .#''a^K"'-M>' • M ^ i € • ̂ ^. M'^::. A A R O N T . B E C K • ^ • r f - F R E D D . W R I G H T C O R Y F . N E W H A N B R U C E S . L I E S E C O G N I T I V E T H E R A P Y O F S U B S T A N C E A B U S E C o g n i t i v e T h e r a p y o f S u b s t a n c e A b u s e Aaron T. Beck, M.D. Fred D. Wright, Ed.D. Cory F. N e w m a n , Ph.D. Bruce S. Liese, Ph.D. T H E G U I L F O R D PRESS N e w York London ©1993 The Guilford Press A Division of Guilford PubHcations, Inc. 72 Spring Street, New York, N Y 10012 www.guilford.com All rights reserved No part of this book may be reproduced, stored in a retrieval s or transmitted, in any form or by any means, electronic, mechanical, photocopying, microfilming, recording, or otherwise, without written permission from the Publisher. Printed in the United States of America. This book is printed on acid-free paper. Last digit is print number: 9 Library of Congress Cataloging-in-Publication Data Cognitive therapy of substance abuse / Aaron T. Beck . . [et al p. cm. Includes bibliographical references and index. ISBN 0-89862-115-1 (he.) ISBN 1-57230-659-9 (pbk.) 1. Substance Abuse—Treatment. 2. Cognitive therapy. I. Beck, Aaron T. [DNLM: 1. Cognitive therapy—methods. 2. Substance Abuse— therapy. W M 270 C6765 1993] RC564.C623 1993 616.86'0651—dc20 DNLM/DLC for Library of Congress 93-5208 CIP To Phyllis, G w e n , Jane, and Ziana P r e f a c e s L-#ubstance abuse is widely recognized as a serious social and legal problem. In fact, the use of illegal drugs may be responsible for more than 2 5 % of property crimes and 1 5 % of violent crimes. Financial losses related to these crimes have been estimated at $1.7 billion per year. Homicides are also strongly linked to drug dealing. Approximately 1 4 % of homicides per year are causally related to drugs. The costs for criminal justice activities directed against drug trafficking on the federal level were approximately $2.5 billion in 1988, compared to $1.76 billion spent in 1986. There are also many health problems caused by these drugs. Alcohol can damage almost every body organ, including the heart, brain, liver, and stomach. Illegal drugs such as cocaine can have a serious effect on the neurological, cardiovascular, and respiratory systems. Cigarettes can cause cancer, heart disease, and more. The most widely used and abused drug in the world is alcohol. In the United States, two-thirds of the population drink alcohol. About ten out of a hundred people have problems with alcohol so serious that they can be considered "alcoholic" or "alcohol-dependent." (Interestingly, this 1 0 % of Americans buys and drinks more than half of the alcoholic beverages!) At least 14 million Americans take illegal drugs every month. Dur­ ing "peak months" this number climbs to more than 25 million users. Some experts have estimated that approximately 2.3% of Americans over 12 years of age have a problem with illegal drugs serious enough to warrant drug treatment. To a large degree, we have tried to put a halt to drug abuse by making drugs illegal. For example, heroin and cocaine are presently illegal in the United States. Cigarette smoking is becoming increas­ ingly proscribed. At one time we tried to stop alcoholism by legal Vll via Preface mechanisms (i.e., prohibition). Obviously, these methods will never make substances completely unavailable. Not all people who use drugs become addicted to them, although many people have asked themselves, "Am I [or is someone else] an alcoholic [or a substance abuser]?" The American Psychiatric Associ­ ation has defined the addictions very specifically. In fact, the official term for an addiction is "substance dependence." There are some specific signs of substance dependence, including (1) heavy use of the substance, (2) continued use even though it may cause problems to the person, (3) tolerance, and (4) withdrawal symptoms. Cultural and historical factors are implicated in substance use and abuse. The patterns and consequences of drug use have been influ­ enced by historical developments, which have had positive and neg­ ative effects. Two centuries ago, the extraction of pure chemicals from plant materials created more powerful medicinal agents. The inven­ tion of the hypodermic needle in the middle of the nineteenth cen­ tury was also a medical boon, which, on the other hand, allowed drug users to circumvent the body's natural biological controls consisting of bitter taste and slow absorption through the digestive tract. Many synthetic drugs developed in the twentieth century had medical appli­ cation but created further opportunities for abuse and addiction. In short, any activity that affects the reward mechanisms of the brain may lead to compulsive, self-defeating behavior. Social, environmental, and personality factors have affected sub­ stance use and abuse in ways that go far beyond the simple pharma­ cological properties of these agents. Alcoholism, for example, is preva­ lent among certain ethnic groups and practically absent among others, such as the Mormons, who require abstinence for group acceptance. O n the other hand, other social subgroups may condition group accep­ tance on using or drinking. The social milieu may influence using. Soldiers used illegal drugs extensively in Vietnam but, for the most part, relinquished heavy drug use after returning home. Impoverished environments have been shown in both animal experiments and human studies to lead to addiction. As pointed out by Peele, the com­ m o n denominator is the lack of other opportunities for satisfaction. Finally, our clinical experiences have indicated that addicted indi­ viduals have certain clusters of addictive attitudes that make them abusers rather than users. Successful treatment depends on clinicians' effectiveness in deal­ ing with these addictive potentials. And what form will this care take? As pointed out by Marc Galanter, president of the American Academy of Psychiatrists in Alcoholism and Addiction, the long-term efficacy of new pharmacological treatments is open to question. "Tricyclics, Preface ix dopaminergic agents, and carbamazapine for cocaine abusers have yet to be substantiated as a vehicle for continuing care. For opiates, naltrexone and buprenorphine offer only a modest niche in the do­ main that was traditionally occupied by methadone maintenance. Intervention in GABAergic transmission may hold promise for alco- hoHsm, but that promise is far from clinical application" (Galanter, 1993, pp. 1-2). W e have written this book in response to the ever-growing need to formulate and test cost-effective treatments for substance abuse dis­ orders, problems that seem to be multiplying in the population in spite of society's best efforts at international interdiction and domes­ tic control and education. W e believe that cognitive therapy, a well- documented and demonstrably efficacious treatment model, can be a major boon to meeting this pressing need. At one time, "drug abuse rehabilitation counseling" was regarded as a specialty area in the field of psychotherapy—now it is apparent that almost all who engage in clinical practice will encounter patients who use and abuse drugs. Therefore, it would be desirable for all mental health professionals to receive some sort of routine training and education in the social and psychological phenomena that com­ prise the addiction disorders. Our volume is intended to provide a thorough, detailed set of methods that can be of immediate use to therapists and counselors—regardless of the amount of experience they might have had with cognitive therapy, or in the field of addictions. Toward this end, we have strived to make our model and our proce­ dures as specific and complete as possible. W e certainly recommend that those who read this book also read the many valuable sources we have cited in the text. Nevertheless, our intention in writing Cog­ nitive Therapy of Substance Abuse has been to provide a convenient, centralized source that is comprehensive, teachable, and testable. Although advances in the field have been made in the form of pharmacological interventions (e.g., antabuse, methadone, and nal­ trexone), 12-step support groups (e.g. Alcoholics Anonymous, Nar­ cotics Anonymous, and Cocaine Anonymous), and social-learning models and programs (relapse prevention, rational recovery, etc.), each of these approaches has posed problems that limit its respective poten­ tial efficacy. For example, pharmacological interventions have pro­ duced promising short-term data but are fraught with compliance and long-term maintenance difficultieŝ atients may not take their chem­ ical agonists and antagonists, and they are prone to relapse when the medications are discontinued. Twelve-step programs provide valuable social support and consistent guidance principles for individuals who voluntarily join and faithfully attend the program meetings, but can- X Preface not address the needs of those who will not enter the programs or who drop out. Social-learning approaches provide sophisticated models of substance abuse and relapse, and hold promise to produce and accumulate empirical data, but thus far the resultant treatments (with very few exceptions) have been less well described than the theories that gave rise to them. Although the cognitive approach that we have explicated is most closely related to the social-learning theories of substance abuse, we want to emphasize that we find value in all of the aforementioned treatment modalities. Cognitive therapy is not in "opposition" to 12- step or psychobiological models of substance abuse. W e have found that these alternative treatment systems may be complementary to our procedures. Many of the substance abuse patients that we treat at the Center for Cognitive Therapy concurrently attend Narcotics Anony­ mous and similar 12-step groups. Other patients take the full spec­ trum of pharmacologic agents, from antidepressants to antabuse, under strict medical guidance. The individualized conceptualization of patients' belief systems and the long-term coping skills (to deal with everyday life concerns, as well as to manage cravings and urges spe­ cific to drug use) that cognitive therapy provides for patients can mesh well with medication and 12-step meetings. The main variable that seems to influence whether or not patients avail themselves of all of these treatment opportunities (once they have been presented to the patients in a feasible manner) is not the practical compatibility of the treatments, but rather the attitudes of the treatment providers] At present, an earlier draft of this book is serving as a treatment manual in a National Institute on Drug Abuse collaborative, multisite study on the respective efficacy of cognitive therapy, supportive- expressive therapy, and general drug counseling. Data obtained from this project will help us to answer two important questions: (1) Does Cognitive Therapy of Substance Abuse succeed as a manual for the train­ ing of competent cognitive therapists for patients with addictions? and (2) Do patients who receive the treatment outlined in the text make demonstrable and lasting gains? In order to answer these questions, therapists are provided with intensive supervision (note: the authors of this text serve in that role), complete with competency and adher­ ence ratings on a regular basis; treatment is not confounded with adjunct medications, urinalyses are routinely conducted, and a host of measures other than drug monitoring per se are being administered and evaluated (to examine changes in mood and global adaptational functioning). Drug abuse is a sociological problem as well as a psychological issue. Factors such as poverty and lack of adequate educational and Preface xi vocational opportunities play a role in the epidemic. However, we believe that it is harmful to assume that low socioeconomic status patients cannot be treated as effectively as those of higher socioeco­ nomic status. While social change is desirable, individual change is not necessarily dependent on it. W e are optimistic that cognitive ther­ apy can serve as an important individual-focused treatment in today's society, and that the data will support this. A c k n o

w l e d g m e n t s w w e would like to offer our thanks to our highly esteemed colleagues in the field of substance abuse treatment and research, Drs. Dan Baker, Lino Covi, Tom Horvath, Jerome Piatt, Hal Urschel, David Wilson, and Emmett Velten, for their extremely help­ ful insights and suggestions on earlier versions of this manuscript. Special thanks are due Dr. Kevin Kuehlwein, an important member of our own cognitive therapy team in Philadelphia, for his thorough evaluations and editorial work on many of the chapters in this book. The input of all of the above has been invaluable during the course of this project. W e would also like to offer our thanks and apprecia­ tion to Tina Inforzato, who did yeoman work in typing this volume, and its many revisions. Without her tireless efforts, this volume would still be "on the drawing board." Xll C o n t e n t s CHAPTER 1 Overview of Substance Abuse 1 CHAPTER 2 Cognitive Model of Addiction 22 CHAPTER 3 Theory and Therapy of Addiction 42 CHAPTER 4 The Therapeutic Relationship and Its Problems 54 CHAPTER 5 Formulation of the Case 80 CHAPTER 6 Structure of the Therapy Session 97 CHAPTER 7 Educating Patients in the Cognitive Model 112 CHAPTER 8 Setting Goals 121 CHAPTER 9 Techniques of Cognitive Therapy 135 CHAPTER 10 Dealing with Craving/Urges 157 CHAPTER 11 Focus on Beliefs 169 CHAPTER 12 Managing General Life Problems 187 CHAPTER 13 Crisis Intervention 211 CHAPTER 14 Therapy of Depression in Addicted Individuals 226 CHAPTER 15 Anger and Anxiety 242 CHAPTER 16 Concomitant Personality Disorders 268 CHAPTER 17 Relapse Prevention in the Cognitive Therapy 292 of Substance Abuse Append ixes 311 References 331 Index 347 xm C H A P T E R 1 O v e r v i e w o f S u b s t a n c e A b u s e T .he fabric of America is profoundly affected by problems of subsAtahnc(e abuse. They are problems that directly affect those millions of Americans who suffer from substance abuse and indirectly touch the lives of millions more in the larger social and vocational networks around them. One in every ten adults in this country has a serious alcohol problem (Institute of Medicine [lOM], 1987) and at least one in four is addicted to nicotine (Centers for Disease Control [CDC], 1991a). Approximately 1 in 35 Americans over the age of 12 abuses illicit drugs (lOM, 1990a). This level of substance abuse has profound social, medical, and psychological ramifications on both the individual and the larger societal levels. The C D C (1991b), for example, estimate that approximately 434,000 people in this coun­ try die each year as a result of cigarette smoking, and many thou­ sands also die as a result of alcoholism (lOM, 1987) and/or illicit drug abuse (lOM, 1990a). It must be emphasized, however, that substance abuse spans many more areas and the toll taken is far greater than these simple mortality figures convey. In this introductory chapter we set the stage for the cognitive therapy of substance abuse. W e begin with an overview of psycho-v active substances and substance abuse, we briefly review the history of psychoactive substance use, we describe the most commonly used and abused psychoactive substances, we discuss cognitive models for understanding substance abuse and relapse, and we scan traditional methods for treating substance abuse. 2 COGNITIVE THERAPY OF SUBSTANCE ABUSE BACKGROUND: PSYCHOACTIVE SUBSTANCES AND SUBSTANCE ABUSE Psychoactive substances are chemicals that affect the central nervous system, altering the user's thoughts, moods, and/or behaviors. The revised third edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-lIl-R; American Psychiatric Associa­ tion [APA], 1987) categorizes psychoactive substances into 10 classes: alcohol; amphetamines or similarly acting sympathomimetics; can­ nabis; cocaine; hallucinogens; inhalants; nicotine; opioids; phencycli- dine (PCP) or similarly acting arylcyclohexylamines; and sedatives, hypnotics, or anxiolytics. Each of these substances has unique prop­ erties and effects. Some substances that are abused have low addic­ tive potential (e.g., hallucinogens), while others have high addictive potential (e.g., crack cocaine). Some are typically smoked (e.g., nico­ tine, cannabis, and crack cocaine); others are ingested orally (e.g., hallucinogens and sedatives); while still others are taken intranasally (e.g., powdered cocaine and inhalants). Some drugs lead the user to feel "up" or energized (e.g., amphetamines and cocaine); some cause the user to feel "down" or relaxed (e.g., sedatives, hypnotics, and anxiolytics); while others (e.g, alcohol and nicotine) simultaneously have both effects on the user. DSM-III-R distinguishes between substance abuse and dependence. Abuse is defined as a maladaptive pattern of psychoactive substance use while dependence (considered more serious than abuse) is defined as "impaired control of use" (i.e., physiological addiction). In this volume, we do not go to great lengths to emphasize this distinction. Instead, we view any pattern of psychoactive substance use as prob­ lematic and requiring intervention if it results in adverse social, voca­ tional, legal, medical, or interpersonal consequences, regardless of whether the abuser experiences physiological tolerance or withdrawal. Further, although we caution against an all-or-none view of addic­ tion and recovery, and although we acknowledge that some patients seem to be more successful at engaging in controlled, moderate sub­ stance use than are others, we advocate a program of treatment that strives for abstinence. In this manner we maximize the patients' chances of maintaining an able and responsible lifestyle, reduce the risk of relapse, and avoid giving patients the false impression that we view a mere reduction in drug use as the optimal outcome. History of Psychoactive Substance Use Psychoactive substances have been used by most cul­ tures since prehistoric times (Westermeyer, 1991). In fact, for centuries Overview 3 psychoactive substances have served many individual and social func tions. O n an individual level, they have provided stimulation, relief from adverse emotional states and uncomfortable physical symptoms, and altered states of consciousness. O n a social level, psychoactive substances have facilitated religious rituals, ceremonies, and medical functions. Egyptian and Chinese opiate use was evident from the earliest writings of these people (Westermeyer, 1991). Marijuana was referenced in India "as far back as the second millennium B.C." (Brecher, 1972, p. 397). Evidence of Mayan, Aztec, and Incan medici­ nal and ritual drug use was evident from their statues and from draw­ ings on their buildings and pottery (Karan, Haller, & SchnoU, 1991; Westermeyer, 1991). Alcohol use goes back to paleolithic times (Good­ win, 1981) and Mesopotamian civilization gave one of the earliest clinical descriptions of intoxication and hangover cures. In modern times the World Health Organization (WHO) has been concerned about drug and alcohol abuse problems on a worldwide scale (Grant, 1986). As early as 1968 the W H O conducted an interna­ tional study of drug use in youth (Cameron, 1968), and in a more recent study (Smart, Murray, & Arif, 1988) drug abuse and preven­ tion programs in 29 countries were reviewed. However, Smart and his colleagues concluded from their review that "the seriousness of the drug problem is well recognized in some countries but not in oth­ ers" (p. 16). Presently the W H O is addressing the issue of alcohol- related problems by developing an international secondary preven­ tion protocol (Babor, Korner, Wilber, & Good, 1987). Drug policies in the United States have been profoundly affected by historical and sociocultural attitudes regarding psychoactive drugs on a spectrum from less restrictive (e.g., libertarian) to more restrictive (i.e., criminal). Between the late 1700s and the late 1800s, for example, psychoactive dnigs (especially narcotics) were widely used in the United States. In fact, Musto (1991) reported that opium and cocaine were legally available during this time from "the local dmggist." A Consumers Union report (Brecher, 1972) described the nineteenth century as "a dope fiend's paradise" due to such minimal restrictions. In the late 1800s and the early 1900s, medical conceptualizations of addiction began to develop, however, influenced to some extent by Dr. Benjamin Rush's (1790) ear­ lier interest in the course of addictions. Magnus Huss, a Swedish physi­ cian, first used the term "alcoholism" in 1849 (lOM, 1990b). At the same time (late 1800s and early 1900s), criminalization of drug use was m- creasingly becoming U.S. policy. In the 1960s and 1970s, however, atti­ tudes about drugs became less restrictive as U.S. sociopolitical attitudes generally became more liberal. Simultaneously, the disease model of addictions was gaining widespread acceptance, partly due to the work ofjellinek(1960). 4 COGNITIVE THERAPY OF SUBSTANCE ABUSE Since the 1980s, the United States has again become less toler­ ant and more restrictive about drugs. At least two explanations can account for this phenomenon: (1) The negative effects of drugs on individuals, families, and society have become more apparent with increased use, and (2) sociopolitical attitudes in the United States generally have become more conservative. At the same time, however, there is increasing controversy about the disease model of addiction ("Current Disease model," 1992; Fingarette, 1988; Peele & Brodsky, with Arnold, 1991) and the criminalization of psychoactive substances (R. L. Miller, 1991). The Most Commonly Used Drugs Alcohol Alcohol is simultaneously a chemical, a beverage, and a drug that "powerfully modifies the functioning of the nervous sys­ tem" (Levin, 1990, p. 1). Approximately 1 0 % of Americans in the United States have a serious drinking problem; 6 0 % are light to mod­ erate drinkers; and the remaining 3 0 % of adults in the United States do not consume any alcohol. Alcohol abuse, however, accounts for approximately 8 1 % of hospitalizations for substance abuse disorders (lOM, 1987). Remarkably, half the alcohol consumed in this country is consumed by the 1 0 % who are heavy drinkers. A larger percentage of men than women drink and a greater percentage of men than women are heavy drinkers. Alcohol initially acts as a general anesthetic, interfering with subtle functions of thought, reason, and judgment (Miller & Munoz, 1976). As blood alcohol concentration (BAC) increases, however, the effects become more intense until gross motor functioning is also affected. At still higher BAC levels, sleep is induced, and ultimately death may occur as a result of respiratory depression. "Alcohol affects almost every organ system in the body either directly or indirectly" (National Institute of Alcohol Abuse and Alco­ holism [NIAAA], 1990, p. 107). Thus with chronic use, alcohol can cause serious multiple medical problems, including damage to the liver, pancreas, gastrointestinal tract, cardiovascular system, immune system, endocrine system, and nervous system. Alcohol has also been strongly linked to the leading causes of accidental death in the United States: motor vehicle accident, falls, and fire-related injuries. Further­ more, approximately 3 0 % of suicides and half of all homicides are alcohol related (lOM, 1987), and estimates of annual deaths related to alcohol use range between 69,000 and 200,000 per year (lOM, Overview 5 1987). In addition, a significant percentage of both violent and non violent crimes are committed under the influence of alcohol (cf. McCord, 1992). Chronic alcohol use can also have other profound negative social consequences, including loss of career, friends, and family. A great deal of physical and sexual abuse, for example, is related to the intoxicated state of the offender (Clayton, 1992; Frances & Miller, 1991; Harstone & Hansen, 1984), and general family dys­ function often is associated with the alcoholism of one or more adult members (Heath & Stanton, 1991). Medical complications can even reach insidiously into the next generation, in that maternal drinking during pregnancy can cause fetal alcohol syndrome and other seri­ ous birth defects. In fact, "prenatal alcohol exposure is one of the leading known causes of mental retardation in the western world" (NIAAA, 1990, p. 139). Illicit Drugs According to the lOM (1990a), at least 14 million persons consume illicit drugs monthly. During peak months this fig­ ures climbs to more than 25 million users. It is estimated that approxi­ mately 2.3% of the U.S. population over 12 years old has an illicit drug problem sufficiently serious to warrant treatment. This statistic is substantially higher, however, for individuals who are incarcerated (33%) or on parole or probation (25%). W h e n these people are included in the epidemiologic data, the estimate of illicit drug use problems in the overall population increases to 2.7%. Regarding

the social costs of illicit drug abuse, it is estimated that more than 2 5 % of property crimes and 1 5 % of violent crimes are related to illicit drug use by the criminal. Financial losses related to these crimes have been estimated at $1.7 billion per year. Homicides are also strongly linked to activities surrounding drug dealing. Approx­ imately 1 4 % of homicides per year are causally related to drugs. The costs for criminal justice activities directed against drug trafficking on the federal level were approximately $2.5 billion in 1988, com­ pared to $1.76 billion spent in 1986. In the following sections we present brief descriptions of the three most commonly used illicit drugs: marijuana, cocaine, and the opioids. In 1972, a Consumers Union report identified marijuana as the fourth most popular psychoactive drug in the world, after caffeine, nicotine, and alcohol (Brecher, 1972, p. 402). Although marijuanas use has declined since its peak in 1979, it still remains the most widely used illicit drug in Western society (APA, 1987; Weiss & Millman, 1991). 6 COGNITIVE THERAPY OF SUBSTANCE ABUSE Marijuana is typically smoked, although it can also be ingested. According to Weiss and Millman (1991), in spite of its generally sedat­ ing effects, marijuana's psychoactive effects in the user are quite varied, "profoundly dependent upon the personality of the user, his or her expectation, and the setting" (p. 160). The health effects of marijuana have been widely debated and remain quite controversial, probably due to the inconsistent effects of the drug on the individual user and across different users. For some time marijuana was considered relatively safe and nonaddictive (Brecher, 1972). Presently, however, it is associated with multiple adverse physical and psychological effects, including labile affect and depression, amotivational syndrome, impaired short-term memory, and pulmonary disease (Weiss & Millman, 1991). According to DSM- III-R, marijuana dependence is characterized by heavy use of the drug (e.g., daily) with substantial impairment. Marijuana dependence also puts one at risk for other psychological problems, as those who are dependent on cannabis are also likely polysubstance abusers or afflicted with other psychiatric disorders (APA, 1987; Weiss & Millman, 1991). Cocaine is a major central nervous system stimulant that produces euphoria, alertness, and a sense of well-being. It may also lower anxi­ ety and social inhibitions while increasing energy, self-esteem, and sexuality. Presently cocaine is among the most widely used illicit drugs. In fact, cocaine use increased in 1991, "despite the Bush adminis­ tration's three-year war against drugs" (Mental Health Report, 1992, p. 5). Clearly, for many people the positive short-term physiological and psychological effects of cocaine maladaptively supersede the dan­ gers associated with acquiring and using the drug. According to Gawin and EUinwood (1988), "The pursuit of this direct, pharmacologically based euphoria becomes so dominant that the user is apt to ignore signs of mounting personal disaster" (p. 1174). Cocaine is an alkaloid (as are caffeine and nicotine) which is extracted from the coca leaf. In its pure form, raw coca leaves can be chewed, although this practice is generally limited to native popula­ tions in the cocaine-producing countries (APA, 1987). In the United States, cocaine is most commonly taken intrana­ sally (i.e., snorted or "tooted") in the powder form of cocaine hydro­ chloride. In this form, the user pours the powder on a hard surface and then arranges it into "lines," one of which is snorted into each nostril (Karan et al., 1991). In powdered form, cocaine hydrochloride can also be mixed with water and administered by intravenous injec­ tion. This process is known as "shooting" or "mainlining" (Karan et al., 1991). Intravenous injection of cocaine results in intense sub­ jective and physiologic effects within 30 seconds Oones, 1987). Overview 7 Cocaine can also be smoked as a paste or in alkaloid form (i.e., "freebased"). In this form it also produces its effects within seconds. Crack cocaine (named for the sound made by the cocaine as it is freebased) is the currently popular form of freebase which is sold in relatively inexpensive, prepackaged, and ready-to-use small doses (Karan et al., 1991). According to Karan et al. (1991), low-cost crack, approximately $2-$ 10 per vial, "has been widely available on the streets in many American cities since 1985" (p. 125), making it easily within the financial grasp of most teenagers and even the impover­ ished. Adding to this high availability is the especially troublesome fact that crack cocaine produces an enormously intense and almost instant high. Crack cocaine is, therefore, extremely addictive, lead­ ing to significant impairment in life functioning after only a few weeks' use on average (Gawin & EUinwood, 1988; Smart, 1991), much faster than, for example, intranasal usage of cocaine. These charac­ teristics of crack cocaine make it especially prone to rapid increase in the prevalence of its abuse. Indeed, many observers suggest that cocaine use has already reached epidemic levels (Weinstein, Gottheil, & Sterling, 1992). In the popular press, for example, a graphic biographical Reader's Digest article describes cocaine as "the devil within" (Ola & D'Aulaire, 1991). This contrasts starkly with the glorification of cocaine in movies and songs of the 1970s and early 1980s, when cocaine was seen as the drug of choice of the affluent and powerful. In the scientific litera­ ture, Gawin and EUinwood (1988) explain that "believing that the drug was safe, millions of people tried cocaine, and cocaine abuse exploded" (p. 1173). These authors report that 1 5 % of Americans have tried cocaine, and 3 million people had abused cocaine regularly by 1986, resulting in "more than five times the number addicted to heroin" (p. 1173). Smart and Adlaf (1990) report also that an increasing num­ ber of cocaine abusers have sought treatment since the 1980s. Cohen (1991) attributes the "cocaine outbreak" to supply factors (e.g., low cost, availability, and high profitability), external factors (e.g., peer pressure and media portrayals of drug usage), internal factors (e.g., hedonism, sociopathy, depression, and life stress), and intrinsic drug factors (e.g., "the pharmacologic imperative"). Strikingly, cocaine abuse occurs and persists in spite of dramatic medical problems that are associated with its use: central nervous system damage, cardiac arrest, stroke, respiratory collapse, severe hypertension, exacerbation of chronic diseases, infection, and psychiatric complications (Estroff, 1987). Because cocaine abuse research has produced fewer pharma­ cological treatment alternatives than has research on some other illicit drugs such as heroin (Alterman, O'Brien, & McLellan, 1991; Covi, Baker, & Hess, 1990; Stine, 1992), and because of the extent and 8 COGNITIVE THERAPY OF SUBSTANCE ABUSE severity of cocaine-related problems, we have placed proportionatel greater emphasis on cocaine and crack cocaine than on other drugs in this treatment manual. The opioids, including heroin, methadone, and codeine, are drugs that pharmacologically resemble morphine. Drugs in this class pro­ duce feelings of euphoria, relaxation, and mood elevation. They also have the potential for reducing pain, anxiety, aggression, and sexual drives (lOM, 1990a), and are considered highly addictive. According to Thomason and Dilts (1991): Opioids have the capacity to commandeer all of an individual's attention, resources, and energy, and to focus these exclusively on obtaining the next dose at any cost. This vicious cycle repeats itself every few hours, 24 hours a day, 365 days a year, for years on end. Comprehending the implications of opioid abuse shocks and stag­ gers the inquiring mind. (p. 103) Although the use of pharmacologic agonists such as methadone (and antagonists such as naltrexone) traditionally has represented an important component of treatment in the heroin abuser, methadone itself is unfortunately subject to various forms of abuse (e.g., black market dealings or use with other drugs). Further, many heroin abusers find methadone to be inferior to the "real stuff," leading to high noncompliance and dropout (Grabowski, Stitzer, & Henningfield, 1984) rates with these programs. Therefore, we posit that pharmaco­ logic approaches (even for heroin) represent an incomplete treatment strategy unless utilized in combination with psychosocial approaches such as support groups and cognitive therapy. Nicotine Cigarette smoking is by far the single most prevent­ able cause of death in the United States. In fact, it has been estimated that 434,000 people died in 1988 due to cigarette smoking (CDC, 1991b). This figure includes those who died of cancer, lung disease, heart disease, house fires caused by careless smoking, and renal and pancreatic disease. Approximately 49.4 million Americans (28.1%) are regular cigarette smokers (CDC, 1991a), despite the fact that cigarette smoking is known to be a leading cause of morbidity and mortality in this country. Since the mid-1970s, however, the number of smokers has admit­ tedly decreased steadily. Historically, more men than women have smoked; however, a higher proportion of men than women have also quit smoking. It has thus been projected that by the year 1995, more Overview 9 women than men will be smokers. Ironically, in spite of cigarettes' historical and advertising linkage with status, wealth, and desirabil­ ity, it is increasingly the case that the socially disadvantaged are over- represented as smokers. The number of minorities, poor, and less educated people who smoke, for example, has been disproportionately higher than those who do not smoke, and this trend is expected to continue (Pierce, Flore, & Novotny, 1989). Nicotine is the psychopharmacologically addictive ingredient in cigarettes. As mentioned earlier, nicotine dependence is included in DSM-III-R, along with the dependence on other psychoactive sub­ stances (alcohol, opiates, cocaine, etc.). Not surprisingly, we have found the addictive process in cigarette smoking to be analogous to the addictive process involved in the other psychoactive substances. Therefore, although nicotine addiction is not associated with the same degree of social, vocational, and legal consequences as is addiction to illicit drugs, its medical hazards and the fact that early-life regular smoking often leads to addiction to "harder" substances (Henning­ field, Clayton, & Pollin, 1990) make it an important area for mental health intervention. Although this volume focuses relatively little on methods specifically geared to smoking cessation, we believe that the same principles of assessment and treatment (e.g., coping with crav­ ings and modifying beliefs) that we outline in this book are highly applicable to the patient addicted to nicotine. Polysubstance Abuse Individuals abusing one psychoactive substance are likely to be simultaneously abusing another substance. In fact, between 2 0 % and 3 0 % of alcoholics in the general public and approxi­ mately 8 0 % in treatment programs are dependent on at least one other drug. A prevalent combination is alcohol, marijuana, and cocaine (N. S. Miller, 1991, p. 198). N S Miller (1991) explains that polysubstance abuse occurs tor multiple reasons. For example, some drugs enhance the effects of other drugs, while some drugs are used to avoid unwanted side effects of other drugs. Some drugs are used to treat drug withdrawal effects of other drugs and, similarly, some drugs are used as substihites for other '^'"^The medical and psychological correlates of polysubstance abus are numerous (N. S. Miller, 1991). They include problems associated with each individual drug (e.g., liver and heart disease associated with alcohol abuse), as well as those more commonly associated with multiple substances (e.g., interaction-induced overdose). 10 COGNITIVE THERAPY OF SUBSTANCE ABUSE Dual Diagnosis: Substance Abuse and Other Psychiatric Disorders The coexistence of substance abuse with other psy­ chiatric disorders is also very common (e.g., Ananth et al., 1989; Brown, Ridgely, Pepper, Levine, & Ryglewicz, 1989; Bunt, Galanter, Lifshutz, & Castaneda, 1990; Davis, 1984; Hesselbrock, Meyer, & Kenner, 1985; Kranzler & Liebowitz, 1988; Nace, Saxon, & Shore, 1986; Nathan, 1988; Penick et al., 1984; Regier et al., 1990; Ross, Glaser, & Germanson, 1988; Schneier & Siris, 1987). In a survey of more than 20,000 Americans conducted by Regier et al. (1990) it was found that individuals with psychiatric disorders were 2.7 times as likely to have alcohol or other drug problems, compared to those without psychi­ atric disorders. In fact, 3 7 % of individuals with substance use disor­ ders had coexisting Axis I mental disorders. From these data it appears that individuals with substance abuse problems should benefit most from therapeutic interventions that simultaneously address their other psychiatric disorders. Cognitive therapy is ideally suited for these individuals, since it has been devel­ oped and tested on patients with depression, anxiety, and personal­ ity disorders (see Hollon & Beck, in press, for a most recent compre­ hensive review).

In fact, an important component of cognitive therapy involves the case conceptualization (Persons, 1989), defined as the evaluation and integration of historical information, psychiatric diag­ nosis, cognitive profile, and other aspects of functioning (see Chap­ ter 5, this volume, for a detailed description of the case conceptual­ ization). When a coexisting psychiatric syndrome is found to exist with a dmg or alcohol abuse patient, for example, the therapist focuses simultaneously on substance abuse and the symptoms of the psychi­ atric syndrome as well as on any factors of interaction (see Chapters 14, 15, and 16, this volume, for more on the treatment of patients with dual diagnoses). RELAPSE P R E V E N T I O N Substance abuse and dependence are characterized both by remission and by relapse. In a classic review by Hunt, Barnett, and Branch (1971) it was found that heroin, nicotine, and alcohol were all associated with similar high rates and patterns of relapse (p. 455; see Figure 1.1). These investigators found that two-thirds of individuals treated had relapsed within 3 months. Many investigators have speculated about the meaning of these findings, most inferring Overview 11 RELAPSE RATE OVER TIME •----•HEROIN ASMOKING OALCOHOL 2weeksJ 6 101112 MONTHS FIGURE 1.1. Relapse rate over time for heroin, smoking, and alcohol addic­ tion. From Hunt, Barnett, and Branch (1971), p. 456. Copyright 1971 by Clinical Psychology Publishing Co., Inc. Reprinted by permission. that they reflect common processes that underlie the addictions. In fact, since the publication of Hunt et al.'s (1971) data, addiction experts have focused on developing and testing comprehensive models of addiction that include all the psychoactive substances, as well as gambling and binge eating. Marlatt and his colleagues (Brownell, Marlatt, Lichtenstein, & Wilson, 1986; Marlatt, 1978; Marlatt, 1982; Marlatt & Gordon, 1985) have made an important contribution to the addiction literature with their cognitive-behavioral model of relapse prevention. According to Marlatt and Gordon's (1985) model (see Figure 1.2), individuals view themselves as having a sense of perceived control or self-efficacy. When they are faced with high-risk situations, this sense is threat­ ened. High-risk situations for the drug abuse patient might include negative or positive emotional or physical states, interpersonal con­ flicts, social pressure, or exposure to drug cues. Individuals faced with high-risk situations must respond with coping responses. Those who have effective coping responses develop increased self-efficacy, result­ ing in a decreased probabiHty of relapse. Those who have relatively fewer coping responses or none at all may experience decreased self- 12 COGNITIVE THERAPY OF SUBSTANCE ABUSE Coping Increased Decreased response self-efficacy probability of relapse Higii-risk situation Decreased Abstinence self-efficacy violation No Initial effect: Increased coping Positive use of probability response outcome substance Dissonance conflict of expectancies and relapse (for initial self-attribution effects of (guilt and perceived substance) loss of control) F I G U R E 1.2. Model of relapse process. From Mariatt and Gordon (1985), p. 38. Copyright 1985 by The Guilford Press. Reprinted by permission. efficacy and increased positive o u t c o m e expectancies about the effects of the drug, followed b y a "lapse" or initial use of a substance. This initial use mi g h t result in w h a t Marlatt calls a n Abstinence Violation Effect (AVE; i.e., perceived loss of control) and a n ultimately increased probability of relapse. T h e w o r k of Marlatt and his colleagues has h a d a profound effect o n knowledge about addictive behaviors. In fact, m o s t current text­ books o n addictions n o w deal with the issue of relapse prevention in some way. Although most of the work on relapse prevention has been generated within the cognitive-behavioral model (e.g., Chiauzzi, 1991), various 12-step programs (e.g. Alcoholics Anonymous) and other advocates of the disease model have recently also increased their emphasis on relapse prevention (e.g., Gorski & Miller, 1986). MODELS OF ADDICTION Numerous theoretical models have been developed to explain addictive behaviors (see Baker, 1988; Blane & Leonard, 1987, for recent reviews). As previously mentioned, the dominant trend Overview 13 among addiction experts is toward developing comprehensive theo­ retical models that explain all addictions. Cognitive Models of Addiction A variety of related cognitive models of addiction have been developed and evaluated (e.g., Abrams & Niaura, 1987; Marlatt, 1978, 1985; McDermut, Haaga, & Shayne, 1991; Stacy, Newcomb, & Bentler, 1991; Tiffany, 1990; Wilson, 1987a, 1987b) since Bandura's (1969, 1977) classic presentations of cognitive social learning theory. Marlatt (1985) describes four cognitive processes related to addictions that reflect the cognitive models: self-efficacy, outcome expectancies, attributions of causality, and decision-making processes. Self-efficacy refers to one's judgment about one's ability to deal com­ petently with challenging or high-risk situations. Examples of high self-efficacy beliefs include the following: "1 can effectively cope with temptations to use drugs" or "1 can say 'no' to drugs." Examples of low self-efficacy beliefs might include the following: "I'm a slave to drugs," "I can't get through the day without drugs," or "I can't get what I want, so I might as well use drugs." Marlatt (1985) explains that low levels of self-efficacy are associated with relapse and high levels of self-efficacy are associated with abstinence. Marlatt (1985) also explains that self-efficacy increases as a function of success; to the extent that individuals effectively choose not to use drugs, they will experience an increased sense of self-efficacy, for example, believ­ ing that their sense of pride is greater than their need for a "high." Outcome expectancies refer to an individual's anticipation about the effects of an addictive substance or activity. Positive outcome expectancies might include the following beliefs: "It will feel great to party tonight," or "I won't feel so tense if I use." To the extent that one expects a greater positive than negative outcome from using drugs, one is likely to continue using. Attributions of causality refer to an individual's belief that drug use is attributable to internal or external factors. For example, an individual might believe the following: "Anybody who lives in m y neighborhood would be a drug user" (external factor), or "I am physi­ cally addicted to alcohol and m y body can't survive without it" (inter­ nal factor). Marlatt (1985) explains that such beliefs most likely would result in continued substance use, since the individual perceives his/ her use to be predestined and out of control. For example, the AVE is an individual's tendency to believe that he/she is unable to control substance use after an initial lapse. That is, the AVE occurs when an individual has had a "lapse" or "slip" (i.e., has used a drug after being 14 COGNITIVE THERAPY OF SUBSTANCE ABUSE abstinent for some time) and attributes this lapse to a "lack of w power" (i.e., an internal causal factor). Under such circumstances, this individual is likely to continue using, resulting in a full-blown relapse. This is analogous to Beck's (1976) description of all-or-none think­ ing; for example, "I've blown it, so I might as well keep using." Marlatt (1985) also describes substance abuse and relapse as a cognitive decision-making process. He demonstrates (with an amus­ ing example) that substance use is a result of multiple decisions (like forks in the road) which, depending on the decisions, may or may not lead to further substance use. He further explains that some deci­ sions initially appear to be irrelevant to substance use ("apparently irrelevant decisions"); however, these decisions ultimately may result in a greater likelihood of relapse because of their incremental push toward higher-risk situations. In his example, Marlatt "innocently" chooses to sit in the smoking section of an airplane after being absti­ nent from smoking for several months. As a result of this decision he is more vulnerable to relapse (by his exposure to other smokers, their smoke, and their offers of cigarettes to him). W e see this same phenomenon in patients who claim to have had every intention of remaining abstinent from alcohol and illicit drugs, only to bhthely accept an invitation to meet a friend at a local tavern, or to cavalierly choose to drive out of the way in order to go past a street corner where drugs are sold. When such patients lapse into alcohol and drug use, it is striking to see how they fail to realize the ways in which they set themselves up for a fall with their decisions that lead up to the actual using incident. Unfortunately, the cognitive models of substance abuse have not been integrated adequately into many addiction treatment programs (lOM, 1990a; Miller & Hester, 1985). This volume provides a focused, step-by-step treatment based on Beck's (1976) cognitive model. It is our hope that the chapters that follow will stimulate increased appli­ cation of this cognitive model to substance abuse treatment across treatment settings and modalities. The Motivation to Change Efforts to examine the treatment of addictions are incomplete without considering the issue of motivation. Miller and Rollnick (1991) address this issue, explaining that most addicts are genuinely ambivalent about changing (rather than resistant, weak- willed, or characterologically flawed). The authors view motivation as a "state of readiness or eagerness to change, which may fluctuate from one time or situation to another" (p. 14). Overview 15 Prochaska, DiClemente, and Norcross (1992) provide a compre­ hensive model for conceptualizing patients' motivation for change. In their work, Prochaska et al. (1992) identify five stages of change: precontemplation, contemplation, preparation, action, and mainte­ nance. In the precontemplation stage, individuals are least concerned with overcoming their problems and they are least motivated to change problematic behaviors. In the contemplation stage individuals are willing to examine the problems associated with their substance use and consider the implications of change, although they may not take any constructive action. They are also likely to respond more positively to confrontation and education, although they may still be ambivalent. In the preparation stage, patients wish to make actual changes and therefore desire help with their problems, although they may feel at a loss as to how to do what is necessary to become drug free. In the action stage individuals have made a commitment to change and they have begun to actually modify behaviors. Prochaska et al. (1992) point out that this is a particularly stressful stage, which may require considerable therapist support and encouragement. In the maintenance stage individuals attempt to continue the process begun in the contemplation and action stages. In recent years, with so much emphasis placed on relapse prevention, the maintenance stage has received increased attention. Prochaska and DiClemente (1986) caution that the process of change is very complex. They explain that "most individuals do not progress linearly through the stages of change" (p. 5). Alternatively, they offer a "revolving door model" (p. 6), based on the assumption that individuals make multiple revolutions around the circle of stages prior to achieving their long-term goals. Furthermore, they observe that some individuals "get stuck" in the earlier stages of change. In the words of Prochaska and DiClemente (1986), "Therapy with addictive behaviors can progress most smoothly if both the client and the therapist are focusing on the same stage of change" (p. 6). To use nicotine dependence as an example, a smoker in the precontemplation stage will benefit little from advice about specific strategies for quit­ ting smoking. The same smoker, however, might respond well to general questions about health maintenance, which might lead to a discussion of the health effects of smoking, which might lead further to a discussion of the benefits of quitting, which eventually might lead to a discussion of specific strategies. It is clear that the field can benefit from an understanding of what makes a patient ready to seek help (Tucker & Sobell, 1992). The Prochaska et al. (1992) stage model is a useful heuristic. However, it is important to note that patients in a precontemplative 16 COGNITIVE THERAPY OF SUBSTANCE ABUSE Stage of change are not impossible to treat (especially if they ar court order to attend therapy). Conversely, patients in the action phase or maintenance phases are not guaranteed to succeed in treatment. The same degrees of vigilance and commitment are required of the cognitive therapist regardless of the substance abuse patient's stage of change. Treatment Outcome Goals Some models of addiction (e.g., Alcoholics Anony­

mous and other disease-model programs) view total abstinence as the only acceptable goal of treatment. Proponents of these models view addiction as an all-or-nothing phenomenon, with any use seen as pathological and abstinence considered a state of "recovering" (rather than "recovered"). Alternatively, proponents of cognitive-behavioral models are more likely to view light or moderate use (i.e., "controlled drinking") as an acceptable goal of treatment in some cases. At one time controlled drinking was extremely controversial (Marlatt, 1983). Presently, however, it is generally accepted that the goals of treatment should vary according to the patient's needs, prob­ lems, and previous response to treatment. Sobell, Sobell, Bogardis, Leo, and Skinner (1992), for example, surveyed problem drinkers to deter­ mine their preference for self-selected versus therapist-selected treat­ ment goals (e.g., abstinence vs. controlled drinking). They found that most respondents preferred setting their own goals and believed that they would be more likely to achieve them; respondents with more serious drinking problems were even more likely to favor self-set goals. In general, we favor a collaborative approach in setting goals with patients. Therefore, to the extent that allowing severely addicted patients to set the modest goal of substance use reduction succeeds in getting otherwise resistant patients engaged in a more complete course of therapy, we are in favor of a controlled substance use approach. In the long run, however, we strongly advocate assisting patients in becoming drug- and alcohol-free. THE TREATMENT OF SUBSTANCE ABUSE A N D DEPENDENCE In reality, most substance abuse treatment programs are eclectic in theory and practice, and they include varying degrees of inpatient and outpatient services, 12-step program attendance, education, psychotherapy, family therapy, support groups, pharmaco- Overview 17 therapy, and so forth. In our view, cognitive therapy can be compat ible with any of these approaches. In fact, many of our drug and alcohol abuse patients attend support groups, have had inpatient detoxification, and take medication. The special strengths that cog­ nitive therapy adds to this battery of approaches are its emphasis on (1) the identification and modification of beliefs that exacerbate crav­ ings, (2) the amelioration of negative affective states (e.g., anger, anxi­ ety, and hopelessness) that often trigger drug use, (3) teaching patients to apply a battery of cognitive and behavioral skills and techniques, and not just willpower, to become and remain drug-free, and (4) help­ ing patients to go beyond abstinence to make fundamental positive changes in the ways they view themselves, their life, and their future, thus leading to new lifestyles. In the following section we present a brief overview of more tra­ ditional treatments of substance abuse and dependence. Alcoholism Treatment Miller and Hester (1980, 1986) have conducted exhaustive reviews of the alcoholism treatment literature. These authors have examined nine major classes of interventions. The four most common were pharmacotherapy, psychotherapy or counseling. Alcoholics Anonymous, and alcoholism education. The five less com­ monly employed approaches included family therapy, aversion thera­ pies, operant methods, controlled drinking, and broad spectrum treat­ ment. Miller and Hester (1986) conclude from their reviews that alco­ holism treatment is best approached as a two-stage process, requir­ ing different interventions at each stage. The first set of interventions should be focused on changing drinking behaviors to abstinence or moderation (e.g., behavioral self-control training). The second set of interventions should be focused on maintenance of sobriety (e.g., social skills training in order to increase confidence in relating to drug- free people). Miller and Hester (1986) also draw some disturbing conclusions, however, about the poor relationship between empirical research and traditional inpatient treatment approaches. Treatment methods that are supported by controlled research include aversion therapies, behav­ ioral self-control training, community reinforcement, marital and family therapy, social skills training, and stress management, whereas approaches actually currently employed as standard practice in alco­ holism programs include Alcoholics Anonymous, alcoholism educa­ tion, confrontation, disulfiram, group therapy, and individual coun- 18 COGNITIVE THERAPY OF SUBSTANCE ABUSE seling. They point out that there is little apparent overlap betwe these lists: Alcoholism treatment programs in the United States do not tend to use treatment methods that have been validated by controlled outcome studies. Furthermore, Miller and Hester (1986) point out that traditional inpatient treatment programs are very expensive, "despite clear evidence that they offer no advantage in overall effectiveness" (p. 163). Concurring in this, McLellan et al. (1992) note that stan­ dard detoxification and "28-day programs" (in spite of their high costs) are insufficient to deal with long-term issues. Clearly, to help drug and alcohol patients deal with more enduring issues, these treat­ ments need to be supplemented with ongoing outpatient treatment that focuses on attitude change and skills acquisition. The Institute of Medicine recently commissioned a National Acad­ emy of Sciences committee to make an exhaustive critical review of the research literature on treatment for alcohol problems (1990b). The committee discovered that interventions included "a broad range of activities that vary in content, duration, intensity, goals, setting, pro­ vider, and target population" (p. 86). The committee's assessment was that "no single treatment approach or modality has been demonstrated to be superior to all others" (p. 86). Its conclusions, published in Broadening the Base of Treatment for Alcohol Problems (1990a), included the following: 1. There is no single treatment approach that is effective for all persons with alcohol problems. 2. The provision of appropriate, specific treatment modalities can substantially improve outcome. 3. Brief interventions can be quite effective compared with no treatment, and they can be quite cost-effective compared with more intensive treatment. 4. Treatment of other life problems related to drinking can improve outcome in persons with alcohol problems. 5. Therapist characteristics are partial determinants of outcome. 6. Outcomes are determined in part by treatment process factors, posttreatment adjustment factors, the characteristics of indi­ viduals seeking treatment, the characteristics of their problems, and the interactions among these factors. 7. People who are treated for alcohol problems achieve a con­ tinuum of outcomes with respect to drinking behavior and alcohol problems and follow different courses of outcome. 8. Those who significantly reduce their level of alcohol consump­ tion or who become totally abstinent usually enjoy improve­ ment in other life areas, particularly as the period of reduced consumpfion becomes more extended (pp. 147-148). Overview 19 The findings of the Institute of Medicine (1990a) coupled with those of Miller and Hester (1986) make it apparent that there is still a profound need for effective alcoholism treatment interventions. It is hoped that the principles introduced in this text will be integrated into, and evaluated in, traditional treatment programs in order to move toward more effective and appropriate alcoholism treatment programs. Illicit Drug Treatment In addition to its report on alcohol treatment pro­ grams, the Institute of Medicine appointed a separate committee (1990a) to review the treatment of drug problems in the United States. Specifically, the committee divided treatments into four classifications: methadone maintenance, therapeutic communities, outpatient non- methadone programs, and chemical dependency programs. These findings (1990a) were similar to those of Miller and Hester (1986). The most empirically validated programs have been metha­ done maintenance clinics for opioid dependency. Some evidence also supported the efficacy of therapeutic communities and outpatient nonmethadone treatment. Nonetheless, "Chemical dependency is the treatment with the highest revenues, probably the second largest number of clients, and the smallest scientific basis for assessing its effectiveness" (lOM, 1990a, p. 18). The Institute of Medicine acknowl­ edges that most of the studies on methadone maintenance were con­ ducted in the 1970s and early 1980s, however. As a result, research has insufficiently addressed the growing cocaine problems in this country. By contrast, this volume will focus heavily on the cognitive therapy of cocaine and crack cocaine addiction. Smoking Cessation Interventions In a report published by the National Cancer Insti­ tute, Schwartz (1987) critically reviewed the literature on smoking cessation interventions. He divided the various methods into 10 cate­ gories: (1) self-care, (2) educational approaches/groups, (3) medica- fion, (4) nicotine chewing gum, (5) hypnosis, (6) acupuncture, (7) physician counseling, (8) risk factor preventive trials, (9) mass media and community programs, and (10) behavioral methods. Schwartz (1987) found considerable variability in cessation rates among these methods. Approximately 1 million Americans per year quit smoking, and most do so on their own through "self-care." In fact, three-fifths of all smokers would prefer to quit on their own, rather than seek group 20 COGNITIVE THERAPY OF SUBSTANCE ABUSE quit-smoking programs (Schwartz, 1987). There are many self-help aids for those wishing to quit smoking, including books, pamphlets, audio cassettes, drug store preparations, correspondence courses, and so forth. Almost all self-care efforts and aids involve some cognitive techniques. In fact, those who successfully quit on their own have higher levels of success expectancy and self-efficacy (areas strongly affected by cognitive interventions) than those who are unsuccess­ ful. Approximately 16%-20% of smokers who quit on their own are abstinent at 1 year (Schwartz, 1987). For those who wish to receive assistance with smoking cessation, there are nonprofit and commercial clinics and groups available. Most of these utilize cognitive methods, including education, self-monitor­ ing, and modifying attitudes about smoking. In a review of 46 group smoking cessation programs, Schwartz (1987) found median cessation rates ranging from 2 1 % to 36%, depending on the length of follow- up and the time the study was conducted. A number of medications have also been tried as aids to smok­ ing cessation over the years. These have included lobeline, mepro- bamate, amphetamines, anticholinergics, sedatives, tranquilizers, sym­ pathomimetics, anticonvulsants, buspirone, propranolol, clonidine, nicotine polacrilex, and most recently transdermal nicotine. Of these, the most promising medications have been those that replace the nicotine from cigarettes with prescription nicotine (i.e., nicotine gum and transdermal nicotine). In fact, the median cessation rates for nico­ tine gum at 6-month and 1-year follow-ups were 2 3 % and 11%. These rates were substantially higher when the gum was used in conjunc­ tion with cognitive-behavioral smoking cessation programs: 3 5 % and 2 9 % (Schwartz, 1987). At the time this book was being written, transdermal nicotine delivery systems had just been approved by the Food and Drug Administration. Hence, substantial field trials of these "patches" have not been conducted. Both hypnosis and acupuncture have been of interest to the gen­ eral public as smoking cessation techniques. However, empirical vali­ dation of these methods has been weak and hirther controlled studies are necessary prior to assuming their efficacy (Schwartz, 1987). SUMMARY Huge numbers of people in the United States are affected by substance abuse. Thousands of books and articles have been written and millions of dollars have been spent on research on the addictions. Nonetheless, there is a noticeable paucity of reliably effec- Overview 21 five substance abuse treatment strategies. For years, however, it h been noted that there are underlying cognitive processes common to the addictions. (Even Alcoholics Anonymous warns alcoholics about "stinkin' thinkin.'") W e believe strongly that understanding and work­ ing with these cognitive aspects more explicitly will help to resolve some of the uncertainty plaguing the field of substance use treatment. In the chapters that follow we strive for a high degree of speci­ ficity in describing the procedures that comprise this approach. A preliminary version of this book currently serves as a therapist manual in an ongoing National Institute on Drug Abuse pilot study compar­ ing cognitive therapy, supportive-expressive therapy, and general drug counseling treatment outcomes for cocaine abusers. Our hope is that Cognitive Therapy of Substance Abuse will continue to serve as a train­ ing guide for further clinical and empirical tests. C H A P T E R 2 C o g n i t i v e M o d e l o f A d d i c t i o n W R Y DO PEOPLE USE DRUGS (AND/OR ALCOHOL)? Some individuals are "generalists" and may use a wide variety of addictive substances almost randomly or depending on their availability. Others are "specialists" and their drug of choice may depend on its specific pharmacological properties as well as its social meanings (e.g., alcohol is often viewed as manly and associated with sports, whereas cocaine is associated with group acceptance and sexual activity). Cocaine may be used because of its stimulant properties- producing a rapid "high," for example. Similarly, amphetamines may be chosen as psychic energizers. In contrast,

barbiturates, benzodiaz­ epines, and alcohol may be preferred because of their relaxing effect and, perhaps, their presumed relief of inhibitions. Hallucinogens are attractive to some to relieve boredom and "expand consciousness." Most people addicted to cocaine have also abused other drugs and/or alcohol (N. S. Miller, 1991; Regier et al., 1990; Stimmel, 1991). There are numerous explanations for why people use—and become addicted to-psychotropic substances. In general, the process of addiction can be understood in terms of a few simple, perhaps obvious, formulas. A basic reason for starting on drugs or alcohol is to get pleasure, to experience the exhilaration of being high, and to share the excitement with one's companions who are also using (Stim­ mel, 1991). Further, there is the expectation that the drug cocaine, for example, will increase efficiency, improve fluency, and enhance creativity. 22 Cognitive Model of Addiction 23 How do people progress from recreational or casual use to regu­ lar use? In time, additional factors may contribute to becoming depen­ dent on the drug. Some people find that drug taking-for example, heroin, benzodiazepines (such as Valium), or barbiturates^rovides temporary relief from anxiety, tension, sadness, or boredom. These individuals soon develop the belief that they can weather the frustra­ tions and stresses of life better if they can turn to drugs and/or alco­ hol for a period of escape or oblivion. People with adverse life cir­ cumstances are more likely to become addicted than are those with more sources of satisfaction (Peele, 1985). For a while, real-life prob­ lems fade into insignificance and life itself seems more attractive. As one patient put it, "If I take coke, m y bad thoughts go away." Fur­ ther, people whose self-confidence is low may find that the drug or alcohol boosts their morale—in the short run. Finally, many individu­ als discover that using drugs provides new social groups in which the only requirement for admission and acceptance is that they are users. If drug using has so many advantages, why should we be con­ cerned with getting people off the "drug habit"? The profound impli­ cations of breaking the law by using illegal drugs (and selling them in order to support their habit) are so obvious that they do not need further elaboration. Regardless of whether the drugs are legal, such as alcohol, or illegal, substance abuse creates serious personal, social, and medical problems (Frances & Miller, 1991; Kosten & Kleber, 1992). A major problem is that the drug seems to take control of addicted individuals. Their goals, values, and attachments become subordinate to the drug using. They cannot manage their lives effectively. They become subject to a vicious cycle of craving, precipitous drops in mood, and greater distress that can be relieved immediately only by using drugs again. The web of external and internal problems leading to and, later, maintaining compulsive drug use is a defining characteristic of addic­ tion. Far from soothing life's pains, the drugs create a new set of prob­ lems-enormous financial outiays (for illegal drugs), threat of or achial loss of employment, and difficulties in important personal relation­ ships, such as marriage. The individual also becomes stigmatized by society-as a "lush" or a "junkie." Finally, of course, chronic use may cause serious medical problems and even death. As pointed out by Peele (1989), the compulsive use of psycho­ tropic agents depends on a wide variety of personal and social fac­ tors. If the environment is malevolent and there is group support for drug use-as in the case of U.S. soldiers in Vietnam-widespread drug use is more likely. W h e n the environment is comparatively less stress­ ful (as when veterans retiirn to civilian life), individuals do not con- 24 COGNITIVE THERAPY OF SUBSTANCE ABUSE tinue excessive use—except for those who had been heavy users prio to military service (Robins, Davis, & Goodwin, 1974). A number of characteristics distinguish addicted individuals from casual users. A major difference, as pointed out by Peele (1985), is that while addicted individuals subordinate important values to drug using, casual users prize other values more highly: family, friends, occupation, recreation, and economic security, to name a few. In addition, drug users may have certain characteristics, such as low frus­ tration tolerance, nonassertiveness, or poor impulse control, that make them more susceptible. Thus, psychological and social factors may be the determinative factors—rather than the pharmacological prop­ erties per se—in converting a drug user into a drug abuser. Support­ ing this hypothesis is the commonly encountered phenomenon in hospital settings where "patients who take opioids for acute pain or cancer pain rarely experience euphoria and even more rarely develop psychic dependence or addiction to the mood-altering effects of nar­ cotics" {Medical Letter on Drugs and Therapeutics, 1993, p. 5). If drug addiction were merely a biological process, we would not expect this to be the case. The sequence of using or drinking is illustrated in Figure 2.1. An addicted individual who is feeling anxious or low decides to have a smoke or a snort. The short-term relief is followed by delayed, longer- term negative consequences: problems about breaking the law, seri­ ous financial problems, family difficulties, and possibly medical prob­ lems. These problems lead to realistic fears of being apprehended, becoming bankrupt, losing a job, disrupting close relationships, and becoming ill. These fears generate more anxiety and lead to craving and further using or drinking to neutralize the anxiety. Thus, a vicious cycle is established. Many other kinds of vicious cycles, which are described in Chap­ ter 3 (this volume), may be created. These involve a number of psy­ chological factors such as low self-esteem, emotional distress, and hopelessness. W H Y NOT STOP IF DRUGS OR ALCOHOL CREATE PROBLEMS? By definition, addicts are people who have difficulty in stopping permanently. They may have started to use voluntarily, but they either do not believe that they can stop or they do not choose to stop voluntarily. At the first sign of medical, financial, or interper­ sonal problems, many users ignore, minimize, or deny the problems Cognitive Model of Addiction 25 Anxiety/Low Mood Using ^k- Flnanclal, Social, Medical Problems FIGURE 2.1. Simple model of vicious cycle. or attribute them to something other than drugs (e.g., they m a y blame their spouse for domestic problems). Others m a y be aware of the problems, but they evaluate the advantages of using as greater than the disadvantages. M u c h of this evaluation is based on avoiding a true assessment of the disadvantages (Gawin & EUinwood, 1988; Gawin & Kleber, 1988). As the problems increase, m a n y users become more ambivalent and begin to vacillate in their decision to use. One factor in maintaining drug use is the c o m m o n belief that withdrawing from the drug will produce intolerable side effects (Horvath, 1988, in press). However, these effects vary enormously from person to person—and from substance to substance—and the impact is greatly enhanced by the psychological meaning attached to the withdrawal symptoms. These meanings are often more salient than the actual adverse physiological sensations in determining the inten­ sity of withdrawal symptoms. Most cocaine abusers participating in detoxification programs, for example, feel better in the early stages after they stop using (Ziedonis, 1992). A major obstacle to eliminating using or drinking is the network of dysfunctional beliefs that center around the drugs or alcohol. Exam­ ples of these beliefs are: "I can't be happy unless I can use," and "I a m more in control w h e n I've had a few drinks." A n individual w h o is contemplating eliminating the use of drugs or alcohol m a y feel sad or anxious. Termination of reliance on drugs or alcohol is seen as a deprivation of satisfaction and solace or a threat to well-being and functioning Qennings, 1991). Stopping m a y mean, for some, remov­ ing the "security blanket" used to cushion dysphoria. Addicted individuals often try on their o w n to stop using or drink­ ing. However, w h e n they experience the craving (often stimulated by low m o o d or exposure to the drugs or related stimuli), they feel dis­ appointed if they restrain themselves from using or drinking. They perceive their feelings of disappointment and distress as intolerable; the thought, "1 can't stand this feeling," upsets them even more. Hence, they feel driven to yield to the craving in order to dispel the 26 COGNITFVE THERAPY OF SUBSTANCE ABUSE sense of loss and relieve their distress. Patients often have a cl of beliefs that seem to become stronger when they decide to stop using. These center around the anticipated deprivation: "If I can't use, I won't be able to bear the pain (or boredom)," "There is nothing left in life for me," "I will be unhappy", or "1 will lose m y friends." These beliefs are elaborated more in the section on low frustration toler­ ance (Chapter 15, this volume). Another set of beliefs centers around the addicted individual's sense of helplessness in controlling the craving: "The craving is too strong," "1 don't have the power to stop," or "Even if I do stop—1 will only start up again." These beliefs become self-fulfilling prophecies. Since the patients believe they are incapable of controlling their urges, they are less likely to try to control them and, thus, confirm their belief in their helplessness in overcoming their addiction. W H Y D O PEOPLE W A N T HELP? There are roughly five stages people go through in seeking help (Prochaska et al., 1992). In the precontemplative stage, they do not even acknowledge to themselves that they have a problem (or else they consider using more important than the problems it causes). In the contemplative stage, they are willing to consider their problems, but are still unlikely to stop using on their own. Individuals in the preparation stage intend to take action to cease their drug and alcohol use, but are uncertain about being able to follow through. In the action stage, patients behaviorally demonstrate a decrease in their drug-taking behaviors and a therapeutic modification in their drug-taking beliefs. Those who are successful enough to reach the maintenance stage have already taken great strides toward a drug-free and alcohol-free life, and are actively working to maintain consistency in this endeavor over a period of months and years. People come to therapy for a variety of reasons. Some users have been arrested for "dealing" or possession and are referred by the courts. Others see their lives deteriorating as a result of the financial, psychological, and interpersonal consequences of using or drinking. Still others are pressured by friends or family. By the time these patients are labeled drug abusers, addicts, or alcoholics, they have often hit a low point in terms of any combination of the following: health, social adjustment, employment and economic status, and psychologi­ cal well-being. Many people with drug and alcohol problems have tried repeat­ edly to "break the habit," only to relapse eventually. Others suffer from Cognitive Model of Addiction 27 a personality disorder (e.g., Mirin & Weiss, 1991; Nace, Davis, & Gaspari, 1991; Regier et al., 1990) and/or a psychiatric syndrome such as chronic anxiety (e.g., Kranzler & Liebowitz, 1988; LaBounty, Hat- sukami, Morgan, & Nelson, 1992; Walfish, Massey, & Krone, 1990) or depression (e.g., Hatsukami & Pickens, 1982; Rounsaville & Kleber, 1986). For some, drug use is simply a manifestation of their mani­ fold difficulties. For others, drugs represent a form of self-medication (Castaneda, Galanter, & Franco, 1989; Khantzian, 1985) to relieve their feelings of distress, sadness, or anxiety. Given the consequences of sustained drug use, it is important to consider the problem in terms of its sociological, interpersonal, and psychological dimensions, in addition to the strictly pharmacologi­ cal properties of drugs. In fact, substance abuse or addiction could be defined as compulsive use leading to a web of entanglement involv­ ing social, economic, and legal problems over which the patient no longer has control. Given their acknowledgment that they are addicted, many of these individuals come to the conclusion that the only way they can manage or even salvage their lives is to receive assistance, professional or otherwise. H O W C A N COGNITIVE THERAPY HELP? Cognitive therapy is

a system of psychotherapy that attempts to reduce excessive emotional reactions and self-defeating behavior by modifying the faulty or erroneous thinking and maladap­ tive beliefs that underlie these reactions (Beck, 1976; Beck, Rush, Shaw, & Emery, 1979). The approach to a particular patient is derived from a thorough concephialization of the particular case. The specific case formulation, in turn, is based on the cognitive model of that disorder. The thor­ ough case conceptualization, including the relationship of early life patterns to current problems, at the beginning stages of treatment differentiates cognitive therapy from some of the other forms of therapy. The approach is (1) collaborative (builds trust), (2) active, (3) based on open-ended questioning to a large degree, and (4) highly structured and focused. As applied to substance abuse, the cognitive approach helps indi­ viduals to come to grips with the problems leading to emotional dis­ tress and to gain a broader perspective on their reliance on drugs for pleasure and/or relief from discomfort. In addition, specific cognitive strategies help to reduce their urges and, at the same time, establish a stronger system of internal controls. Moreover, cognitive therapy 28 COGNITIVE THERAPY OF SUBSTANCE ABUSE can help patients to combat their depression, anxiety, or anger, w frequently fuels addictive behaviors. A major thrust of cognitive therapy of substance abuse is to help the patient in two ways: (1) to reduce the intensity and frequency of the urges by undermining the underlying beliefs, and (2) to teach the patient specific techniques for controlling or managing their urges. In a nutshell, the aim is to reduce the pressure and increase control. When the patient's addiction is related to a coexisting psychiatric disorder, that condition also needs to be addressed by the cognitive therapist. Cognitive therapy is carried out in several ways. The therapist helps the patient to examine the sequence of events leading to drug use and then to explore the patient's basic beliefs about the value of drugs, alcohol, and nicotine. At the same time, the therapist trains the patient to evaluate and consider the ways in which faulty think­ ing produces stress and distress. Therapists help patients to modify their thinking so that they can gain a better grasp of their realistic problems and can disregard pseudo-problems derived from their faulty thinking. In addition, through rehearsal and practice, patients are trained to build up a system of controls to apply when confronted with strong urges. The techniques the therapist uses include a painstaking evalua­ tion of the short-term and long-term benefits and disadvantages of using: the cost-benefits analysis (also called the advantages-disadvan­ tages analysis; see Chapters 9 and 10, this volume). The therapist also helps the patient to find more satisfactory ways of coping with real­ istic problems and unpleasant feelings without turning to drugs or alcohol for relief. They also work together to structure the patient's life so that other sources of pleasure are made available (cf. Havassy, Hall, & Wasserman, 1991). Since many patients have a low frustra­ tion tolerance (Ellis, Mclnerney, DiGiuseppe, & Yeager, 1988), they are shown how their self-defeating attitudes about themselves and their capabilities lead to overreacting when they encounter obstacles, delays, or thwarting (Chapter 15, this volume). The therapist also demonstrates how patients can approach these obstacles as problems to be solved rather than as barriers to their goals. Many patients who suffer from difficulties in asserting themselves in an appropriate way are likely to be dominated and even exploited by other people, and thus are prone to experience frequent impatience, anger, and disappointment. By learning new interpersonal skills, the patients are able to assert their rights more effectively. The same type of assertion can help them to refuse when others coax them to start Cognitive Model of Addiction 29 using. Refusal can take on a new meaning for them^standing up for themselves, putting long-term interests before short-term gains, and becoming desensitized to derogatory or profane epithets. One of the main features of cognitive therapy is the use of "Socratic questioning." By skillfully asking questions, the therapist leads the patient to examine areas that the patient has closed off from scrutiny, for example, the true frequency and quantity of drug use, the actual losses from the addiction, and the quality and effects on interpersonal relations. Also, questioning leads patients to generate options and solutions that they have not considered. Finally, this approach puts patients in the "questioning mode" (as opposed to the "automatic impulse" mode) so that they will start to evaluate more objectively their various attitudes and beliefs. In a sense, stopping drug use or drinking is a technical problem. The patients coming for help would like to stop using but they do not know how. Many of them have tried to stop many times but have been unsuccessful. Cognitive therapy provides them with tools that will enable them to stop and maintain the abstinence from drugs or to moderate their drinking and smoking. Moreover, they can apply these same useful techniques to their daily problems and thus have a more enjoyable, more fulfilling life. D O SUBSTANCE ABUSERS H A V E ADDITIONAL PSYCHIATRIC PROBLEMS? Many of the patients seeking—or referred for—treat­ ment of addictions have a "dual diagnosis" (Mirin & Weiss, 1991; Regier et al., 1990). By this we mean that in addition to their diagno­ sis of addiction, they also have a syndromal diagnosis (Axis I), such as depression, or a diagnosis of personality disorder (Axis II), or a com­ bination of both. A good conceptualization takes into account the vari­ ous ways in which the patients' psychological problems play them­ selves out. For example, a patient with a dependent personality disorder centered around a poor self-concept may become depressed following a rejection and seek to counteract the depressed feelings through using and/or drinking. Linking these behaviors may be a common thread, such as "I am too weak or fragile to make it on m y own." This belief may lead to clinical depression when interpersonal supports are removed. The same belief promotes using or drinking when the patient is confronted with a difficult problem or a stressful situation: "I can't handle this without a drink (or drug)." 30 COGNITIVE THERAPY OF SUBSTANCE ABUSE WHY DO PEOPLE RELAPSE AFTER NOT USING FOR A SUBSTANTIAL PERIOD? Many individuals handle the withdrawal symptoms, if present, and go for significant periods without using but then relapse—sometimes, for no apparently compelling reason (Carroll, Rounsaville, & Keller, 1991; Tiffany, 1990). The problem seems to lie in the fact that these individuals have not become "inoculated" to the external or internal conditions that can trigger the craving and undermine the control. These circumstances fall into the category of "people, places, and things," which is described in 12-step programs. This category includes situations such as associating with compan­ ions or sex partners who urge one to have a "hit" or drink, visiting a place where one has previously used or drunk, seeing drug parapher­ nalia, or receiving one's paycheck. These individuals also may expe­ rience a craving for the substance if they are feeling sad, bored, or anxious. Some individuals have a lapse when an unusual stressful situation occurs: death of a friend or relative, serious argument with a spouse, or loss of a job. One of the underlying reasons why recovering addicts are still prone to react with powerful urges to various stimulus (high-risk) situations is that their basic beliefs regarding the relative advantages and disadvantages of drug taking have not changed substantially. They may have acquired a number of strategies for controlling their drug- taking behavior, but they have not significantly modified the attitudes that help to fuel the craving. Consequently, when their controls are weakened, perhaps as a result of stress, and their urges are stimulated, for example by exposure to a high-risk situation (a situation that activates their drug-using beliefs), they are vulnerable to lapse by using or drinking a minimum or moderate amount. This lapse is accentu­ ated by a sense of helplessness or hopelessness: "It proves I can't control m y urges"; "I will never be able to beat this problem." As they are swept back into the drug-using cycle, the lapse becomes a relapse. Sometimes, patients may lapse for no discernible reason—that is, they have not been exposed to a high-risk situation (Tiffany, 1990). The probability of such a lapse is increased any time the ratio of the perception of control to the intensity of craving is decreased; that is, when control is weakened by fatigue and a gradual slippage of the constructive beliefs (anti-indulgence behefs) and/or an increase in the desire to use or drink, based, for example, on tran­ sient unpleasant feelings. The degree of commitment to abstinence may simply decrease with the passage of time-perhaps because of fading of memories of the bad effects of using or drinking (Gawin & Cognitive Model of Addiction 31 EUinwood, 1988; Velten, 1986). At this time, a "normal" degree of craving may lead to a lapse. If the patient's reaction is, "My control must be pretty poor if I give in to such mild craving," he/she may progress into a relapse. The basic beliefs that have been dormant but become stimulated by exposure to the stimulus (high-risk) situations include notions such as "If I use, I can handle m y problems better," "Having a smoke or hit will make life more enjoyable," or "I need a drink to overcome my anxiety." As soon as these beliefs are activated, the individual experiences an exacerbation of craving. The patient's attempts at self- confrol are undermined by permission-related thoughts (stemming from the beliefs) such as "I can do it this once and stop," or "There's no reason why I should continue to deprive myself." There is, thus, a continuing conflict between the attitudes concerned with control­ ling the urge and those attitudes favoring yielding to the temptation (or, more strictiy, initiating the behavior that would satisfy the urge). P H E N O M E N A OF ADDICTION Cravings and Urges In helping patients deal with their substance use prob­ lems, it is crucial to have a full understanding of the phenomena associated with drug use. Craving refers to a desire for the drug, whereas the term urge is applied to the internal pressure or mobiliza­ tion to act on the craving (Marlatt, 1985, and Horvath, 1988, use the terms in a similar way). In short, a craving is associated with wanting and an urge with doing. The two terms are often used interchange­ ably, but it is useful to separate them. Cravings represent a strong desire for a particular type of experi­ ence, for example, the pleasure from eating, relaxation from smok­ ing, or the gratification from sex. The fulfillment of the wish may be labeled the consummation and the means, the consummatory act. When one form of consummation is not available, an individual may turn to another form. For example, if there is no satisfaction in sight for yearning for affection, an individual may reach for a sweet or a beer instead. An urge is the instrumental sequel to a craving. A person desires to experience a "high" or relief from discomfort and feels a pressure to act to obtain this experience. Marlatt and Gordon (1985) define an urge as a behavioral intention to engage in a specific consumma­ tory behavior. Urges may be regarded as compulsions when the indi­ vidual feels incapable of resisting them. Thus, an urge may be insti- 32 COGNITIVE THERAPY OF SUBSTANCE ABUSE gated by an unpleasant feeling state (such as anger or anxiety) or anticipation of an unpleasant stressful event. The ultimate goal of consummating the urge is a reduction of the instigating state, whether it be a craving for excitement or a desire to relax. The delay between the experience of craving and implementa­ tion of the urge does provide an interval for a therapeutic interven­ tion—for the technical application of control or what is called, in common parlance, "will power," which we define as an active pro­ cess of applying self-help techniques, not simply a passive enduring of discomfort. Additionally, fostering a delay between the craving and the use of drugs allows for the natural diminishing of the acute crav­ ing episode (Horvath, 1988), thus lowering the chances that the

patient will act on the craving (Carroll, Rounsaville, & Keller, 1991). Urges are governed by the anticipated consequences, for example, reward for doing something or pain for not doing it. The urge may be accompanied by a positive feeling when it is driven by a positive expectation or a negative feeling when it is driven by expectation of unpleasantness unless the urge is consummated. Some people con­ fuse urge with "need." They will say "I need a smoke" or "I need a drink" as though they cannot survive, or at least function, without it. Such a belief is, of course, spurious and becomes a focus for thera­ peutic interventions. Cravings and urges tend to be automatic and may become "auton­ omous"; that is, they can continue even though the individual tries to suppress or abolish them. They may become imperative and are not easily dissipated even if blocked from being carried out. At this point, the word "compulsion" seems most appropriate to describe cravings and urges. W e see compulsions most clearly in obsessive- compulsive disorder, in which the individual experiences strong pres­ sure to engage in a repetitive act in order to ward off some feared event. Addictive behaviors incorporate some of the same characteris­ tics. The Role of Beliefs Dysfunctional beliefs play a role in the generation of urges. The beliefs help to form the expectation, which then molds the urge. For example, a patient with a serious drinking problem had the following beliefs: "If I am 'amusing and friendly' I will receive lots of praise" and "If I have a drink I will be more entertaining." He translated these beliefs into a specific expectation for receiving praise when an opportunity arose for entertaining people. The expectation, then, led to the urge to "show off." However, he was uncertain of his Cognitive Model of Addiction 33 success unless he had crack cocaine first. His expectation of succe was enhanced by his belief in the stimulating or disinhibiting effect of cocaine. As it happened, he would usually "overshoot the mark" and become so excited that people considered him "pathetic." Following Bandura (1982), Mariatt and Gordon (1985) have refined the concept "beliefs about the positive effect of using" into "positive outcome expectancies." Research by Brown, Goldman, Inn, and Anderson (1980) has shown that the expectancies of alcoholics fall into six factors: that drinking will (1) transform experiences in a positive way, (2) enhance social and physical pleasure, (3) increase sexual performance and satisfaction, (4) increase power and aggres­ sion, (5) increase social assertiveness, and (6) decrease tension. A simi­ lar set of expectations is associated with drug use (see Drug Belief Questionnaire in Appendix, this volume). The "Drug Habit" The habit of taking substances for relief or pleasure differs from the way the term "a bad habit" is generally understood. A particular "habit," such as grimacing when frustrated or leaving clothes on the floor, is a repetitive pattern—but it is not experienced as a craving or a need. For the drug abuser the immediate response to a relevant situation is subjective, namely, a craving or an urge. There is a delay between the stimulus and the consummatory act, such as preparing the syringe or the powder. What are chained to the stimu­ lus, thus, are the cravings and urges. Through continual repetition, the chain becomes stronger. In contrast to the habits involved in skilled acts such as driving, the pattern of drug taking is compulsive and dysfunctional. In addition, the skilled acts are based on volun­ tary decisions, whereas drug-taking cravings are involuntary (even though the control of the urges is voluntary). Because of the differ­ ence between using and the habits of everyday life, the term "drug habit" is probably a misnomer. Through a process of "stimulus generalization," the addicted individual is likely to respond with craving to an increasingly broader range of stimulus situations. Whereas originally the individual might have felt the craving for a drink or smoke only in a group, he or she now may experience it when upset, bored, or lonely. With the bind­ ing of the craving to more and more stimuli, there is a concomitant expansion of the dysfrinctional beliefs about drug use. Whereas ini­ tially the belief might be "I should take a smoke to be part of the group," the beliefs may build up to "I need a smoke to be accepted" and later to "I have to take a snort to relieve m y loneliness and dis- 34 COGNITIVE THERAPY OF SUBSTANCE ABUSE tress." The urges, thus, become more generalized and more impera­ tive in keeping with the broadening content of the beliefs. Furthermore, the rebound dysphoria experienced particularly after a "cocaine crash" (Karan et al., 1991; Ziedonis, 1992), for example, leads to a renewal of the craving in order to counteract this low feel­ ing. The consequence of the repetition of emotional distress leading to craving to indulgence to temporary relief of dysphoria is the develop­ ment of beliefs such as "I need a hit in order to feel better." When a drug or alcohol is taken to relieve stress-related or naturally occur­ ring tension, anxiety, or sadness, it tends to reinforce the belief "1 need the drug," as well as "I can't tolerate unpleasant feelings." The Control/Urge Equation There is a common belief that addicted individuals have little or no control over their urges and behavior or that the craving is irresistible. O n the surface, this seems to be true because these people seem to be driven by such a powerful force that they engage in addictive behavior even though they recognize its destruc- tiveness; many make repetitive abortive attempts to control their behavior and will say that they know they want to confrol their behav­ ior but simply carmot. This common observation of their cravings and urges overwhelming any resistance has led to the principle expressed by Alcoholics Anonymous: "I recognize that I am powerless." Their perception of "being out of control" has the positive bene­ fit of inducing addicted people to seek professional help rather than continuing to waste energy in futile attempts to exercise confrol—often followed by self-castigation for not successfully counteracting the urge. Developing control is a technical problem to a large extent. Learning specialized techniques for reducing craving and establishing some measure of control is generally necessary for those who are truly addicted. On the one hand, the sources of craving need to be explored. On the other hand, the notion of total loss of control is simplistic and does an injustice to the potential internal resources available to the individual. In actuality, most people who abuse drugs do exer­ cise control most of the time. When the urge is not strong or the substance is not currently available, they are able to abstain. They do not necessarily go off in wild pursuit of the drug at the first sensa­ tion of craving. There is a qualitative difference between the wish to use (to experience "benefits" of the drug) and the wish to control the urge. The craving activates a drug-taking routine: The individuals' sources for consummating the urge are scanned, a plan emerges, the body becomes mobilized to act, and the physiology shifts to a recep- Cognitive Model of Addiction 35 five state (e.g., the parasympathetic nervous system goes into an a vated state). Since craving is an "appetitive state," it is accompanied by a variety of bodily sensations somewhat akin to hunger or an unpleasant yearning for someone or something. This kind of appe­ tite operates according to the pleasure principle, in contrast to the wish to control the urge, which operates according to the reality principle. The wish not to use, thus, to control, is not expressed in visceral terms (as is craving) but is experienced as a sort of mental state. It has a sttong cognitive component, specifically, decision-making. What powers the decision-making is a sense of resolution or commitment that is felt in the musculature (in contrast to craving, which is more visceral). Thus, the two opposing motivations—craving and self-control (or will power)—are qualitatively different. Parallel to the decision not to use (refusal state) is the decision to indulge (permission giving). Permission giving and permission refusal are akin to gatekeepers. Their relative'strength determines whether the gates will open or close. There is more conscious (vol­ untary) participation in the gatekeeping than in the craving; there­ fore, the individual can reflect and decide whether or not to indulge. If the craving is strong, the decision to refuse/abstain may be too weak to control it. If the balance favors refusal, the using does not occur. Even when the urge is strong, addicted individuals can abstain at times, particularly if the drug is not immediately available. It is important to recognize that addictive behavior is related to the bal­ ance of control versus urge. Put in more abstract terms, the ratio of the strength of the control to the strength of the urge influences whether the individual will abstain or use. The formula or ratio power ofcontiol/power of urge may be used as a guide for intervention. Treat­ ment is focused on increasing this ratio. It does not require a super­ human effort to change the relative strengths. It may simply involve reducing the denominator (urge) or increasing the numerator (con­ trol) or, preferably, doing both. Beck et al. (1979) have used the analogy of the votes in Congress for a declaration of war to illustrate how suicidal behavior may be modified. A somewhat similar analogy may be applied to a decision to use. To declare war requires a simple plurality, a margin of one vote of the yeas over the nays. However, just as in the case of sui­ cide, if the decision is postponed or the relationship of yea to nay votes is changed in favor of the nays, the progression to action is arrested. In the case of declaration of war, lobbying for a few votes for peace may forestall the fateful action; in the case of addiction, strengthening the votes for abstinence can reverse the tendency to use. In the long run, however, it is necessary to build a solid "major­ ity" to forestall relapse. 36 COGNITFVE THERAPY OF SUBSTANCE ABUSE The point to this analogy is that it is not necessary to eliminate cravings totally or to institute absolute control. It is sufficient to change the relative strengths of the two parts of the equation. A change involving reduction of craving or increase in control may interrupt the drug-using progression in the short run. Since the goal is usually permanent abstinence, a durable improvement requires enough last­ ing change in the ratio to provide a sufficient margin of safety. Treat­ ment, thus, is directed toward both halves of the equation: increas­ ing control and reducing craving. Increasing Control Many addicted individuals simply have not developed the skills to control temptation. If such a skill deficit exists, one part of the therapy is directed toward increasing self-control skills. A vari­ ety of methods can be used to increase control. These techniques can be practiced in the therapist's office. The basic procedure is to repro­ duce stimulus conditions that will elicit craving and then to rehearse control behaviors as the craving is stimulated. For example, the indi­ vidual is asked to imagine a situation in which she is offered crack cocaine. She then imagines ways in which to refuse the offer. Or she might imagine feeling blue or anxious and then desiring relief from the discomfort. She then pictures what she will do when craving occurs: divert herself by calling a friend, become engaged in some pleasant activity, or read a flashcard detailing rational responses to cognitions related to craving. Another approach involves dealing directly with permission- giving thoughts. This exercise is carried out in the form of a debate. The patient mentally verbalizes or rehearses reasons for giving per­ mission to indulge and, at the same time, presents a rebuttal to this argument. At some point, however, it is necessary to identify and evaluate the underlying beliefs regarding permission giving and per­ mission refusing. Ultimately, of course, the therapist needs to help the patient reduce the craving by dealing with its various psychological and social sources. These sources may cover very broad domains of

the patient's life ranging from low frustration tolerance to marital problems. "Will Power" In the context of drug using, "will power" refers to a deliberate conscious decision (plus sufficient drive and technical self- help know-how to enforce it) to halt or delay the implementation of Cognitive Model of Addiction 37 an urge. When the urge to use is low or absent, the individual's dr to abstain from further use may appear to be quite strong. However, when the temptation is strong, the will power may become attenu­ ated. Marlatt and Gordon (1985) consider will power in terms of the strength of the commitment not to use or drink. Commitment means attaching a value to a particular goal so that it supersedes other con­ tradictory goals. Thus, the allocation of importance to abstinence can power the resolve to resist cravings. The successful application of will power when cravings and urges are aroused depends on a number of factors. An individual may make a serious commitment to stop smoking, drinking, or using but may not have the technical skills to fulfill the commitment. The applica­ tion of this technical knowledge can greatly increase the amount of leverage when the resolve to abstain is opposed to cravings and urges. Further, core beliefs about oneself (e.g., whether one is effective or helpless) may affect one's capacity to apply will power to controlling urges. W e must caution that patients tend to misconstrue the mean­ ing of will power, seeing it as an almost masochistic battle to main­ tain an unceasing state of discomfort in the face of drug urges (Tiffany, 1990). Clinicians must emphasize to patients that they will be taught to modify their beliefs and behaviors (cf. Washton, 1988) so that positive self-image and lifestyle changes will take place. This, along with the natural dissipation of cravings over time (Horvath, 1988), will help patients to feel good about resisting drug use in the long mn, as opposed to feeling deprived and in pain. According to the myth of the "rational man" (e.g., in jurispru­ dence or economics), an individual weighs the risks and benefits of a given action and makes a rational decision. In the case of the addicted individual, however, the objective cost-benefit analyses, or advantages-disadvantages calculations, are thrown off by the momen­ tary appeal of using, drinking, or smoking. The immediacy and reli­ ability of the effect of the drug and the subjective certainty that some desired effect will be achieved right away contrasts with an uncer­ tain, possibly undesirable consequence in the future. Some individu­ als become oblivious to the negative consequences when they expe­ rience the craving (Gawin & EUinwood, 1988). Others simply shrug off the long-range effects with the attifride "I'll take m y chances," or rationalize, "It won't hurt if I give in this one time." O n the other hand, a number of individuals are able to summon up, on their own, arguments and unpleasant memories that deter them from yielding to the temptation. In any event, there is always a con­ flict when individuals try to utilize will power to forestall yielding to their urges. O n the one hand, for example, an individual experiences 38 COGNITIVE THERAPY OF SUBSTANCE ABUSE the craving (and the anticipated relief or pleasure) and, on the o the voice of reason and restraint (and the anticipated deprivation and distress). After many unpleasant experiences, one may be able to issue oneself warnings of the dangers of indulgence when exposed to a high- risk situation or when aware of the lowering of one's resistance. Whether one will be able to heed these warnings to oneself depends to a large extent on one's access to techniques to implement them. Addictive Beliefs In our work, we have been impressed by the common­ ality of certain beliefs across various types of addictions (cocaine, opiates, alcohol, nicotine, and prescription drugs) and various addicted individuals. Even individuals susceptible to binge eating or general­ ized overeating show these types of dysfunctional beliefs (Heatherton & Baumeister, 1991; Lingswiler, Crowther, & Stephens, 1989; Zotter & Crowther, 1991). The addictive beliefs characterize those individu­ als after they have become addicted (i.e., they are characteristic of the disorder), however, and cannot in themselves be considered predis- positional to addiction. Nonetheless, the addictive beliefs do contrib­ ute to maintaining the addiction and provide the groundwork for relapse. Addictive beliefs may be considered in terms of a cluster of ideas centering around pleasure seeking, problem solving, relief, and escape. The specific items will vary depending on the type of preferred sub­ stance. Among the dysfunctional ideas are (1) the belief that one needs the substance if one is to maintain psychological and emotional bal­ ance; (2) the expectation that the substance will improve social and intellectual functioning; (3) the expectation that one will find plea­ sure and excitement from using; (4) the belief that the drug will energize the individual and provide increased power; (5) the expecta­ tion that the drug will have a soothing effect; (6) the assumption that the drug will relieve boredom, anxiety, tension, and depression; and (7) the conviction that unless something is done to satisfy the crav­ ing or to neutralize the distress, it will continue indefinitely and, possibly, get worse. In addition to these expectations/beliefs, the patients have a variety of beliefs relevant to justification, risk taking, and entitlement. These attitudes fall into one category of "permission-giving beliefs," such as "Since I'm feeling bad, it's O K to use," "I've been having a hard time; therefore, I'm entitied to relief," "If I take a hit, I can get away with it," "The satisfaction I get is worth the risk of relapsing," or "If I give in this time, I will resolve to resist the temptation next time." Cognitive Model of Addiction 39 Predispositional Characteristics A number of characteristics of the drug abuser, how­ ever, may have existed prior to drug use and thus may be considered predispositional. These characteristics center around (1) general sen­ sitivity to their unpleasant feelings or emotions—for example, they have a low tolerance for the normal cyclical changes in mood; (2) deficient motivation to control behavior^hus, instant satisfaction is more highly valued than control; (3) inadequate techniques for con­ trolling behavior and coping with problems—therefore, even when motivated to exert restraint, they do not have the technical knowl­ edge to follow through with it; (4) a partem of automatic, nonreflective yielding to impulses; (5) excitement seeking and low tolerance for boredom; (6) low tolerance for frustration (low frustration tolerance in itself rests on a complex set of beliefs and cognitive distortions); and (7) relatively diminished future time perspectives, such that the individual's attention is focused on here-and-now emotional states, cravings, and urges and on the actions for relieving or satisfying them. None of the attentional resources are devoted to the consequences of these actions. Low frustration tolerance (LET) seems to be an important precur­ sor to drug using (Chapter 15, this volume). Specifically, a number of dysfunctional attitudes magnifying the usual everyday sources of fmstration lead to excessive disappointment and anger. Among the components of this belief complex are attitudes such as (1) things should always go smoothly for m e or things should not go wrong; (2) when I am blocked in what I am doing, it is awful; (3) I cannot stand being frustrated; (4) other people are to blame for m y being thwarted, and they should be punished; and (5) people deliberately give m e a hard time. When individuals with LFT find that their activity is blocked or their expectations are thwarted, they are likely to (1) greafly exagger­ ate the degree of loss resulting from thwarting, (2) exaggerate the long- range consequences of this loss, (3) blame whomever they think might be responsible for thwarting, (4) experience excessive anger, (5) have a sfrong desire to punish the offender, and (6) importantly, overtook other ways of achieving their goal, such as problem solving. The result of this sequence of events is that an individual becomes overmobilized to attiack the offender. Since there is rarely a legitimate avenue for expressing the hostile impulses, the individual is left in a highly energized state, full of tension and anger. At some point, such individuals find that drug taking may reduce the highly volatile state and relieve the pent-up tension. Of course, the use of drugs for this 40 COGNITIVE THERAPY OF SUBSTANCE ABUSE purpose is at best only a temporary remedy and in the long run is self-defeating because the individual never learns ways of coping directly with frustration and solving the contributing problems. Con­ sequently, LFT is perpetuated, as are the beliefs regarding helpless­ ness. S U M M A R Y Many addicted individuals have characteristics that predispose them to drug abuse. These predispositional factors include (1) general exaggerated sensitivity to unpleasant feelings, (2) deficient motivation to control behavior, (3) impulsivity, (4) excitement seek­ ing and low tolerance for boredom, (5) low tolerance for frustration, and (6) in many cases, insufficient prosocial alternatives for gaining pleasurable feelings, and a sense of hopelessness in ever achieving this goal. LFT is characterized by exaggeration of the degree of loss result­ ing from thwarting, blaming other people for any frustration, a strong desire to punish the offender, and overlooking other ways of prob­ lem solving. Each of these predispositional factors is addressed in the course of cognitive therapy. The sequence of addiction often follows a vicious cycle proceed­ ing from anxiety or low mood to self-medication by using or drink­ ing. This behavior, in turn, produces and/or exacerbates financial, social, and/or medical problems, which lead to further anxiety and low mood. Patients often ascribe their drug and alcohol use to "uncon­ trollable cravings and urges." However, certain dysfunctional beliefs tend to fuel these cravings. Abusers tend to ignore, minimize, or deny the problems resulting from their drug use or attribute these prob­ lems to something other than the drugs or alcohol. An important factor in maintaining psychological dependency is the belief that withdrawal from the drug will produce intolerable side effects. In actuality, through careful clinical management these side effects gen­ erally turn out to be tolerable. Another important set of core beliefs centers around the addicted individual's sense of helplessness in con­ trolling the craving. Cravings are associated with wanting gratification or relief, whereas urges are concerned with doing something to provide a grati­ fication or relief. The delay between the experience of craving and the implementation of the urge provides an interval for therapeutic intervention. Cravings and urges tend to be automatic and may become autonomous; the thrust of therapy is to provide voluntary methods for managing them. Patients tend to equate the strong crav- Cognitive Model of Addiction 41 ing with an imperative "need" and an uncontrollable urge. Although the craving leading to drinking and using is involuntary, controlling the urge is voluntary and can be adopted even though the patient may feel helpless. Increasing the ratio of the subjective power of control to the subjective power of the urge may be used as a guide for inter­ vention. Cognitive therapy is a system of psychotherapy that attempts to reduce self-defeating behavior by modifying erroneous thinking and maladaptive beliefs and teaching techniques of control. In the cogni­ tive therapy of drug abuse, the specific case formulation forms the basis for the therapeutic regimen. This formulation, in turn, is based on the cognitive model of addictions. The therapeutic approach consists of undermining the urge by weakening the beliefs that feed into the urge and, at the same time, demonstrating to the patient various ways of controlling and modi­ fying their behavior. Cognitive therapy of substance abuse is charac­ terized by the following: (1) It is collaborative (builds trust), (2) it is active, (3) it is based, to a large degree on guided discovery and empir­ ical testing of beliefs, (4) it is highly structured and focused, and (5) it attempts to view the drug or drinking problem as a technical prob­ lem for which there is a technical solution. C H A P T E R 3 T h e o r y a n d T h e r a p y o f A d d i c t i o n A b-ccording to the

cognitive perspective, the way people interpret specific situations influences their feelings, motiva­ tions, and actions. Their interpretations, in turn, are shaped in many instances by the relevant beliefs that become activated in these situ­ ations. A social situation, for example, m a y activate an idiosyncratic belief such as "Cocaine makes m e more sociable" or "1 can be more relaxed if I have a beer (or a cigarette)," and lead to a desire to use, drink, or smoke. Specific beliefs such as these constitute a vulnerability to substance abuse. Activated under particular predictable circum­ stances, the beliefs increase the likelihood of continued drug or alco­ hol use (i.e., they stimulate craving). Beliefs also shape the individual's reactions to the physiological sensations associated with anxiety and craving (Beck, Emery, with Greenberg, 1985). Beliefs such as "1 cannot tolerate anxiety" or "I must give in to this hunger" will influence the person's reactions to these sensations. Individuals with such beliefs are likely to be hyperattentive to these sensations. Even a low-level degree of anxiety or craving can elicit a substance-using belief such as "I must take a hit (or drink) to relieve m y anxiety (or satisfy m y craving)." The activation of substance-using beliefs is illustrated in the expe­ rience of Les, a chronic cocaine user, w h o experienced a sudden crav­ ing for cocaine while attending a party. In this scenario, his acute urge to use was related to his sense of social isolation within a group. His underlying belief, "I can't stand it without cocaine," was activated by his sad feelings at seeing other people having a good time using drugs. Les lived in a rundown neighborhood in which there was a great deal 42 Theory and Therapy 43 of drug fraffic. He had a longstanding belief, "I'll never get out this awful environment." This belief (not the environment per se) led to chronic feelings of sadness and hopelessness. The belief underly­ ing his chronic urge to use cocaine was "I need some coke to get through the day." This case illustrates the coexistence of acute cravings and urges related to a specific situation with more chronic urges related to the patient's general life situation. The combination of these beliefs made Les prone to addiction. LAYERS O F BELIEFS There were several levels of beliefs underlying Les's addictive behavior: (1) his more general basic belief that he was "trapped" in a noxious environment; (2) his belief that the only way he could escape from his environment and his unpleasant feelings was to take drugs; and (3) the belief that he "needed" drugs to relieve any unpleasant feelings. Added to these drug-related beliefs was a basic belief that he did not belong and was not accepted as a member of his peer group. This cluster of beliefs made Les vulnerable to addic­ tive behavior; that is, they fed into a compulsive urge to relieve his distress through drug taking. The essence of a large proportion of addictive behaviors, consist­ ing of the types of general and specific beliefs held by this patient, are illustrated in Figure 3.1. The addictive beliefs (Chapter 2, this volume) seem to derive from either one or a combination of core beliefs (sometimes referred to as "core schemas"). The first set of dysfunctional core beliefs has to do with personal survival, achievement, freedom, and autonomy. Depend­ ing on the precise nature of the patient's vulnerability, the core belief that is expressed m a y have a content such as any of the following: "I am helpless, trapped, defeated, inferior, weak, inept, useless, or a fail­ ure." The second set of dysfunctional core behefs is concerned with Core Beliefs Emotions Addictive Beliefs "I am trapped/ Sad or "Drugs are an escape." alone." angry "Drugs make me more sociable." Addictive Behavior Go to a crack house FIGURE 3.1. Sequence of core beliefs and addictive beliefs. 44 COGNITIVE THERAPY OF SUBSTANCE ABUSE bonding with other individuals or to a group. This set of beliefs is concerned with lovability or acceptability. The various permutations of the core belief m a y take the following form: "I a m unloved, unde­ sirable, unwanted, repulsive, rejected, different, socially defective." Such core beliefs constitute a specific sensitivity or vulnerability: W h e n circumstances (e.g., social rejection) that are relevant to the core belief arise, they trigger the belief (e.g., "I a m defective") and lead to distress. Les had a double set of core beliefs revolving around the notions "I a m helpless" and "I a m undesirable." W h e n he noted the difficult conditions in his neighborhood, the first belief was triggered and took the form "I a m trapped." O n c e this notion took hold, he believed himself incapable of improving his lot, saw the future as hopeless, and felt frustrated and sad. The specific addictive belief-was then trig­ gered: "The only w a y to get relief is to take a hit." In a group situation his automatic thought was "I don't belong." This thought stemmed from his other core belief, "I a m unaccept­ able." These beliefs converged o n the addictive belief: "The only way to get accepted is to use coke." T h e relation between his two core beliefs, his automatic thought, his addictive belief, and his craving is illustrated in Figure 3.2. The same sort of constellation of core belief, addictive belief, and craving m a y apply whatever the instigating factor and whether the form of relief is alcohol, illegal drugs, legal drugs, or tobacco. The sequence generally proceeds from (1) a core belief, such as a nega­ tive view of the self (helpless, undesirable) and/or a negative view of the environment (noxious, oppressive), and/or a negative view of the future (hopeless), to (2) unpleasant feelings, such as dysphoria or anxi­ ety. From there, the addiction-prone individual experiences (3) crav­ ing and psychological dependency o n drugs (e.g., "1 need cocaine to m a k e m e feel better). Core Belief Automatic Thought Emotions "I am "I am trapped in this Sad or helpless." bad environment." frustrated .r Core Belief Addictive Belief Conclusion "I am "I don't belong unless I "1 need the drug" undesirable." use." \f Craving FIGURE 3.2. Interaction of multiple beliefs. Theory and Therapy 45 It is important to note that the perception of a noxious environ­ ment is not limited to inner-city individuals. Privileged individuals who perceive their job, family, or marital situation as inimical, who experience the same sequence of discouragement over life circum­ stances and have negative views of themselves and their future, may turn to drugs as a form of escape. In depression (Chapter 14, this volume), the negative view of the self, the current circumstances, and the future often is exaggerated. After patients modify their depressive thinking, the therapist often finds that compulsive drug use is dimin­ ished (Woody et al., 1983). Individuals like Les become habitual users because they regard using as a way of gaining or maintaining social acceptance. They have addictive beliefs such as "I can't let m y friends down . they will reject me if I don't use." (This fear, of course, may be realistic and one of the goals of therapy may be to help the patient to develop friendships with nonusers.) One patient greatly admired his cousin who was addicted to cocaine. The patient constantly used crack when he was with his cousin. The instigating factor each time was a desire to please his cousin. Eventually, using became embedded in his sys­ tem of coping with his fear of becoming socially ostracized. S E Q U E N C E O F BELIEFS Although the core beliefs represent the background of the addictive beliefs, they are not immediately apparent unless the patient is depressed (Chapter 14, this volume). The addictive beliefs may be more accessible. These addictive beliefs are activated in a specific sequence. First in the sequence are anticipatory beliefs. Initially these take a form such as "It will be fun to do this . . It's okay to try it occasionally." As the patient gains satisfaction from using, he/she often develops romanticized beliefs predictive of gratification or escape: "1 will have an hour or so of sheer pleasure . I wiU feel less sad/anxious . It wiU be a sweet oblivion." Some beliefs are predic­ tive of increased efficacy or socialization: "I will perform better . I will be more entertaining and will be accepted into the group." As the individuals start to rely on the drug to counteract feelings of disfress, they develop relief-oriented beliefs, such as "I need cocaine in order to function . I can't continue without it. I will feel well again if I use . I need the drug . I can't control the craving . I must have it or I'll fall apart." Note the imperative quality of these beliefs: "I must have a smoke to make it through the day." The acti­ vation of these beliefs then leads to cravings. 46 COGNITFVE THERAPY OF SUBSTANCE ABUSE Activating Anticipatory Craving situation beliefs Drug-seeking Permissive < plan of action beliefs FIGURE 3.3. Sequence of anticipatory and permissive beliefs. Since addiction-prone individuals may have some conflict about using (e.g., medical, financial, social, or legal consequences of using), they generally develop a facilitating or permissive belief, such as "1 deserve it" or "It's all right, I can handle it. Since I'm feeling bad, it's all right to use . . Nothing else is going right; this is the only right thing in m y life." The relation of these beliefs is illustrated in Fig­ ure 3.3. The sequence of these beliefs formed by Les is illustrated in Fig­ ure 3.4. His uneasiness in a social situation triggers the anticipatory belief "I will feel better if I use," which is immediately followed by a craving and then the plan of action to call his cousin for a "hit." CONFLICTING BELIEFS In the various stages of cocaine use the patient can have conflicting sets of beliefs, such as "I should not use cocaine" versus "It's O K to use this one time." Each behef can be activated under different circumstances or even at the same time. The balance between the relative strength of each belief at a given time will influence whether the patient uses or abstains. (Of course, the availability of the drug will also be a determining factor.) Sometimes the individual experiences a conflict between the desire to use and the desire to be free of drugs. This ambivalence may be formulated as a conflict between two beliefs: "It's O K " (permis­ sive) versus "It's not O K " (abstinent). The conflict between these beliefs results in discomfort or m a y increase the individual's current discomfort. Paradoxically, the individual m a y experience an even greater pull toward using in order to relieve the uneasiness produced by the conflict. The belief "I need relief from this feeling" becomes more potent and may tip the scales in favor of using. In therapy, patients learn skills to cope with the discomfort and to test out and restructure their belief that using or drinking is the most usefial way of dealing with discomfort. Theory and Therapy 4 7 Social 1 will leei situation Craving better If." Call cousin "It's OK." , _ FIGURE 3.4. Simple model of Les's substance use (maps onto Figure 3.3). A C T I V A T I O N O F BELIEFS IN S T I M U L U S SITUATIONS Drug-using beliefs and desires typically are activated in specific, often predictable, circumstances, which we term "stimu­ lus situations." These are also labeled "cues" (Moorey, 1989). How­ ever, depending on the patient's current mood and self-control, the degree of riskiness of a situation may vary considerably from time to time. That is, a situation that is manageable at one time may be stimu­ lating enough to promote drug use at another time. These circum­ stances, which can be external or internal, correspond to what Marlatt and Gordon (1985) term "high-risk situations." These situations stimu­ late the craving to "smoke, shoot, snort, or swallow drugs." Examples of external stimulus situations are a gathering of friends using cocaine, contact with a

drug dealer, or receiving a weekly pay­ check. Internal circumstances (or cues) include various emotional states such as depression, anxiety, or boredom, which can trigger drug- using beliefs and, consequently, craving for the drug. As shown in Figure 3.5, drug use may be regarded as represent­ ing the final common pathway of the activation of the cluster of the aforementioned beliefs. Cognitive therapy is aimed at modifying each of the categories of beliefs: anticipatory a n d permissive, as well as the underlying core beliefs (e.g., "I a m frapped") that potentiate these drug- Activating Beliefs Automatic > Craving/ stimulus: activated thoughts urges • Internal cues • External cues t \f Continued Focus on Instrumental Facilitating use or strateoies beliefs relapse (action) (Pe rmi 3sion) F I G U R E 3.5. Complete model of substance use. 48 COGNITIVE THERAPY OF SUBSTANCE ABUSE related beliefs. The therapist attempts to introduce or reinforce more adaptive beliefs relevant to each of the classes of beliefs. Other tech­ niques are concerned with dealing with major life problems (see Chapters 12 and 13, this volume) or personality difficulties or disor­ ders (see Chapters 14, 15, and 16, this volume) leading to drug use. As shown earlier, craving is aroused in a specific situation and seems to arise as a reflex reaction to the stimulus. However, the situ­ ation does not directly "cause" the craving: Interposed between the stimulus and the craving is a drug-related belief that is activated by the situation and an automatic thought derived from this belief. For example, w h e n he was feeling sad, Les would get the thought "If I take a hit now, I will feel better." His underlying belief was: "I can't stand discomfort. I need a fix to make the discomfort go away." The sequence then proceeded to craving, to facilitating beliefs ("It's O K this time"), to an actual plan for obtaining the drug, and finally to using. These beliefs can be ascertained by direct questioning and the use of inventories (see Appendix, this volume). The sequence proceeds so rapidly that it is often viewed as a "conditioned reflex" (O'Brien, 1992). The automatic thought, in par­ ticular, seems to be almost instantaneous and can be captured only if the patient learns to focus on the chain of events. Figure 3.6 illustrates the sequence from the activating stimulus to the implementation of the plan to get the drug. It should be noted that each step offers an opportunity for a cognitive intervention. Using the method of guided discovery (Beck et al., 1979), for example, the cognitive therapist questions the meaning attached to the activating stimulus, the relief-oriented belief that taking a fix is the most desir­ able solution, the permission-giving belief ("I can do it without harm"), and the implementation plan (the decision to look around for money). Les had a very low tolerance for unpleasant feelings, whether sadness, anxiety, or sheer boredom. His belief regarding the neces­ sity for alleviating feelings of distress was activated w h e n he attended a party. His drug-taking beliefs centered on the anticipation of reUef Feeling sad "If I take a fix I will feel better.' "What the hell." Craving Purchase and Look around to "I can do It this use drugs get the money. time without any harm." F I G U R E 3.6. Example of Les's drug-using sequence (maps onto Figure 3.5). Theory and Therapy 49 from any negative feelings. Other examples of his anticipatory rel oriented beliefs were: "There is only one way for m e to have fun," "I can't stand the withdrawal symptoms," "I feel better knowing it's there," and "If I don't take a hit regularly, I will feel much worse." It should be noted that the patient's permissive thoughts about the harmlessness of drug taking stemmed from a simplistic (and deceptive) set of beliefs. He believed that since he only snorted cocaine, he could not be addicted: He saw himself as being safe from addic­ tion provided he did not smoke crack. In fact, one of his typical per­ missive thoughts was, "I'm O K since I don't smoke crack." "Spontaneous craving" (i.e., craving in the absence of an obvi­ ous external stimulus) is also often observed. For example, a patient with a 5-year history of cocaine use reported having a dream about using cocaine. Upon awakening, he "felt high." Next, he started day­ dreaming about the last time he had used cocaine. This imagined scenario in turn activated the belief, "Life is more fun when I use," and was followed by the automatic thought, "I love this stuff." A permission-giving belief was also activated, "There is no harm in this." His attention then focused on checking to see whether he had enough money to buy cocaine. Although the craving appeared to be sponta­ neous in this case, the patient's mental state during the dream and upon awakening set the stage for daydreaming about using. This imagery served as a catalyst for the permission-giving thoughts. His attention then focused on implementing his craving and shut out any consideration of the ill effects of using. INFORMATION PROCESSING: MEANING, SYMBOLISM, AND RULES In referring to the kinds of circumstances (external or internal) that excite the craving-using cycle, we generally use the term "stimulus situations" or "triggers" rather than "high-risk sifrra- tions" introduced by Mariatt and Gordon (1985). Although many situ­ ations have a high probability of setting the craving-using pattern into motion, their effect varies from person to person and even for the same person over time. By conceptualizing these situations in terms of their stimulus properties and meanings, we can align our concept of drug use and abuse with concepts regarding stress (Beck, 1993), syndromal disorders (e.g., depression; Beck et al., 1979), and person­ ality disorders (Beck, Freeman, & Associates, 1990). While the term "high-risk situation" fits nicely into a descriptive model, the formulation in more cognitive terms can fit our observa- 50 COGNITIVE THERAPY OF SUBSTANCE ABUSE tion into an explanatory model. This model, encompassing concepts of the activation of beliefs, symbols, information processing, and motivation, provides a broader framework for understanding and psychological intervention. Although we use the terms "stimulus situations" and "stimulus properties," it should be noted that the actual situation is neutral. It becomes a stimulus if a person attaches a special meaning to it. For example, an addicted individual looks at a cocaine pipe and other paraphernalia and becomes excited and experiences craving. Another person, indifferent to drugs or not knowledgeable about the parapher­ nalia, simply sees a pipe. For the first person, the pipe is a symbol, a coded message, packed with meaning. The meaning is not inherent in the pipe but in the individual's personal symbolic code (embed­ ded in his or her information or cognitive processing system). The individual automatically applies this code when he/she perceives the paraphernalia, for example, and consequently experiences pleasure and craving. The therapist's task is to help the patient to decode the symbol. If one "unpacks" its meaning, it would read something like this: "The pipe means taking a hit, which will give me pleasure." The pipe and the concept of pleasure have become fused so that the expectation of pleasure in the future gives pleasure now and leads to craving. The drug abuser may seem to be stimulus bound. Any depiction of or reference to drugs on television, radio, or magazines, for exam­ ple, may be sufficient to excite the individual. The addicted person is actually "schema driven"; that is, Les's reactions are produced by inter­ nal cognitive structures, labeled schemas, that contain the code, for­ mulas, or beliefs that attach meaning to the situation (see Beck, 1967, for a complete description of schemas). Thus, a schema containing the belief "Using is necessary for m y happiness" will be primed when the person is exposed to a relevant situation. Similarly, a schema containing the belief "I cannot be happy unless I am loved" will be activated if the person perceives that he or she has been rejected by a lover and, thus, will feel sad. The experi­ ence of the sad affect will, in turn, be processed cognitively by behefs such as "I can't stand sadness," "I need relief by using." The indi­ vidual then experiences craving. The therapeutic application of this explanatory model involves attaching more importance to modifying the individual's belief sys­ tem than to simply getting him to avoid or cope with high-risk situ­ ations. Since some "situations" (such as internal states) are unavoid­ able and other sihiations (e.g., exposure to drug-related situations) may be inevitable (Childress, Hole, & DePhilippis, 1990; Moorey, 1989; Theory and Therapy 51 O'Brien, McLellan, Alterman, & Childress, 1992; Shulman, 1989), the best outcome can be derived from changing the beliefs that make these situations risky. Les, for example, often compared himself with other people more successful than he. W h e n he saw such a person, his negative beliefs ("I'm inferior" and "I'm no good") were activated. Thus, the mean­ ing attached to the perception of the other person was a self-devalu­ ation, leading to sadness. He also attached a meaning to sadness: "My life is intolerable . I can't stand the pain." Following the activation of the belief "I need dope to ease the pain," Les experienced craving. In therapy, each of these beliefs was explored. The proposed mechanism for therapeutic change consists of align­ ing the belief system more closely with reality. Since the beliefs are maladaptive (e.g., "I need the drug [or alcohol] in order to function"), it is necessary either to modify these beliefs or to substitute more functional beliefs (or both). The process of change, however, involves more than simple modification of the beliefs. The therapist and patient need to work together to improve the patient's system of controls (e.g., by practic­ ing delay of gratification) and to learn coping techniques such as anticipating and solving problems. Thus, the therapeutic goals are (1) conceptual change and (2) tech­ nical development of proficiency in coping. Cognitive Blockade W h e n they are not experiencing craving, patients are generally able to recognize the disruptive effects of the drug on their lives. However, once the drug-taking beliefs are activated, a "cogni­ tive blockade" inhibits awareness of or attention to the delayed long- term consequences of drug use (Gawin & EUinwood, 1988; Velten, 1986) and increases the focus on immediate instrumental strategies, such as searching for money to buy drugs. As these beliefs become hyperactive, recognition of the drawbacks of drug use become attenu­ ated. W h e n Les was not feeling sad, he was convinced that using cocaine was bad for him, but once his craving was stimulated, he had difficulty in remembering his reasons for not using. His attentional processes were predominantly allocated to using. The immediacy of the stimulus and the activated meanings shut out serious consider­ ation of long-range consequences. This kind of "tunnel vision," in which the individual's attentional resources are devoted almost totally to the immediate situation, has been demonsfrated in cognitive psychology experiments (Beck, 1991). 52 COGNITIVE THERAPY OF SUBSTANCE ABUSE For example, very hungry individuals will be hypersensitive to sti relevant to food or eating and will be relatively insensitive to other signals. The introduction of danger stimuli, however, will shift the attention to the danger stimuli and away from food stimuli. Clinical states show the same type of phenomenon. Information that is con­ gruent with the clinical condition will be processed very rapidly and memories congruent with the state can be rapidly recalled, but the patient has trouble gaining access to stored information that is not congruent with the clinical condition. Depressed patients, for example, quickly assimilate negative information about themselves but block out positive information. Also, they recall negative information much better than positive information (Beck, 1991). Similarly, patients hav­ ing a panic attack readily respond to suggestions that they are expe­ riencing a serious condition but have problems in recalling benign explanations for their attacks or even in applying reason to counter­ act the catastrophic interpretations they are making (Beck, 1986). A somewhat similar phenomenon may be observed among many individuals addicted to drugs, alcohol, or nicotine. Although when sober they may be quite adept at reeling off (with sincerity and

con­ viction) the reasons for not using, drug users have difficulty in recall­ ing or attaching the same significance to these reasons once they are in the throes of a specific drug-using episode. Since all their atten­ tion is focused on the mechanics of obtaining the drug, the reasons for using at that time become very salient and the contradictory rea­ sons become inaccessible or insignificant. This phenomenon is termed the "cognitive blockade" because of blocking out the incongruent (i.e., the corrective, realistic) informa­ tion. The therapeutic task is to lift the blockade, as it were, through a variety of tasks. One approach is to deliberately activate the crav­ ing cycle in the office (e.g., through imagery) and, while the craving is strong, review the reasons for not using. Of course, sufficient time must be allotted for this maneuver to preclude the craving's being maintained following the session (Childress et al., 1990). A similar strategy involves the preparation of flashcards (listing reasons for not using) which patients will read when they experience craving in the natural environment. SUMMARY At the core of the problem of the addicted individual is a set of addictive beliefs which appear to be derived from core beliefs such as "1 am helpless," "I am unlovable," or "I am vulnerable." These Theory and Therapy 53 core beliefs interact with life stressors to produce excessive anxiety, dysphoria, or anger. These stressful or stimulus situations do not directly "cause" craving, but they activate the drug-related beliefs that lead to the craving. Although w e use the term "stimulus situation," it should be noted that the situation itself is neutral. The meanings, derived from the beliefs, that are attached to a situation are what cause the individual's craving. Individuals with beliefs that they cannot tolerate anxiety, dysphoria, or frustration, for example, will tend to be hyperattentive to these sensations and m a y build up expectations that they can relieve the sensations only through using or drinking. Thus, w h e n an unpleasant affect arises, the individual attempts to neutralize it by using or drinking. A specific sequence of drug-related beliefs leading to drinking or using m a y be delineated. First is the activation of anticipatory beliefs relevant to obtaining pleasure from using or drinking. These antici­ patory beliefs usually progress to relief-oriented imperative beliefs, which define using or drinking as a dire necessity and stipulate that the craving is uncontrollable and must be satisfied. The anticipation of pleasure or relief leads to the activation of craving and facilitating 01 permissive beliefs, such as "I deserve it" or "It's O K this time," which legitimize using or drinking. Finally, the instrumental plans, which have to do with plans or strategies for obtaining drugs or alcohol, are propelled by the imperative craving. M a n y individuals have conflicting beliefs regarding the pros and cons of using. At times they are locked in such an unpleasant struggle between these opposing beliefs that, paradoxically, they m a y seek dmgs simply to relieve the tension generated by the conflict. The therapeutic application of this model, consisting of modify­ ing the individual's belief system, goes beyond teaching the individual to avoid or cope with "high-risk situations." C H A P T E R 4 T h e T h e r a p e u t i c R e l a t i o n s h i p a n d I t s P r o b l e m s A , , collaborative relationship between the therapist and the patient is a vital component of any successful therapy. The most brilliantly conceived interventions will be reduced in effective­ ness if the patient is not engaged in the process of treatment. All the support and effort that the therapist m a y put forth in an effort to help the patient will make little impact if the therapist has not gained some measure of the patient's trust. While this seems to be relevant to almost every type of patient, it is most especially true of the substance-abusing population. Numer­ ous potential factors interact to create an almost adversarial relation­ ship between the therapist and the drug-abusing patient at the begin­ ning of therapy and during the course of treatment. These factors include: 1. Drug-abusing patients often do not enter treatment on a vol­ untary basis. 2. Patients often maintain highly dysfunctional presuppositions about therapy. 3. Patients often are not very open and honest, at least at the start of therapy. 4. Patients may be currently involved in felonious activities, thus presenting confidentiality dilemmas. 5. Patients view their therapist as part of the "system," and not as an ally. 54 The Therapeutic Relationship 55 6. Patients have a difficult time believing that their therapist r cares about their problems. 7. Patients look askance at therapists w h o m they perceive to differ from them markedly in terms of demographics and attitudes. 8. Therapists may maintain negative presuppositions about drug- abusing patients. Many of these patients do not come into therapy of their own volition. Some are given an ultimatum by their significant others (e.g., spouse, children, or parents) or employers, while others are remanded by the courts following criminal legal proceedings (Frances & Miller, 1991). Consequently, the drug-abusing patient may enter the ther­ apist's office with any number of counterproductive automatic thoughts, such as "I don't want to be here; I'm only here so m y wife will get off m y back," "I'll just tell this doctor what he wants to hear, and then I'll blow out of here," "This whole therapy thing is like doing real easy time compared to prison; I'll just go along with this and do what I want to do anyway," "I don't really have a problem; maybe I'll show up for therapy, and maybe I won't," and "I'm not going to tell this shrink anything that can be used against me; m y life is nobody's business but m y own." The list could go on and on. To complicate matters further, drug-abusing patients typically enter therapy playing their cards close to their vests, and therefore conceal the kinds of automatic thoughts listed above. The therapist must actively probe for them, as the patients often will not divulge them in an unsolicited fashion (Covi et al., 1990). Another factor that militates against the ready formation of a positive therapeutic relationship is that substance abuse often repre­ sents felonious behavior. As such, patients are highly motivated to be dishonest in self-reporting their substance abuse activities. Although the vast majority of therapeutic interactions represent privi­ leged communications between therapist and patient, drug-abusing patients are typically well schooled in covering their tracks. As the stakes are high, such patients may simply decide it is best to take no chances, and therefore will not readily admit to drug-abuse-related behaviors. Furthermore, some actions of the patients may be serious enough threats to themselves or to the general public that the thera­ pist may legally and ethically be required to contact the authorities (e.g., when the patient admits that a drug-related murder has been arranged, or when the patient calls the therapist and claims to have taken a drug overdose in order to attempt suicide). Since therapists should inform their patients about the limits of confidentiality at the outset, drug-abusing patients will come to know 56 COGNTTIVE THERAPY OF SUBSTANCE ABUSE what information they cannot safely reveal. If they do come forth such sensitive material, the therapist is placed in the uncomfortable position of having to serve as society's watchdog, and may in the process completely discourage the patient from continuing with much needed treatment. This point highlights another more general factor that adds to the difficulty in forming a working alliance with drug-abusing patients-̂ iamely, that such patients often view the therapist as an agent of the police, the courts, "the system," or a more privileged socio­ economic class. Such patients find it hard to believe that their thera­ pists will sincerely try to help them with their problems, or will treat them with honesty, respect, and positive regard. As a result, the patients tend to dread and avoid therapy sessions. They may take con­ frontational statements from the therapist as confirmation that the therapist is working against them, while positive statements from the therapist may be seen as naive, manipulative, insincere, or patroniz­ ing. This places the therapist in a "damned if I don't, damned if I do" position, which, left unaddressed, may sabotage therapy before it gets started. Yet another stumbling block to the formation of a healthy thera­ peutic relationship is the perceived demographic and/or attitudinal differences between therapist and patient. For instance, the patient might think, "This doctor is probably rich and has everything she wants in life. There's no way that she could possibly understand what it's like to struggle every day of your life like I do. H o w in the worid can she help me? The rules of her world just don't apply to mine. Whatever she says is just bullshit." Another thought might be, "I wonder if this therapist ever used drugs. If he did, then he's no bet­ ter than me, so why should I listen to him? If he didn't, then how can he know what it's like to be hooked? Only someone who's been there could know what he's talking about." Similarly, the therapist may have maladaptive beliefs about the patient, such as "This guy is a low-life. At best he's going to waste m y valuable time, and at worst he's going to be a liability or a threat to m y personal safety," or "These types of patients are beyond help. They have a chronic disease for which there is little hope for cure or rehabilitation. Therefore, there's not much point in investing too much of m y time or energy," or "I can't relate to this patient at all. 1 wouldn't associate with him (or her) in 'real life' so I don't think I'll be able to form a working bond with this patient here in the office either." Admittedly, working with drug-using patients can be highly stress­ ful; therefore we strongly encourage therapists to engage in regular The Therapeutic Relationship 57 peer supervision with colleagues in order to receive professional support and objective advice. Such consultations can help therapists to avert burnout, and to combat their own dysfunctional beliefs pertinent to working with the drug-abusing populations (cf. Weiner & Fox, 1982). W e acknowledge that the obstacles are formidable. However, based on extensive clinical experience, we believe it is possible to establish a positive, collaborative therapeutic relationship with the substance abuser. W e consider this to be the case even when such patients exhibit severe concomitant Axis II disorders, such as para­ noid, narcissistic, and/or antisocial personalities (see Chapter 16, this volume). To be sure, the task is difficult, and frequently trying. At the same time, freating the substance-abusing patient can be reframed as represeriting a growth-enhancing challenge for the therapist. The skills of developing therapeutic alliances with difficult populations (e.g., substance abusers and borderline patients), comprise the "art" of therapy, and as such are very much a measure of the competency of the mental health professional. This chapter presents guidelines for facilitating the formation and maintenance of an adaptive and functional therapeutic relationship with the drug-abusing patient. Case illustrations are provided in order to highlight various techniques and strategies, as well as to demon­ strate how things can go awry. The central messages of this chapter are that (1) a positive therapeutic relationship does not occur by chance—it can be actively constructed, (2) treating the drug-abusing patient requires careful and vigilant attention to the vicissitudes of the interactions between the therapist and the patient, and (3) the management of the therapeutic relationship with the drug-abusing patient is neither a straightforward nor an overwhelming task. ESTABLISHING R A P P O R T The initial interactions between the patient who is just entering therapy and the therapist are extremely important. Even when dmg-abusing patients are self-referred, they often have a great deal of ambivalence about seeking ongoing contact with a therapist (Carroll, Rounsaville, & Gawin, 1991; CarroU, Rounsaville, & Keller, 1991; Havassy et al., 1991; Institute

of Medicine, 1990b). From the very start, such patients will be sizing up their therapists to determine if they can be trusted and if they know what they are doing (Perez, 1992). A perceived negative experience with the therapist can lead such patients to choose never to return for further sessions. For those patients who 58 COGNTTIVE THERAPY OF SUBSTANCE ABUSE are constrained to continue with therapy as per the terms of their parole or probation, the lack of a positive start to treatment may lead to the kinds of negative expectations that foster passive resistance or contentious behavior in session. The introductory session in cognitive therapy typically involves the dual aims of establishing rapport with the patient, and socializ­ ing the patient into the cognitive model. W e suggest that the thera­ pist adhere to both these aims, but place special emphasis on the aim of establishing rapport. The basic therapeutic tasks of listening, reflec­ ting, and demonstrating genuineness and positive regard must not be given short shrift at this stage. While it is also useful to describe the cognitive model, it is important to minimize psychological jargon, and to stay as close as possible to ordinary language. This will help the wary and distrustful patient to view the therapist as being more of a "real person." For example, the cognitive therapist would be ill-advised to speak in the following manner: "We're going to be examining your thinking processes, to under­ stand the kinds of cognitive distortions that lead you to engage in maladaptive behaviors such as drug abuse and antisocial activities." Instead, a preferable alternative phrasing would be: "Mr. X, I'd like to tell you a little bit about cognitive therapy, and I'd like you to feel free to ask m e any questions you might have about what goes on here in treatment. W e try to understand how you see things—your thoughts about yourself, about life, about using dmgs, and about other things. The reason for this is that it's very important for me to understand where you're coming from and what you're going through. It's also important because you might learn some things about yourself that could help you turn your life around to be more the way you want it. What do you think of that?" The therapist in the above example does not go into depth in describing cognitive therapy, but he sets some of the groundwork. It is more important that the therapist come across as being understand­ ing and reasonable. If the patient remains in treatment for a suffi­ cient period of time, there will be many opportunities to elaborate on the specifics of cognitive therapy, and to teach the patient the relevant cognitive and behavioral skills. It is important that therapists communicate in as nonjudgmental a manner as they do with their non-substance-abusing patients. Most clinicians can sympathize with patients who are depressed or anxious but may have less tolerance for those who break the law and cause misery for their families because of their own substance abuse behav- The Therapeutic Relationship 59 iors. Therefore, therapists need to monitor their thoughts and verb behaviors so that they do not project an air of disdain or preachiness in the therapy session (we discuss this in more detail later in the chapter). The patient's drug abuse behaviors and cognitions need to be discussed as representing a problem, without implying an attack on the patient's morals or character. Additionally, therapists can facilitate the development of rapport by focusing on other areas of their patients' distress as well. Since many of these patients are in treatment by virtue of having reached points of crisis in their lives (Kosten, Rounsaville, & Kleber, 1986; Sobell, Sobell, & Nirenberg, 1988), many of them have dual diagnoses (Castaneda et al., 1989; Evans & Sullivan, 1990; Nace et al., 1991; Rounsaville et al., 1991), thus making it appropriate to address such areas of concern as dysphoric mood, feelings of shame and low self- esteem, general difficulties in coping with life stressors, family prob­ lems, and the like. W h e n therapists demonstrate that they are inter­ ested in the entirety of the patients' well-being, and are not simply seeking to stop their "bad" drug using, patients may begin to see their therapist as an ally. In this manner, therapists show that they are interested in getting to know the patient as a person, not simply as an addict. Therapists then gain a better chance at calling patients' attention to the fact that substance abuse is an important causal fac­ tor in their overall emotional, interpersonal, and physical malaise. This motivates patients to consider the cessation of substance abuse as a major ongoing goal of therapy. Another useful rapport-building technique nicely doubles as a procedure to begin to educate patients about the cognitive model. Here, therapists freely ask their drug-abuse patients what they think about coming into therapy. Such questions can involve asking about patients' doubts and concerns, as well as their expectations, goals, and hopes for therapy. It is especially important to inquire about these thoughts during the initial therapeutic contact, to maximize the like­ lihood that the patient will return for a second session. Otherwise, the patient may harbor misgivings about ongoing sessions, and quietly exit therapy after one session without ever offering a clue that such intentions were present. As illustrated earlier, these techniques serve two functions. First, they communicate a willingness to hear the patient's point of view, and show that the patient will have input into the treatment. Second, they allow the therapist to point out how certain thoughts (e.g., doubts about therapy) can lead to certain emotions (e.g., hopelessness and dysphoria) and behaviors (e.g., quitting therapy) that have a great impact on the patient. After discussing these doubts, the patient may have a more optimistic outlook on therapy. If the patient also feels 60 COGNITIVE THERAPY OF SUBSTANCE ABUSE better emotionally, the therapist can seize on this as a live exam of cognitive therapy at work—positive thinking corresponds with positive mood. The following dialogue between patient (PT) and thera­ pist (TH), based on one of our court-referred cases, illustrates this: PT: {interrupts the therapist to ask a terse question) How many ti do I have to come here [to therapy sessions]? TH: Well, as I understand it, as often as you and I believe it makes sense that you come here. That might be once a week, perhaps more often, perhaps less, and we'll be meeting either until it's clear that you're no longer in need of regular sessions, or until the end of your probation period. Do you have some ideas in mind? PT: Yeh, I have some ideas, (long pause. patient frowns and has a scowling look) TH: I take it you're not too pleased about being here. PT: You got that right. TH: I'd like to hear you out if you're willing to tell me what's on your mind right now. PT: What's to tell? I have to come here, and that's that. I ain't got no choice. So what else is new? TH: H m m m {sympathetically). You're pretty down and maybe pissed oft that you have to come here. And it feels to you like it's some­ thing that was forced on you. PT: Yeh. TH: And that this isn't the only thing that's been forced on you? PT: Yeh. TH: I'd tike to hear more about it. PT: I'm just tired of the whole thing, {long pause) TH: Go on. I'm listening. PT: I did my time. Two years of m y life. And now I'm supposed to be free, but no. I have to check in with m y parole officer, and I have to give urines [toxicology screens each week], and I can't travel without permission, and I have to go see a head shrinker, and everything else. TH What is your opinion about all of this? PT: It sucks. TWHel l, I suppose that I wouldn't be too pleased myself if I were going through what you're going through right now. I don't think I'd take too kindly to having all these appointments. The Therapeutic Relationship 61 PT: It's like, I'm always being checked up on. And being monitored. I'm sick of it already. It's as bad as when I was in jail. TH: Are you saying that you view coming to therapy here as being "checked up on?" PT: Yeh. {sarcastically and incredulously) Tell m e you're not here to check up on m e and report things to m y PO about me. TH: Well, you got part of it right, that's for sure. I am responsible for sending an attendance report to the parole office each month. I mean, after all, they are paying for your treatment and they want to see that you're getting something out of it and not just blowing it off. If you're not here, then it probably tells them that you're not getting any ongoing help. If you're not getting any ongoing help, then you don't stand as good a chance of remaining free of drugs, and you might violate parole and wind up in jail again. I don't think that they want you to have to go back to jail again, and neither do I. PT: What's it to you? TH: Well, I like to think I'm doing something worthwhile for people. I'd feel proud of myself and happy for you if our weekly meet­ ings had something to do with getting this drug and prison monkey off your back once and for all so you can get back to living your own life again. M y main goal is not just to check up on you. PT: It's just such a hassle, you know. TH: I know. [Therapist makes a conscious decision not to address this automatic thought at this time, but rather chooses to com­ miserate with the patient in order to build rapport] PT: I guess I have to come here. But I don't have to like it. TH: Well, that's true. You're the final judge on whether this whole therapy thing is worth anything to you. But I'd like to think that we could work together so that you can get something for your troubles. I'm not here to "shrink your head." I'm a psy­ chologist. A therapist. I'm here to help you solve some prob­ lems. I can't do it alone, though. I need your assistance. I may be an "expert" in psychology, but you're the expert on you. I have to respect that. PT: Well, yeh. TH: What would you like to get out of therapy so that it's much more than just being monitored? Something for you. Therapist and patient went on to talk at some length about the patient's goals for therapy, and the patient's mood brightened and 62 COGNITIVE THERAPY OF SUBSTANCE ABUSE her anger diminished. Before the end of the session, the therapist helped the patient to summarize the contents of the session, with special emphasis on an important point that paved the way to social­ ization into the cognitive model. The main point was that when the patient thought only about the down side of therapy, she felt sad and angry. However, when she opened up her mind to other possible uses of therapy, she acquired more information, thought of more useful ideas, and felt more hopeful. In short, she learned an important les­ son about how untested thoughts could adversely affect her emotions, as well as her capacity for solving problems. She also learned that it was important to get all the facts before passing judgment on a situ­ ation (such as being in a therapist's office for the first time), espe­ cially when the situation seemed very negative to start with. As highlighted by the preceding dialogue, it is useful to elicit the patient's negative thoughts about therapy. Therapists need to be able to hear the patient's complaints without feeling personally attacked. They may be tempted to engage in an argument with such a patient, and/or to dismiss the complaints as being pure folly. They need to resist such a temptation, lest the patients regard their expectations about the adversarial nature of therapy as confirmed. A sympathetic elicitation of

the patient's thoughts, followed by sincere involvement by way of questioning and direct, honest, humble feedback, will be a boon to the establishing of rapport. As patients attempt to engage in the process of treatment, thera­ pists can help facilitate the establishment of rapport by giving posi­ tive verbal reinforcement for the patients' pro-therapy behaviors and attitudes. For example, therapists can provide encouragement and praise to patients for demonstrating good attendance, promptness, active participation in sessions, and cooperation with therapeutic homework assignments (e.g., writing down the disadvantages of using drugs each time the patient experiences a strong urge to go out to make a "score"). Such positive feedback from therapists helps patients to feel supported, to understand their role in therapy, and to decrease their anxieties and negative expectations about the process of work­ ing with mental health professionals. BUILDING T R U S T Trust does not develop immediately. It cannot be asked for, and it cannot be artificially rushed. Only through the therapist's consistent professionalism, honesty, and well-meaning actions over a period of time can trust enter fully into the therapeu- The Therapeutic Relationship 63 tic relationship. It does no good for the therapist to say merely, worry, you can trust me." It is far more realistic to admit that there is little reason for the patient to trust the therapist in the beginning, but that "I hope that in time you will decide for yourself whether or not I can be believed and trusted." Unfortunately, trust can be impaired or lost relatively quickly, and therefore it must be nurtured and managed in a delicate, painstaking fashion. In short, therapeutic trust with the substance-abusing popu­ lation is difficult to establish, and may be more difficult to maintain. Furthermore, even if the patient learns to trust the therapist, there may be little reason for the therapist to trust the patient. Inaccurate and/or incomplete reporting by patients is a frequent phenomenon with this population, a situation to which the therapist must remain sensitive. Nevertheless, since the professional is held to a higher stan­ dard of behavior than is the patient, the therapist must be willing to continue benevolently to assist the substance-abusing patient, even if that patient has been untruthful. Later, we discuss ways in which the therapist can confront such dishonesty on the part of the patient, yet continue to strengthen the therapeutic relationship and work toward greater progress in treatment. The following suggestions and illustrations are offered to assist the cognitive therapist in achieving and holding on to this most valu­ able therapeutic asset. The basic elements of trust building are very simple and undra- matic. They include behaviors that consistently demonstrate the ther­ apist's genuine involvement in the therapeutic process, and com­ mitment to being available to the patient. Such behaviors include (1) being available for therapy sessions on a regular basis, (2) being on time for sessions (even if the patient is not), (3) returning patient telephone calls in a prompt manner, (4) being available for emergency intervention (e.g., by giving the patient a telephone number where the therapist can be reached in case of the need for crisis interven­ tion), (5) showing concern and being willing to try to contact the patient if he or she fails to keep an appointment, and (6) remaining in touch with the patient (and available for the resumption of outpa­ tient cognitive therapy) if inpatient hospitalization, detoxification freatment, halfway house rehabilitation, or reincarceration takes place during the course of the therapeutic relationship. Therapists foster trust when they assiduously avoid making dis­ paraging comments about the patient, the patient's family members, other substance abusers with w h o m the therapist has had contact, or any socioeconomic, ethnic, or gender group. Even if the therapist makes the derogatory comment about someone else, the patient may 64 COGNITIVE THERAPY OF SUBSTANCE ABUSE think that this is how the therapist truly thinks of him or her wh not working in the role of "therapist," and such a remark may foster the patient's possible belief that the therapist is insincere in his or her show of respect. Trust is also built when therapists serve as role models who have "clean" lifestyles and attitudes. Offhanded comments by therapists about their own "partying" or "getting buzzed" clearly are contra- indicated. Such statements give drug-abusing patients a confusing mixed message. This message may lead the patient to perceive the therapist as a hypocrite who operates on a "Do as I say, not as I do" policy. Related to this issue is the situation that arises when patients ask therapists about their own experiences with drug use. Certainly, thera­ pists are under no obligation to answer this type of question. A typi­ cal appropriate response would be, "I know you're curious about it, but I'm going to have to decline to answer your question. W e really have to stick to talking about issues that are relevant to you." At the same time, therapists may use their discretion in choos­ ing whether to answer. A brief, honest reply may go a long way toward fostering the patient's sense of trust for the therapist. For example, the therapist might answer, "No, I've never used any drugs on more than a try-and-see basis, and even that was fifteen years ago. I was playing with fire, and I guess I'm lucky it never progressed. But I've seen enough misery in the lives of those who've gotten into more regular drug use to know that I'd be a damned fool to ever try any­ thing again." Another honest answer could be, "No, I've never used drugs. I was always too afraid that I might like them. But really, we need to focus back on you because this is your session." Those thera­ pists who have used drugs in the past may choose to be silent about this matter or may use the experience to make rare but relevant self- disclosures as a way of keeping a patient engaged in treatment or to drive home an important point. The goal here again is to nurture the therapeutic relationship, not to get sidetracked from the work of therapy. SETTING LIMITS While it is crucial that therapists strive to work in a collaborative fashion with their drug-abusing patients, they must take care not to become oversolicitous to the point that patients know they can take advantage of their therapist. Limits must be set (Moorey, 1989)-for example, that a therapy session will not be held if it is de­ termined that the patient is in an inebriated or drug-intoxicated state. The Therapeutic Relatioruhip 65 Another such limit might be that the therapist will not condone "a little bit" of drug use. Therapists can establish such ground rules without sabotaging the therapeutic relationship if they take care to maintain a respectful tone, and reiterate their commitment to act in ways that are in the best therapeutic interest of their patients (Newman, 1988, 1990). When one of our patients arrived drunk to a session, the following dialogue took place: TH: Walt, pardon me for asking this . and if I'm mistaken please accept m y apology. but have you had something to drink before coming to this session? PT: I had a few. N o big deal {belches to be humorously obnoxious). TH: H o w many is "a few"? PT: You know, a few. TH: Walt, I think you're intoxicated. PT: I'm fine. I can hold m y beer pretty good. TH: Walt, we've discussed this before. If you're in an altered state of mind . and believe me, drinking "a few" means that you're in an altered state of mind . there's no point in going through with this session. I have no reason to believe that you'll be able to pay serious enough attention to what we do here to warrant continuing with this session. PT: Shit man, you're making a big deal out of nothing. TH: Walt. PT: I'm fine I tell you. TH: Walt. PT: I shouldn't have said anything. TH: Walt. I'm glad you were up front with me. I respect you for it. I'm depending on you to be a man and tell m e the real story to m y face. It's just that we can't go through with this session. That was our agreement, and I think we should stick to our agreements. PT: Shit, man. TH: Did you drive here? PT: No, I was beamed down {sneers). TH: I have something important to ask you. I need to ask you to hang out in the waiting room for a couple hours until you're sober enough to drive safely. 66 COGNITIVE THERAPY OF SUBSTANCE ABUSE PT: Doc, I don't got time for this shit. I got here fine, and I'll home fine. TH: Walt, you've worked too hard to get to this point to mess up now. If you get pulled over, or worse, you're risking going back to jail. I don't want to see that happen to you. What's a couple of hours to ensure your freedom? You can have m y newspaper to keep you occupied for awhile. The patient ultimately complied with this therapist's request. The limit was clearly set, but the tone of the communication was neither critical nor controlling. The therapist emphasized that he was look­ ing out for the patient's welfare, and this had a lot to do with the patient's compliance and willingness to continue actively with cog­ nitive therapy. When the therapist sets a limit, sticks to it, and does so in a respectful way, trust is fostered and the patient learns to have respect for the therapist as well. Parenthetical to the above, it is necessary that the therapist be amenable to continuing with therapy once the patient is in compli­ ance again after a slip (Mackay & Mariatt, 1991). Since many drug- abusing patients frequentiy test limits, no gains will be made if thera­ pists are disinclined to go forward with therapy when their patients engage in defiant and/or manipulative behaviors. Therapists serve their drug-abusing patients best when they follow through on predeter­ mined agreements on how to deal with counterproductive patient behavior but also show genuine support and encourage the patients to "get with the program" again. The above vignette brings up the issue of the role of alcohol in the illicit drug-abusing patient's life and therapy. While we believe that it is theoretically possible for illicit-drug-abusing patients to con­ tinue to drink alcoholic beverages on a casual basis during treatment, in practice our experience tells us that the use of alcohol undermines their abstinence from drugs such as cocaine and heroin. One reason is that the use of alcohol lowers patients' inhibitions. Patients have reported that when they are drinking they are less likely to think about the compelling reasons for staying free of drugs. Even when they can stay focused on the disadvantages of drug use, patients report that they are less apt to care about the long-term consequences of their behavior than when they are sober. Thus, they are more likely to resume the use of harder substances. Further, when patients use alco­ hol as a "substitute" for drugs such as cocaine or heroine, their con­ sumption quickly escalates to levels indicative of abuse and depen­ dence. Therefore, we discourage the use of alcohol durtng patients' treatment and recovery from illicit drugs. The Therapeutic Relationship 67 PROTECTING CONFIDENTIALITY As alluded to previously, there are limitations to con­ fidentiality. Therapists should spell this out to their patients from the very start. The following monologue may serve as a model: "Mr. A, I want you to know that almost everything we discuss here will be kept just between you and me, unless you want rne to talk to someone else about your situation or you otherwise give m e permission. So, for the most part, things that you tell m e here will be kept confidential. But I want to inform you that there are certain exceptions to this rule. If you tell m e something that indicates that you or someone else is in danger, and you're not willing to help me fix the situation so that everyone is safe, then I am legally obligated to contact the authorities and anybody else who

may be personally involved. This includes situations in which you intend to kill your­ self or someone else, or where you are causing harm to a child. Another such situation would be where you have the AIDS virus, but you're not telling your sexual partners or making any attempts to protect them from infection. Please hear m e out. I can promise you this: If it comes to pass that I have to break confidentiality in order to protect you or someone else, I will make every possible effort to let you know that I'm going to do this. I don't want to do things behind your back. That's not m y style. I'd rather that you know exactly where I'm coming from. In fact, if the authorities have to be con­ tacted, I'd be more than happy to stand by you while you make the phone call. If you cooperate in this way, and I support you, we can solve most any problem. What do you think about all that I've just said? Do you have any questions?" (If the patient has been referred by a parole office district, the following can be added to the monologue): "You should also know that I am obligated by law to let your parole officer know whether or not you are attending these therapy sessions, and to let him know if you are arriving on time. I don't have to tell him if you have started using drugs again, but he'll be asking you to submit to giving urines on a regular basis, so he'll have his own way of knowing whether you've started up again." Patients will not be pleased to hear this, but they will appreciate the explanation and the warning. The alternative, namely, that the therapist necessarily breaks confidentiality without first alerting the patient to this possibility, will at the very least seriously undermine trust in the therapist. 68 COGNITIVE THERAPY OF SUBSTANCE ABUSE MAINTAINING CREDIBILITY Yet another way in which therapists can establish and maintain their credibility as trustworthy professionals is by being willing to admit that they do not know everything, and/or that they were wrong about something. To highlight this point, one of our patients asked his therapist if the therapist could use hypnosis to cure him of his crack addiction. The therapist admitted that he had no training in hypnosis, and therefore could not perform this technique. Instead, he explained a bit more about cognitive therapy and worked with the patient to formulate a goal list. In a later session, the patient stated that he knew that the therapist was "for real" because the thera­ pist admitted that he did not know how to perform hypnosis. The patient added, "How did 1 know what you could do for m e and what you couldn't? N o w at least 1 know that if you say you can do some­ thing for me, you can actually do it-and if you can't, you tell me you can't. I wouldn't know what to believe if you always said you could help me with everything." In another instance, the therapist was waiting for his patient to arrive for her session. After 20 minutes, the patient telephoned. Before the patient could explain herself, the therapist launched into a mini- lecture on the importance of attending therapy sessions on time. Just then, someone else got on the line. It was the patient's parole officer, who proceeded to explain to the therapist that he had been respon­ sible for the patient's delay in leaving the parole office. Half an hour later, when the patient arrived for her session, the therapist immedi­ ately apologized for jumping to the conclusion (a cognitive error) that she was remiss in her obligation to attend therapy. He pledged that he would "get evidence" next time before passing judgment. He then asked the patient if she had any negative thoughts or feelings about this situation. She smiled and replied, "Not anymore." In sum, humility, honesty, and aboveboard communication from the therapist will help to bring about the development of the all- important qualities of trust and rapport in the therapeutic relationship. MAINTAINING A SPIRIT OF COLLABORATION When both the therapist and the patient are actively working together, rather than in opposition or in stagnant passivity, there is the greatest potential for therapeutic change. Cognitive therapy takes such a collaborative approach, whereby therapists communicate The Therapeutic Relationship 69 that they take their patients' points of view very seriously, downp their own role as an "all-knowing" paragon of authority and power, and stress the importance of mutual work toward discovery and posi­ tive change (Beck et al., 1979). In doing so, tiierapists do not have to take an overly lenient stance with regard to their patients' problematic drug use and drug-related behaviors, nor must they remain neutral regarding their opinions about drug abuse. Therapists can communicate a fijndamental posi­ tive regard for their patients as individuals without condoning their abuse of substances. This separation of patients from their behavior may seem contrived to some degree, but it is just such a stance that may facilitate the spirit of the therapist and patient working as a team to fight the patient's drug abuse problems. In any event, the differ­ ences between the patient's personality when he or she is using drugs versus when he or she is free of drugs are typically so striking that it is not really difficult to mentally separate the patient from the abuse- related behaviors. A key element of collaboration is compromise. Therapists must not allow themselves to be manipulated or conversely to become dictatorial in their dealings with their substance abuse patients. It is strongly advised that therapists take a firm stance, neither encourag­ ing power struggles nor acquiescing fully to patients' threats and idle promises. Therapists best demonstrate both their strength of will and their character, as well their willingness to collaborate, by being flex­ ible. On a small scale, this quality is demonstrated when therapists allow their patients some say in what gets discussed during the therapy hour. In a situation in which the therapist believes that the patient's chosen therapeutic agenda is too tangential to be valuable, the thera­ pist would do well to agree to spfend a limited amount of time on the patient's preferred topic, while noting for the record that other issues need to be discussed as well in order for treatment to have its stron­ gest impact. Such a strategy fosters a positive working alliance. O n a larger scale, therapists may need to use diplomatic skill just to keep their patients from bolting from treatment. For example, a patient who loathed the fact that he was indeed in the role of a patient wanted to use therapy contacts as nothing more than "bitch sessions." In this manner, the patient could blame everyone else for his troubles and not have to face the fact that he himself had problems that needed attention. When the therapist highlighted this point, the patient threat­ ened to discontinue treatment. After a long discussion (in which the therapist remained calm and carefully worded his comments), it was agreed that the even-numbered sessions would be reserved for com­ plaining about others, but that the odd-numbered sessions would 70 COGNTTIVE THERAPY OF SUBSTANCE ABUSE focus on the patient's problems with anger, depression, and drug abuse. For good measure, the therapist thanked the patient for being "so open minded and a good sport." Ironically, once the patient began to utilize the odd-numbered sessions to discuss his personal issues and drug abuse tendencies, he spontaneously began to use the even- numbered "bitch sessions" to do the same. RESISTING C O L L U S I O N W I T H T H E PATIENT Many substance-abusing patients, on ascertaining that their therapists are supportive and genuinely trying to help, will try to take advantage of the situation. They do this by asking their thera­ pists to single them out for special treatment, to conceal information from their parole officers, to ignore obvious trouble signs, and in general to assume the role of "enabler." Therapists then find them­ selves in the dilemma of trying to reassert the therapeutic ground mles without alienating their patients (cf. Newman, 1990). As difficult as this task might seem, it is essential if therapy is to continue in a fmitful direction. As we've mentioned previously, the therapeutic relationship can be preserved if the therapist communicates straightforward hon­ esty and expresses a desire to continue to provide therapeutic assis­ tance. One patient, "Charleen," called her therapist at home late at night, asking for the following "favor": PT: I'm sorry to bother you so late, but I really need you to help me out. TH: OK. What's going on? PT: I'm on m y way home from a [support group] meeting, and my boyfriend thinks I'm out messing around and getting high and he said he's going to kick me out if I stay out late again. Could you call him and let him know that I've been to a meeting and that everything's cool? [Before saying anything in reply, a number of thoughts were al­ ready racing through the therapist's mind. For starters, he realized that he had no way of knowing whether or not what Charleen was saying was true. Second, he recognized that this request was an inappropri­ ate use of therapeutic telephone privileges. He decided to engage the patient in further dialogue before passing judgment and before agree­ ing to do anything.] TH: Charleen, you know that I want to help you out any way that I can, but I have to admit that I'm uncomfortable with how this all sounds. The Therapeutic Relationship 71 PT: What do you mean? {getting annoyed) TH: Well, you're asking m e to comment on something I have no knowledge of. Now, if you had just been to m y office and we had had a session, and you wanted m e to call to let him know, then I would do it. But this is different. It would make much more sense for you to call your boyfriend yourself and let him know where you are, or just return home as usual. If I call, he's going to think that I'm giving him an alibi for you, and that will just raise his suspicions further. Have you thought this through? PT: So what are you saying, that you're not going to help m e out? Thank you very much, you're a great therapist {angry, sarcastic tone). TH: Charleen, I'm more than happy to help you to deal with a prob­ lem or a situation, but I can't act to make it go away for you. There are certain things that you have to take responsibility for yourself. This is one of those things. PT: So what am I supposed to do if m y boyfriend throws m e out? TH: If that happens, call m e again and we'll try to do some prob­ lem-solving. Can you call m e from your mother's house if that happens? PT: I don't want to go to m y mother's house! TH: You don't have to want to go there. I'm just asking if you can call m e from there if you have to. PT: Yeh. I guess. TH: OK. Do you want to schedule an appointment for tomorrow so we can discuss this whole matter at greater length? PT: I don't know {disgusted tone). TH: Please level with me, Charleen. Have you been using [drugs]? PT: No! TH: Can I depend on you to stay away from drugs until tomorrow when we can get together and have a session? PT: Yeh, yeh. This dialogue illustrates the fact that therapists can offer appro­ priate therapeutic support without having to allow themselves to get sucked into playing the role of enabler. A certain degree of collabo­ rative compromise was called for here. The therapist was unwilling to call the boyfriend for the patient, but he did express a willingness to receive another late-night telephone call in order to help the patient 72 COGNITIVE THERAPY OF SUBSTANCE ABUSE deal with a potential crisis. (Although therapists at the Center f Cognitive Therapy routinely provide patients with

their home tele­ phone numbers for use in emergency situations, we realize that some therapists may prefer instead to make use of an intermediary such as an answering service. In either case, we believe that it is necessary for patients to be able to make contact with their therapist after hours in the event of critical situations.) APPEALING T O PATIENTS' POSITIVE SELF-ESTEEM As many substance abusers evidence defiant attitudes and/or pathological levels of self-importance, it is often necessary for the therapist to appeal to patients' narcissism in order to elicit col­ laboration from them. This does not have to entail gross hyperbole on the part of the therapist. If fact, such an approach is contraindicated as the intelligent patient will rightly see it as an insincere, manipula­ tive ploy. Rather, the therapist needs to focus on some of the patient's actual strengths and positive points, and express appreciation for these qualities. This approach serves to strengthen rapport and to elicit greater cooperation. The following clinical vignette demonstrates an appeal to the patient's sense of entitlement in order to defuse his anger toward the therapist. The problem arose when the patient did not show up for his session, and instead called 5 hours later to say that he had gotten a fiat tire on the way to the therapist's office. The dialogue (a con­ densed version of the actual interchange) proceeded in the following manner: TH: Walt, we've talked about how important it is for you to get to sessions on time, and to keep me informed of your whereabouts. The fact that you waited five hours to call me concerns me. PT: {Exasperated) I was on the road. I couldn't get to a phone. I didn't have a spare tire so I had to wait to get help. There was no way 1 could call any sooner. TH: Walt, ninety percent of m e wants very much to believe you, but I have to be honest with you—ten percent of m e has m y doubts. I can't help but wonder whether your lateness in getting in touch with me is drug related. [The patient responded very angrily, vilifying the therapist for being "such a hard-ass" and for insulting the patient by "calling me The Therapeutic Relationship 73 a liar." The therapist answered with a reply that was geared to use Walt's narcissism in the service of repairing the therapeutic relation­ ship.] TH: Walt, I'd like to believe everything you say to me. But you and I both know that you have a lot of skill and experience in cov­ ering your tracks. You could easily outsmart m e if I'm not care­ ful. If I just blindly believe everything you tell me, then I'm a fool, and frankly, I think you deserve better than to have a fool for a therapist. This latter statement achieved its intended effect of disarming th patient's hostility long enough to get him to agree to come in for a session early the next day. Later in treatment, the therapist and Walt were discussing Walt's unsafe sexual habits. Walt noted that he did use condoms when he had sex with prostitutes, but refused to wear one with his many "girl friends," stating facetiously that it was against his religion. Therapist and patient discussed these practices at length, trying to get a handle on the automatic thoughts and beliefs that led him to act so reck­ lessly in this era of the AIDS epidemic. Additionally, the therapist attempted to focus Walt's attention on the dangers involved in his sexual behavior by noting the pros and cons of wearing condoms. Finally, when it seemed that these tactics were falling on deaf ears, the therapist resorted to making an appeal to Walt's intelligence by saying: TH: The fact that you wear condoms with hookers is a smart move. I wouldn't expect anything less than a smart move where you're concerned. You're very good at taking care of number one. So it confuses m e how you would stop short of doing the smart thing with your girl friends as well. It just doesn't seem like you, Walt. It's out of character for you to leave any loose ends like that [no pun intended]. You normally have all your bases cov­ ered [again, no pun intended]. This approach effectively pitted Walt's desire to be seen as an intelligent person against the "macho" rules that governed his unsafe sex practices. It allowed the therapist to be confrontive without dam­ aging rapport or collaboration. In other cases, we have helped bring our patients back into a collaborative mode by appealing to their sense of justice, their posi­ tive feelings for involved significant others, their survival skills, their integrity, their potential abilities to be positive role models for others, and other personal attributes. 74 COGNITIVE THERAPY OF SUBSTANCE ABUSE MANAGING POWER STRUGGLES In spite of the therapist's best efforts to maintain an ongoing positive therapeutic relationship with the drug-abusing patient, there will almost certainly be times when therapist and patient are at odds, and when negative feelings will be rather intense on one or both sides. However, this does not have to spell doom for the working alliance. W e rely on the following guidelines for managing such power struggles: 1. Don't fight fire with fire. 2. Maintain honesty. 3. Remain focused on the goals of treatment. 4. Remain focused on the patient's redeeming qualities. 5. Disarm the patient with genuine humility and empathy. 6. Confront, but use diplomacy. 1. Don't fight fire with fire. When a patient becomes hostile, lou intransigent, and/or verbally abusive, it does little good for the thera­ pist to respond in kind. In fact, such a reaction on the part of the therapist could potentially lead to a dangerous escalation of the con­ flict. Instead, therapists must show confidence and conviction in their position in a matter-of-fact way. Concern and strong feelings can be expressed (e.g., "Ms. G, I urge you to reconsider your intentions in this matter. I am greatly concerned that you are headed for a big-time fall if you go ahead with your plans to attend that dealer's party!"); however, it is advisable that such sentiments be expressed in a way that communicates a genuine concern for the patient's well-being and best interests. A controlling or disrespectful response (e.g., "You're dead wrong! If you go to that party you're an idiot! I simply can't allow you to do it.") will undermine the therapeutic alliance and probably will not effectively control the patient's behavior anyway. Instead, the strategy advocated here is more akin to the philosophy espoused in Asian martial arts that states that a strong opponent must not be fought head on but rather through leaning back and allowing the adversary's misguided brute force to carry him past you, to stag­ ger, and to fall. 2. Maintain honesty. During times of conflict with a drug-abus­ ing patient, there is often a great temptation to try to appease the patient artificially through reassurances that are less than completely truthhil (e.g., getting a patient "oft your back" by telling him that it won't really matter too much if he continues to be late for therapy The Therapeutic Relationship 75 sessions). Not only is it unwise to reinforce patients' maladaptive interpersonal behavior by capitulating to them, it also sets up the therapist to look like a liar if the therapist later reverses his/her posi­ tion or otherwise reneges on the reassurances. Instead, the therapist must be willing to "take the heat," and not simply say things that the patient wants to hear in order avoid the unpleasantness of a power stmggle. 3. Remain focused on the goals of treatment. W h e n therapist and patient are at odds, it is extremely helpful if the therapist calls atten­ tion to mutually set goals. In effect, therapists can remind both them­ selves and their patients that a disagreement in one area does not alter the fact that there are fundamental areas of agreement and collabora­ tion in other areas. One therapist diffused a heated exchange by tell­ ing his ex-football player patient, "We may not agree on whether we should run the ball, or pass, but we have to remember that we're on the same team and we both want to get into the end zone." 4. Remain focused on the patient's redeeming qualities, as well as your own {as therapist). Power struggles are often fueled in part by the therapist's cognitive biases. This happens when the therapist reacts to an aversive power struggle by focusing only on the patient's irri­ tating qualities, and glossing over his/her strengths. Similarly, the therapist may lapse into dysfunctional self-blame (regarding the lack of the patient's therapeutic cooperation and progress), thus engen­ dering more ill feelings. In such instances, it is extremely helpful for therapists to use cognitive therapy procedures on themselves in order to notice and modify the following types of automatic thoughts that might be exacerbating negative interactions with patients: • "This patient is a loser. He'll never listen to me." • "This patient is so dense. I'm going to have to beat this guy over the head with m y point of view until he agrees with me." • "Why can't I reach this patient? What am I doing wrong? I'm ready to give up on working with this patient." • "Maybe I'm not cut out to work with such a patient. I don't like being reminded of m y shortcomings, so this patient is really on m y shit Ust." • "You just can't compromise and be reasonable with these people. If you give them an inch, they take a light-year. There­ fore, I will not budge from m y position one iota." • "Why did I ever take on the responsibility of treating this patient in the first place? I must have been an idiot. I almost wish this patient would get arrested so I can be rid of this case." 76 COGNITIVE THERAPY OF SUBSTANCE ABUSE Obviously, the aforementioned automatic thoughts are very del­ eterious to the therapist, the patient, and the prospects for the con­ tinuation of treatment. Therapists would do well to focus on their own idiosyncratic automatic thoughts, to produce the kinds of rational responses that would diminish the anger, frustration, and exaspera­ tion that escalate power struggles and undermine problem solving and therapeutic collaboration (Weiner & Fox, 1982). Examples of such rational responses might be: • "There have been a number of sessions in which the patient and I worked very well together. Those were very rewarding experiences that 1 must not forget. • "This patient is not dumb. He's convinced he has his reasons for defying the therapeutic plan the way he's doing. Let me try to understand his resistant automatic thoughts and beliefs, rather than simply label him a troublemaker." • "My worth as a therapist does not hinge on m y patient believ­ ing everything 1 say, doing everything I suggest that she do, and staying free of drugs for the rest of her life. I'd like for her to be compliant and to make progress, but the fact that she sometimes thwarts this doesn't prove that she can't succeed in therapy with me, and it certainly doesn't prove that 1 should throw in the towel with all drug-abusing patients." • "If 1 keep m y cool, present m y point of view resolutely, and also show that I'm willing to be flexible within reason, I'll probably get a lot more therapeutic mileage out of this con­ flict than I will if I become strident or stubborn." • "This power struggle is a great opportunity to get at some really hot interpersonal cognitions!" 5. Disarm the patient with genuine humility and empathy. Fre­ quently, drug-abusing patients will become angry if they perceive the therapist to be flaunting their authority over the patient or acting with a holier-than-thou air. This perception can lead the patient to fight against the therapist's position in order to reassert some measure of control. This implies that it is important for therapists to be aware of the possibility that the patient is viewing him or her in this negative way, and to respond with behavior that gives the patient evidence to

the confrary. For example, one of our patients suffers from diabetes and frequently neglects his medical care as a sign of defiance, much in the same way that others might choose to go on a hunger strike. Ray and his therapist often engaged in power struggles over whether The Therapeutic Relationship 77 or not Ray should consult his medical doctor. Finally, after a gre deal of heated disagreement, the therapist resorted to a more humble, empathic approach: "Ray, I'm not trying to give you a hard time. Who am I to tell you how you should run your life? I'm just worried about you, man. 1 get this mental picture of you in a diabetic coma and it alarms me. 1 don't want this to happen you. I want to keep working with you and I want to see your life become happier and healthier again, but instead I worry that when you walk out that door I'm not going to see you anymore because you're going to wind up dead. I guess that's why I come on so strong about going to see your doctor. Do you see where I'm coming from, Ray?" 6. Confront, but use diplomacy. As mentioned earlier, therapists must be prepared to confront their drug-abusing patients when they break therapeutic ground rules (Frances & Miller, 1991), but a tone of respect and concern must prevail (Newman, 1988). A particularly effective method of subtle confrontation involves the therapist's use of the patient's own words in order to make a point. For example, a patient may say in a given session, "I know I have to stay on top of myself—I can't let down m y guard when things are going well because that's when I always get stupid and think I can go back to using again." Later, this same patient may betray his own words by asking for a discontinuation of treatment because "everything's cool in m y life now," a statement that the therapist evaluates to be a gross oversim­ plification and distortion. Rather than telling the patient that he's fooling himself and then hounding him into staying in therapy, the therapist can use the patient's earlier statement as evidence against his current position: "I'm a littie confused right now. You're telling m e that every­ thing's cool right now and that you can leave therapy. But you told me something—and I wrote it down here because I was so impressed with what you said—that it would be times just like now that you would have to stay on top of yourself, because you know that you're prone to relapsing when you think everything is going great and you let your guard down. Now, I took what you had to say very seri­ ously, and I thought you really knew the story. It seems that what you said would apply to this situation we're in right now. What do you think?" The above example also highlights the importance of the therapist's documenting important patient statements for future use in session. 78 COGNITIVE THERAPY OF SUBSTANCE ABUSE Confrontation is often called for when the therapist suspects that the patient is lying (about his/her whereabouts during a missed therapy session, about level of abstinence, etc.). Here, it is useful for the therapist to develop a repertoire of carefully worded statements that "nicely" say the equivalent of "I think you're lying." Such state­ ments include but are not limited to: • "I don't get the feeling you're being completely straight with me right now." • "I'm going to ask you the same question again. This time please level with me. Whatever the story is, I'll try to help you in any way that I can." • "Are you sure you're telling m e the whole story here? It sounds like there's some stuff you're leaving out." • "1 get the feeling that you're struggling to try to tell m e some­ thing, but you're not sure you can get the words out. Take your time—I'll listen to whatever news you have for me." • "Are you being honest with yourself here?" • "I hope you're not fooling yourself right now." • "Usually the things you say make a lot of sense, so I'm a little confused right now because I have to admit that what you're saying to me at this moment doesn't make sense to me." • "Are you willing to prove what you're saying? I'd like you to show me up by proving it. But if you can't, I'm not sure I can completely buy what you're telling me." • "You know, this is one of those instances where your intelli­ gence works against you. The fact that you're so smart means that you're capable of bullshitting m e and making it sound golden. Now I know that you're smart, and that means that I have to wonder whether you're telling m e the fruth, especially at times like these when your excuses and alibis are extremely convincing and clever." S U M M A R Y This chapter has emphasized the vital importance of establishing a positive therapeutic relationship with the drug-abusing patient. Along the way, we have noted the difficulties that are entailed in this task, and have proposed methods by which to actively nur­ ture and maintain a functional working alliance. W e have illustrated ways that therapists can engender a sense of rapport, trust, and col­ laboration with their drug-abusing patients, without having to collude The Therapeutic Relationship 79 with their patients' dysfunctional beliefs and behaviors. Finally, we have emphasized the role of confrontation in the therapeutic relation­ ship, and demonsfrated that this need not lead to the therapist and patient becoming adversaries. In fact, an honest, humble, direct approach can allow the therapist to use the therapist-patient interac­ tions to make significant headway in treatment. C H A P T E R 5 F o r m u l a t i o n o f t h e C a s e A d. M. good case formulation helps the therapist to understand the complexity of the substance abuser. By weaving together the patient's history, constellation of beliefs and rules, cop­ ing strategies, vulnerable situations, automatic thoughts and images, and maladaptive behaviors, the therapist has a better understanding of how patients become drug dependent. The case formulation also helps to answer many of the following questions: 1. Why did the patient start using drugs? 2. H o w did using drugs lead to abuse and dependency? 3. W h y has the patient not been able to stop on his/her own? 4. How did key beliefs develop? 5. How did the patient function prior to using drugs? 6. What interpretations can we make about high-risk circum­ stances as they relate to using drugs? A well-formulated case helps to give direction to the session (Per sons, 1989). The therapist is guided to ask important relevant ques­ tions and to develop strategies and interventions that are most likely to succeed. Without a case formulation, the therapist is proceeding like a ship without a rudder, drifting aimlessly through the session. CASE FORMULATION The essential components of a case conceptualization are as follows: 80 Formulation of the Case 81 1. Relevant childhood data 2. Current life problems 3. Core beliefs or schemas 4. Conditional assumptions/beliefs/rules 5. Compensatory strategies 6. Vulnerable situations 7. Automatic thoughts and beliefs (especially drug related) 8. Emotions 9. Behaviors 10. Integration of the above data Relevant childhood data are those early experiences that contrib­ uted to the development and the maintenance of core beliefs. These experiences are not necessarily traumatic but are early messages that children receive about themselves that help to form the foundation for their positive and negative views of themselves. For example, a patient might come from a family where one member is an alcoholic and unpredictable. The message that the patient might receive is that "alcohol is a way to cope" and "people are unpredictable." Some patients come from homes where they are often put down and their acceptance is dependent on "perfect behavior." These patients might develop the core belief "I'm unwanted," "I'm unlovable," or "I'm bad." Current life problems comprise the full spectrum of difficulties that dmg-abusing patients experience in their lives as they enter freatment— problems that franscend the simple abuse of mind-altering substances, that will need additional attention in treatment (cf. Sobell et al., 1988). These problems commonly include relationship difficulties, unem­ ployment, health problems, legal trouble, low motivation, unstable living arrangements, hopelessness, and others. As therapists concep­ tualize these difficulties, they attempt to determine which of the patients' problems contribute to the onset of the substance abuse, which problems are sequelae of the drugs, and which are both causal and consequential factors. Therapy with substance abusers is incom­ plete without a treatment plan to address the kinds of life problems mentioned above. Core beliefs or schemas are the most central and important beliefs that reflect how patients view themselves. W e have found that these beliefs generally fall into two categories: (1) "I am unlovable" or (2) "I am helpless." It is important to note that core beliefs might not necessarily be manifested by these exact words, but there can be derivatives or correlates of the core belief. For example, "I am help­ less" might be expressed in such terms as "1 am inadequate," "I am poweriess," "I am trapped," "I am inferior," "I am ineffective," "1 am 82 COGNITFVE THERAPY OF SUBSTANCE ABUSE incompetent," "I am weak," or "I am vulnerable." The belief that " am unlovable" might be expressed as "I am unattractive," "I am unde­ sirable," "I am rejected," "I am unwanted," "I am uncared for," or "I am bad." Conditional assumptions/beliefs/rules help patients to cope (for better or worse) with their core beliefs. These assumptions can be in a positive or negative form. A conditional positive assumption might be the following: "If I do everything perfectly, then I will be wanted and accepted by others." The negative counterpart to this assumption might be, "I am unlovable if I am not accepted by everyone." Compensatory strategies are those behaviors that also help patients to cope with their core beliefs. On the surface, compensatory strate­ gies seem to work. However, the problem with many compensatory strategies is that they are often compulsive, inflexible, inappropriate, energy depleting, and not balanced by adaptive strategies. In addition, these compensatory strategies often still do not prevent the patient from having hidden doubts, secret fears, and negative self-concepts. A typical compensatory strategy for substance abusers is the use of drugs in order to feel more confident or feel better about themselves. However, it should be noted that the use of drugs is not limited to being a compensatory strategy. People use drugs for many reasons. However, we have found that in the drug-dependent patient, drug use can clearly be demonstrated as one of several coping strategies to "remedy" the sense of helplessness or hopelessness. Vulnerable situations are best described as those problematic cir­ cumstances in which core beliefs and drug-related beliefs become activated. An example of this is the cocaine addict who has been abstinent for several months and is faced with the situation of going into a neighborhood where he has previously purchased cocaine. He has an image of the last time he used, which is followed by strong urges and cravings. This, in turn, activates a drug-related belief such as "The urges and cravings make me use." Automatic thoughts stem from the activation of core beliefs, con­ ditional beliefs, and drug-related beliefs. Some typical automatic thoughts of substance abusers are: "I can't stand the urges and cravings," "Just a littie bit won't hurt," and "Go for it. You deserve it. You've worked hard all week." These automatic thoughts often potentiate patients' urges and cravings to use drugs and/or alcohol, and provide them with impe­ tus to enact plans to procure the drugs (Beck, Wright, & Newman, 1992). Emotions are usually associated with particular automatic thoughts or beliefs. Patients who abuse drugs often are unaware of the cogni- Formulation of the Case 83 five processing that precedes a particular emotion, such as anger, anxiety, or sadness. However, through therapy, patients can be taught to be more aware of the thinking

process that is associated with their emotional life. The patient's behaviors are the end products of the vulnerable situations, and the activation of beliefs, automatic thoughts, and emotions. C o m m o n dysfunctional behaviors include actively seeking drugs, using drugs, engaging in irresponsible activities (e.g., unpro­ tected sex), abusive interpersonal confrontations, avoidance of self- help activities, and others. The integration of the above data is the most challenging and most important step in the ongoing process of conceptualizing the patient's life and problems. Here, therapists piece together all the information into a "story of the patient's life" that provides plausible explanations for the patient's difficulties and suggests treatment recommendations that may break into the patient's self-defeating patterns and vicious cycles. For example, the therapist may posit the following: "The patient was subject to a frequent barrage of harsh disap­ proval in childhood, and came to believe that he was inadequate and unlovable. These core beliefs have been carried into adulthood, where the patient experiences chronic discomfort in social situations where he believes that he will not measure up. The patient took to using cocaine in the belief that it would make him feel confident enough to make positive impressions on others. Unfortunately, this dysfunc­ tional compensatory strategy has led to compulsive use of cocaine, leading further to a depletion of his money and endangering his marriage. These life problems have fed back into the patient's cycle of anxiety, sadness, low self-worth, and renewed belief that the only way to be accepted is to become outgoing through the use of cocaine. As a result, his drug, financial, and marital problems have worsened, and his sense of helplessness and hopelessness have increased." CASE STUDY The following case illustrates in more detail the ten essential components of a case formulation. The patient (described in the integrative example above), David, is a 40-year-old white male. He has been married for eight years and has one child. His complaints at intake evaluation included high anxiety and a long history of alcohol and cocaine abuse. He reported recently feeling more anx- 84 COGNITFVE THERAPY OF SUBSTANCE ABUSE ious in social situations, and he feared that if his anxiety got w he might have a relapse and start using cocaine and alcohol. In other areas of his life, he was working and received a good salary; however, he was $40,000 in debt as a result of his cocaine "habit." His mar­ riage was "on the rocks," and he also suspected that his wife was an alcoholic. Upon completion of his intake evaluation, David met the DSM- III-R criteria for polysubstance use, with cocaine as his preferred drug, social phobia, and generalized anxiety disorder. The social phobia was the area on which David wanted to work first. David felt an urgency in this regard because it was the holiday season and he had several business obligations that required his attendance at social functions such as dinner-dances and parties. David felt that if he did not learn to cope with his anxiety in these situations, he would lose control and start using cocaine again. David grew up in a household where his father was seen as a workaholic and someone who "drank too much." David stated that his mother was nurturing but somewhat timid around her husband. In school, David did not do well. He received mostly C's and D's and only stayed in college for one year. David first began drinking at about age 9. Because of his father's business, the family was involved in many social activities and David would often go around drinking out of the glasses of some of the guests. By age 13, David already had experimented with alcohol, marijuana, speed, and diet pills. As a child David was often humiliated and degraded by his father, usually at social events, after his father had been drinking heavily. O n one occasion after his father called him "stupid," he ran outside and sat under a tree and felt humiliated, worthless, and helpless. On another occasion, he ran out onto a pier and sat there feeling ashamed and helpless. These were significant childhood events for David, and they served as the foundation for some of his core beliefs and com­ pensatory strategies. His typical style was to run away and avoid unpleasant situations. Later in life, David realized that alcohol and drugs helped him to cope with unpleasant emotions. Since drugs and alcohol worked so well, David did not develop many other strategies for coping with unpleasant emotions. Under relevant childhood data, we can see that there were several incidents when David was shamed by his father. These incidents helped to form his core belief, "I am unloved, unwanted." He later developed a conditional assumption for coping, "If I do everything perfectly, then people will like me." David had several compensatory strategies, such as always to strive to do things perfectly or to avoid doing things that were unpleasant. Other strategies included avoid- Formulation of the Case 85 ing showing others how he really felt, and using alcohol and drugs. After using cocaine, David felt especially confident that he could do "everything perfectly," which in turn led him to believe that he was loved and wanted by others. A vulnerable situation occurred when David was invited to a din­ ner party at a friend's house. Prior to going to the friend's house, David was acutely aware of the fact that he was becoming anxious and ner­ vous. He was also aware of the fact that his automatic thoughts cen­ tered on such ideas as "I'll screw up," and "They will see m e trem­ bling," and he imagined himself being "overcome with anxiety" and eventually running out of the house. This, in turn, led to taking a drink and snorting a line of coke before going to the party. From this example, the clinician can see the relationship between the development of David's core belief, his conditional assumptions, and his compensatory strategies, as well as their cumulative impact on a vulnerable situation—being invited to a dinner party at his friend's house (see Figure 5.1). Once again, we need to remember that these compensatory strategies tend to be rather compulsive, inflexible, inappropriate at times, energy depleting, and not balanced by other adaptive strategies. In addition, in spite of the compensatory strate­ gies, the patient still tends to have hidden doubts and secret fears about coping. GATHERING DATA FOR CASE FORMULATION The Case Summary and Cognitive Conceptualization Worksheet is an excellent form for compiling data that will be used in the case formulation. This worksheet is divided into eight main sections: I. Demographic Information II. Diagnosis III. Inventory Scores IV. Presenting Problem and Current Functioning V. Developmental Profile VI. Cognitive Profile VII. Integration and Conceptualization of Cognitive and Develop­ ment Profiles VIII. Implications for Therapy The demographic information section is where the therapist collect such information as the patient's age, sex, race, religion, employment 86 COGNITIVE THERAPY OF SUBSTANCE ABUSE Relevant Childhood Data Father was alcoholic. H/lother took verbal abuse from father. David often humiliated by father. Core Belief(s) I'm unloved, unwanted. Conditional Assumptions/Beliefs/Rules If I do everything perfectly, then people will like m e and I'll feel com­ fortable. If I show others how I really feel (anger), they will abandon me. Compensatory Strategy(ies) Use drugs If you are uncomfortable. Don't do anything unless you are 1 0 0 % sure you can accomplish it. Don't show others how you really feel. Situation # 1 Situation # 2 Situation # 3 Invited to a dinner party. Automatic Thought Automatic Automatic "I'll screw up." Thought Thought 'They will see m e trembling." Meaning of the Meaning of Meaning of Automatic Thought the Automatic the Automatic "People won't want Thought Thought to be around me." Emotion Emotion Emotion Fear; apprehension T Behavior Behavior Behavior Took a drink. Did a line of coke F I G U R E 5.1. Cognitive conceptualization diagram developed by Judith S. Beck. From J. S. Beck (in press). Copyright Guilford Press. Reprinted by per­ mission. Formulation of the Case 87 status, marital status, and other pertinent identifying characteris This is standard information that would be a part of any psychologi­ cal evaluation. In the diagnosis section, it is advantageous to formulate a diag­ nosis on all five axes of DSM-III-R. Clinical syndromes are designated on Axis I. O n Axis II, developmental disorders and personality disor­ ders are noted. Physical disorders and conditions pertinent to the patient's psychological difficulties are presented on Axis III. Severity of psychosocial stressors is identified on Axis IV. The level of sever­ ity of psychosocial stressors ranges from code 1 (none) to code 6 (cata- sttophic), such as the death of a child, the suicide of a spouse, or a devastating natural disaster. Axis V can be determined from the Global Assessment of Functioning Scale, which has a code number descend­ ing from 90 to 1, with 90 signifying abstinence and ideal coping, and progressively lower numbers indicating an increasing severity of drug use or deficits in coping and functioning. All the data on the five axes will have an impact on the clinician's understanding of the patient, and in the subsequent designing of the treatment plan. Inventory scores, such as the Beck Depression Inventory, Beck Anxiety Inventory, and Beck Hopelessness Scale (discussed later), are listed in this section. Intake scores plus scores from the first six ses­ sions are reported. There is also an extra column in order to note the scores of the most recent session. These inventory scores are extremely important because the therapist can quickly see general trends and patterns—changes for the better or for the worse. The presenting problem and current functioning section describes the patient's current difficulties and focuses on such areas as employment, concurrent psychiatric disorders, nature of drug use, criminal activ­ ity, interpersonal problems, and other data. This is a cross-sectional analysis of the patient's current functioning. The developmental profile examines the patient's social history, educational history, medical history, psychiatric history, and voca­ tional history. In addition, relationships with parents, siblings, peers, authority figures, and significant others over the life span are also noted. It is also important to ascertain any significant events or trau­ mas in the patient's formative years or recent past. This longitudinal analysis is akin to paging through a family photo album. The thera­ pist can see the patient in different stages of development. This retro­ spective analysis also includes an evaluation of the patient's introduc­ tion to psychoactive substances and how the problem became a full-blown addiction. The cognitive profile section addresses the manner in which the patients process information. The patients' typical problem situations 88 COGNITIVE THERAPY OF SUBSTANCE ABUSE are noted, and the corresponding automatic thoughts, feelings, and behaviors in these situations are outlined. In addition, possible core beliefs, conditional beliefs, and drug-related beliefs are described in this section. The integration of cognitive and developmental profiles takes into consideration the patient's self-concept and concept of others. It also focuses on the interaction of life events with cognitive vulnerabili­ ties, as well as compensatory and coping strategies. An important part of this section is a description of how self-concept and concept of others might have played roles in the onset and progression of sub­ stance abuse. This section is illustrated by the case of Mike, a 31-year- old cocaine addict. The patient lives with his parents in a rundown neighborhood where there is high unemployment and high crime rates. He grew up around drugs and alcohol, and his mother and all his siblings have had problems with drugs and alcohol. Mike is now serving five years probation for insurance fraud. The patient's work history is poor. After dropping out of high school, Mike found only unskilled labor jobs, and he is currently unemployed. There is lots of dealing in his neighborhood; Mike has sold drugs in the past and knows there is lots of fast money in deal­ ing. Mike sees himself as a loner and does not have any real friends. His problematic beliefs are "I'm no better than the rest of my fam­ ily," "I'll never get a job," "I can't get away from it (drugs)," "Deal­ ing is the only way out of here (urban ghetto)," and "Using

is the only way to cure the boredom." His circumstances and beliefs have led to the following behavioral patterns: brief periods of abstinence from drug and alcohol followed by solitary use of alcohol with Valium, which, in turn, leads to intermit­ tent use of crack cocaine, and then to daily use of crack cocaine. Mike's case shows many of the cognitive factors (among other factors) that can influence drug use (see Figure 5.2). The section on implications for therapy examines some of the fol­ lowing areas: 1. The patient's initial "aptitude" for cognitive interventions; 2. The patient's personality characteristics, such as "sociotropic" or "autonomous"; 3. The patient's motivations, goals, and expectations for therapy; 4. The therapist's goals; and 5. Anticipated difficulties in treating the patient. In this section, the clinician hypothesizes how psychologically minded the patient is. For example, is the patient aware of the nature and severity of his or her problems, and does he or she have the ability Formulation of the Case 89 Unemployed—Lots of free time Til never get a job." Long family Drugs easily Poor work history history of drug available Quick money dealing and alcohol use X "I'm no better "I can't get "Dealing Is the only than the rest away from it.' way out of here." of my family." Loner; no non- social support "Using Is the only way to cure the boredom." Mike's Drug Use FIGURE 5.2. Beliefs and other factors contributing to Mike's d m g use. to self-monitor automatic thoughts? The patient's capacity for access­ ing automatic thoughts and beliefs certainly has important implica­ tions for the pace of treatment. In addition, personality characteris­ tics—for example, sociotropic or autonomous—can provide the therapist with s o m e indication as to the conditions under which the patient might relapse, for example, the sociotropic person in situa­ tions in which there is social pressure, and the autonomous individual w h e n blocked from reaching his/her achievement goals. The patient's motivation, goals, and expectations for therapy are noted and dis­ cussed o n the conceptualization form. Also noted are the therapist's goals for treatment, and h o w compatible these are with the patient's goals. Finally, it is also useful to anticipate difficulties that might arise during the course of therapy that might warrant special attention. For example, if the patient has a history of periodic homelessness, this will need to be addressed early in treatment lest the patient suddenly "disappear" from treatment and be unreachable by mail or telephone. A case study illusfration of the Cognitive Conceptualization Work­ sheet (for patient "D.D.") follows. 90 COGNTTIVE THERAPY OF SUBSTANCE ABUSE CASE SUMMARY AND COGNITIVE CONCEPTUALIZATION WORKSHEET Dr. R. D.D. 1/10/92 Therapist' Name Patient's Initials Date Session # I. Demographic Information Ms. D is a 38-year-old, white, single female who is currently unemployed. She lives alone and has recently broken up with her boyfriend. She was in school but stopped going to class this month. II. Diagnoses Axis I: Cocaine abuse Alcohol abuse Major depression, recurrent Axis II: Avoidant personality disorder Histrionic personality disorder Axis III: N o physical illness reported Axis IV: Code 2 (Mild)—Not attending her college classes Axis V: GAP Code 60—Moderate depressive symptoms; not function­ ing well in school; difficulties eating, sleeping, and concen­ trating III. Inventory Scores Sess. Sess. Sess. Sess. Sess. Sess. Latest Intake # 1 # 2 # 3 # 4 # 5 # 6 Sess. BDI 25 26 20 21 17 17 16 16 BAI 2 1 1 12 11 12 13 13 BHS 11 11 12 12 12 10 7 7 Other General Trend of Scores: BDI and BHS scores are improving; how­ ever, her BAI scores have worsened over the past six sessions. (Higher scores indicate greater symptomatology.) IV. Presenting Problem and Current Functioning There were three presenting problems: (1) history of alcohol and cocaine use (though she reported that she had not used in the past 30 days), (2) moderate number of depressive symptoms and related fear that the symptoms would get worse, and (3) worry and fear that she might start using drugs and alcohol, progressing toward total relapse. {continued) Formulation of the Case 91 V. Developmental Profile A. History (family, social, educational, medical, psychiatric, voca­ tional) The patient was born on the East Coast and spent most of her life in an urban setting. Her father had numerous businesses and her mother was a homemaker. W h e n D was 13, her mother and father divorced. The patient liked elementary school but was anxious. She "hated" high school. D went through inpatient detox in 1985, and previously suffered from major depression in 1987. B. Relationships (parents, siblings, peers, authority figures, signifi­ cant others) The patient described her father as a loving, dedicated man. She stated that he was a heavy drinker^unpredictable when he was dmnk. Her mother was the "perfect mother," always there for the family. D was the oldest of five children. She stated her relation­ ship with all of them was "great." C. Significant events and traumas The patient described three significant events: (1) her parents' divorce, (2) her unhappiness throughout high school, and (3) her realization in 1985 that she had a d m g and alcohol problem. VI. Cognitive Profile A. The cognitive model as applied to this patient 1. Typical current problems/problematic situations: Situations that can lead to her taking drugs: (a) W h e n she is around former drug friends. (b) W h e n there is a breakup in a significant relationship. (c) W h e n bored and alone. 2. Typical ATs, affect, and behaviors in these situations: Automatic Thoughts: "They still use." "I'll never find someone who really cares." "I can't stand the boredom." Affect: Angry Depressed Hopeless Behavior. Uses alcohol first, then cocaine B. Core beliefs (e.g., "I a m unlovable") "I a m unlovable." "I a m undesirable." "I a m powerless." "I a m weak." {continued) 92 COGNITIVE THERAPY OF SUBSTANCE ABUSE C. Conditional beliefs (e.g., "If I fail, I a m worthless") "If I do what is expected of me, then people will accept me." "If I do things perfectly, then I feel competent." D. Rules (shoulds/musts applied to self/others) "I must be accepted by others or I'm worthless." "I must be emotionally in charge or there is something wrong with me." VII. Integration and Conceptualization of Cognitive and Develop­ mental Profiles A. Formulation of self-concept and concepts of others The patient believed she had to do the "right" thing as a child or her father would push her away. The patient could not always please her father predictably because his drinking led to erratic and "fickle" treatment of his children. Father left mother without any explanation; led to D's belief that men are not to be trusted. B. Interaction of life events and cognitive vulnerabilities Boyfriend Beliefs: "I a m D feels sad, leaves her unlovable" and depressed, "Men can't be hopeless tmsted" get activated C. Compensatory and coping strategies Avoids doing things that she feels she cannot do perfectly. Tendency to use drugs and alcohol when she is upset. D. Development and maintenance of current disorder Low fmstration tolerance for anxiety, boredom, and depression. Drug-related beliefs such as "Cocaine is the only way to relieve the boredom." VIII. Implications for Therapy A. Aptitude for cognitive interventions (rate low, medium, or high, and add comments, if applicable): 1. Psychological mindedness: very good 2. Objectivity: good 3. Self-awareness: very good 4. Comprehension of cognitive model: very good 5. Accessibility and flexibility of automatic thoughts and beliefs: very good General adaptiveness: very good 7. Humor: Excellent (continued) Formulation of the Case 93 B. Personality characteristics: sociotropic vs. autonomous Sociotropic: Strong need for attachment to others. Achievement needs are far less pronounced. C. Patient's motivation, goals, and expectations for therapy Strong motivation to stop using dmgs and alcohol. Other goals are realistic (i.e., would like to finish college). D. Therapist's goals 1. Teach patient to monitor, examine, and respond to negative automatic thoughts. 2. Help her to acquire skills for coping with d m g and alcohol urges and cravings. 3. Improve D's problem-solving skills. E. Predicted difficulties in therapy 1. Lapse could turn into a relapse if patient does not contact the therapist as soon as possible, which she might not do if she feels ashamed of her behavior and expects the therapist to criti­ cize her. 2. Patient will tend to minimize her problems (e.g., as she did when she described her relationships with family members in glow­ ing terms in spite of serious conflicts). 3. Patient still maintains contact with drug friends who may try to sabotage her abstinence goals. ADDITIONAL DATA FOR THE CASE CONCEPTUALIZATION In addition to the clinical interview, self-report inven­ tories provide data that are important in the conceptualization of the case. The following is a list of such questionnaires and scales. 1. Beck Depression Inventory 2. Beck Anxiety Inventory 3. Beck Hopelessness Scale 4. Dysfunctional Attitude Scale 5. Beliefs about Substance Use Scale 6. Relapse Prediction Scale 7. Craving Beliefs Questionnaire 8. Sociotropy-Autonomy Scale Beck Depression Inventory The Beck Depression Inventory (BDI) (Beck, Ward, Mendelson, Mock, & Erbaugh, 1961) is a self-report scale composed 94 COGNITIVE THERAPY OF SUBSTANCE ABUSE of 21 items, each comprising four statements reflecting gradations the intensity of a particular depressive symptom. The respondent chooses the statement that best corresponds to the way he or she has felt for the past week. The scale is intended for use within psychiat­ ric populations as a measure of the symptom severity of depressed mood and as a screening instrument for use with nonpsychiatric populations. Beck Anxiety Inventory The Beck Anxiety Inventory (BAI) (Beck, Epstein, Brown, & Steer, 1988) is a 21-item, self-report instrument designed to measure the severity of anxious symptoms. The BAI overlaps only minimally with the BDI and other measures of depression while measuring anxiety. Beck Hopelessness Scale The Beck Hopelessness Scale (BHS) was developed by Beck, Weissman, Lester, and Trexler (1974) to measure negative expectancy regarding the future. The BHS is composed of 20 true-false items assessing the expectation that one will not be able to overcome an unpleasant life situation or attain the things that one values in life. The BHS has demonstrated predictive validity for completed sui­ cide (Beck, Steer, Kovacs, & Garrison, 1985). Dysfunctional Attitude Scale The Dysfunctional Attitude Scale (DAS) (Weissman & Beck, 1978) is a self-report scale composed of 100 items. It was developed to assess underlying assumptions and beliefs that consti­ tute schemas by which individuals construe their life experiences. Beliefs about Substance Use The Beliefs About Substance Use inventory is a self- report scale composed of 20 items that can be scored on a range from 1 to 7. A "1" indicates that the person totally disagrees with the state­ ment. A score of "7" means that the person totally agrees with the statement. This scale measures many of the commonly held beliefs about drug use (see Appendix 1, page 311). Formulation of the Case 95 Relapse Prediction Scale The Relapse Prediction Scale (RPS) is a 50 item self- report scale. Each item is composed of situations that typically are reported to trigger urges for cocaine or crack. Each situation is rated on two dimensions: "Strength of Urges" and "Likelihood of Using," with all situations being rated on a 0-5 scale (0 = none to 5 = very high) (See Appendix 1, page 313). Craving Beliefs Questionnaire The Craving Beliefs Questionnaire (CBQ) is a self-report scale that measures beliefs about the craving phenomenon as it pertains to cocaine and crack. Each of 28 items is rated on a 1-7 scale (e.g., 1 = totally disagree and 7 = totally agree) (See Appendix 1, page 312). Sociotropy-Autonomy Scale The Sociotropy-Autonomy Scale (Beck, Epstein, & Harrison, 1983) is a measure of two broad personality dimensions that are associated with depression (Beck, 1967). One is "sociotropy," which refers to the degree of importance a person places on interper­ sonal affiliation in order to be happy. The second is "autonomy," referring to the degree to which a person believes he or she must achieve and attain success in order to be happy. Each of the 60 questions asks the respondent to rate the percent­ age of time that a

statement applies to himself or herself. Half of the questions indicate a sociotropic personality style, and the other half indicate an autonomous personality style. One example of a socio­ tropic item is, "I find it difficult to say no to people." There are five possible responses-this appUes to m e (1) 0%, (2) 25%, (3) 50%, (4) 75%, (5) 100% of the time. Sociotropy and autonomy subscores are summed separately; therefore, a person may be high on both scales or low on both scales. S U M M A R Y The purpose of this chapter has been to provide the therapist with a comprehensive methodology for achieving a sound case formulation. W e began with a rationale supporting the importance of a good case formulation, and suggested key questions for the clinician to ask 96 COGNITIVE THERAPY OF SUBSTANCE ABUSE when treating substance abuse patients. Next, we introduced what w consider the ten essential components of the formulation: (1) relevant childhood data, (2) current life problems, (3) core beliefs, (4) condi­ tional assumptions/beliefs/rules, (5) compensatory strategies, (6) vul­ nerable situations, (7) ATs, (8) emotions, (9) behaviors, and (10) inte­ gration of the data. Each component was described in detail and pertinent examples presented, followed by an illustrative case study. Next, we reviewed methods for gathering and organizing data for the case formulation. W e introduced the Cognitive Conceptualization Worksheet, provided an explanation of its use, and noted examples to aid in the understanding of the use of this form. This chapter con­ cluded with a description of eight self-report inventories used in pro­ ducing information toward a sound case formulation. C H A P T E R 6 S t r u c t u r e o f t h e T h e r a p y S e s s i o n T , he structure of the therapy session is one of the more noticeable Xahnd< essential characteristics of cognitive therapy. Stmcture is important for the following reasons: (1) Within a typical 50-minute session, substance abusers often present a large amount of material to discuss, either longstanding or acute crises, yet there is a limited amount of time. Structuring the session provides the oppor­ tunity to make maximum use of time. Patient and therapist collaborate to most effectively handle problems in the time allowed. (2) Struc­ ture assists in focusing on the most important current problems. (3) Learning new skills, such as better problem solving, requires hard work. Structuring the therapy session sets the tone for a working atmo­ sphere. (4) Structured sessions fight against therapy drift, whereby continuity from session to session is lost. Knowing the elements of the structured session facilitates adherence to the cognitive model and minimizes the chances that drift will occur. This chapter focuses on eight important elements of the struc­ ture of a session: 1. Setting the agenda 2. Mood check 3. Bridge from last session 4. Discussion of today's agenda items 5. Socratic questioning 6. Capsule summaries 7. Homework assignments 8. Feedback in the therapy session 97 98 COGNITFVE THERAPY OF SUBSTANCE ABUSE SETTING THE AGENDA Time is precious. Setting an agenda helps to make efficient use of time and provides a focus for the therapy session. It also teaches patients to set priorities, usually a skill deficiency in impulsive drug-addicted individuals. Because they spend a consider­ able amount of time seeking, using, or recovering from their drug use, patients often spend little time focusing on solving the other problems that are plaguing their lives. Setting agendas has a positive effect on the therapeutic alliance as well. It reinforces the collaborative agreement between patient and therapist as each party has an opportunity to contribute to the pro­ cess of therapy. It allows patient and therapist to target specific goals (see Chapter 8, this volume) for the session and to discuss the appro­ priateness of focusing on specific topics. It also sets the stage for modeling better ways of resolving conflicts, for example, when the patient's agenda item seems incompatible with what the therapist wants to discuss. This is illustrated in the case in which the patient says, "I want to give you all the details . I just want to get it off my chest. It makes me feel better." In order to preserve collaboration, the therapist might reach an agreement with such a patient that a certain portion of the session can be used to "let off steam" but may also suggest that other topics will also need to be covered, such as ambivalence about abstinence, continued drug use, and triggers to using. Some patients have a low tolerance for anxiety and therefore avoid bringing up topics that provoke discomfort. W h e n therapists provide a rationale for putting such topics on the agenda in spite of the dis­ comfort the topics evoke, they help to avoid power struggles between themselves and their patients. Therapists also make good, collabora­ tive use of the agenda by demonstrating empathy for their patients' reluctance to discuss certain hot topics, such as their spouses' sub­ stance abuse problems. At times, therapists need to be flexible in setting agendas. Some­ times patients come to a session in crisis, such as after being fired from a job or being left by a spouse. These types of problems may require immediate attention, superseding ongoing issues. Likewise, a lapse or relapse should be dealt with immediately because patients who have used often feel hopeless about their ability to stay off drugs, and thus are at increased risk for a full relapse. This in turn often leads to feeling hopeless about therapy and may precipitate a prema­ ture flight from treatment. A key point to remember is the importance of the therapist's not structure of Therapy Session 99 being rigid or dictatorial in setting and following agendas. For ex ple, when it becomes clear that a high-priority agenda item will re­ quire most of the session to addresss adequately, the therapist needs to be willing to shelve less important topics. Also, therapists can modify agendas by periodically checking the number of agenda items to be covered and the amount of time left in the therapy session. If there is insufficient time, patient and therapist then collaborate on deciding which agenda items might need to be postponed. The following is a transcript of the beginning of a therapy ses­ sion in which the therapist and patient are setting an agenda collab­ oratively. In reading this transcript, keep in mind that the therapist is working with the patient to set an appropriate agenda with a spe­ cific target problem, to keep the agenda suitable for the amount of time available in the therapy session, and to prioritize the topics. TH: Well, what are we going to focus on today? PT: Some things, but you know . m y burden now . m y thing is that I need a job. TH: That is something important to put on the agenda for today. Are there other things that we need to talk about? For example, your current frequency of drug use? PT: No, I'm doing all right as far as m y drug things are concerned. TH: H o w much of anything have you used since the last time I saw you? PT: Nothing. TH Nothing? PT: Nothing. I go to m y meetings now. TH No drinking? No alcohol? PT: Nothing. TH OK. PT: When I wake up in the mornings now, I really don't have that craving for drugs. Do you know what I mean? So, now I have to just put this energy into getting up in the morning and get­ ting out and getting a job. That's a real problem; let's make sure we get to that. TH: OK. What I will do is write on the board a list of things that we need to cover. W e might not be able to get to everything today. First we have "finding a job"-difficulty getting up in the morn­ ing to go looking for one. The next thing I was going to put there had to do with "cravings." So, at some time today, I would like to talk with you about what happened that led to your last 100 COGNTTIVE THERAPY OF SUBSTANCE ABUSE slip. The whole point of doing this is for you to get more familiar with what happened so you can recognize when you are feel­ ing bad, what that usually leads to, and to try to come up with some ways to keep it from going all the way down to your using again. To the alcohol, then to the coke, then to the heroin. Oh, we also need to go over the homework from last week. PT: Finding a job is the most important. TH: OK. Maybe we can start with that. Is there anj^hing else you want us to focus on? PT: No, this is good. As this brief transcript illustrates, the therapist set the stage focusing on two primary goals for treatment: reducing drug use, "What happened that led to your slip?" and doing problem solving, "Find­ ing a job . difficulty getting up." The therapist asked two of three important questions that should be asked at every session: (1) Have you used since the last session? (2) Have you had any urges/cravings to use? and (3) Are there any situations coming up before our next session where you might be at risk to use? (This third question was not asked by the therapist.) M O O D CHECK Since depression, anxiety, and hopelessness are inter­ nal stimuli that have the potential to trigger continued use and/or relapse, it is important to monitor these (and other) states. Therapists should pay special attention to feelings of hopelessness as it has been shown that a chronic, marked negative view of the future is one of the best predictors of suicide (Beck, Steer, et al., 1985). It is desirable to have the patient complete the BDI, BAI, and BHS at every session (see Chapter 5, this volume, for descriptions of these instruments). Scores and their meanings should be discussed with the patient, especially if there are substantial changes in scores. Sometimes there can be a change in mood as measured by these instruments, but the patient seems unaware of the change. Therefore, the thera­ pist should ask the patient if he or she is aware of changes in his or her mood. The therapist might say, "Your score on the BDI is higher this week, which may indicate that you have been feeling more depressed. Do you agree with that?" Important points to remember are (1) mood is an important vari­ able with regard to drug use and relapse, (2) hopelessness is one of structure of Therapy Session 101 the best predictors of suicide, (3) mood levels should be measured each session, and (4) therapists should discuss scores obtained from the BDI, BAI, and BHS with their patients. B R I D G E F R O M LAST SESSION Drug and alcohol abusers often have chaotic lives; therefore it is easy for therapists to get drawn into a pattern of jump­ ing from one topic to another in a disjointed fashion. Therapists should think carefully as to how they will stay focused and maintain continuity across therapy sessions. They should ask themselves, "How do the present agenda items relate to what was discussed in the pre­ vious session, and how do these items relate to the overall goals of treatment?" The therapist also reviews the patient's feedback about the pre­ vious session. There are two ways to accomplish this. First, the thera­ pist asks the patient if there is any unfinished business from the most recent session, including any negative reactions he or she might have had. Second, the therapist may reflect on the Patient's Report of Therapy Session (see Appendix 5, page 324), which patients are asked to complete after each session. Usually this is brief; however, some responses might require considerably more attention and time to address. For example, one patient reported after the last session that he did not expect to make any progress in that session, that he did not in fact make any progress, and that he did not

expect to make progress in future sessions. The therapist, recognizing that this feed­ back indicated that the patient held very negative views about therapy, suggested that this be discussed at some length in the current ses­ sion. To get a sense of the patient's world, it is helpful to review briefly the patient's life during the past week. Therapists can use activity schedules to structure this review. Therapists must encourage their patients to keep this review as brief as possible, so that it does not deteriorate into idle chit-chat about the patient's general goings-on that takes up valuable time in the session. DISCUSSION OF TODAY'S A G E N D A ITEMS When therapists and patients proceed to discuss the agreed-on agenda items for the session, they must bear in mind the following points. First, it is important to prioritize the list of topics. It is not always possible to discuss every item within the time con- 102 COGNITIVE THERAPY OF SUBSTANCE ABUSE straints of a given session. Some topics will need to be shelved u the following session. Therefore, it makes the most sense to deter­ mine which topic or topics are essential to discuss in the present session, and to discuss these topics first. By doing so, therapists can avert unfortunate problems such as an entire session being used to discuss a patient's complaints about his car troubles, only to find out as the sessions ends that the patient went on a drinking binge after his wife walked out on him. Clearly, this latter topic needed to be discussed first and foremost, not just for 2 minutes at the tail end of the session. Second, therapists must be alert to patients' tendencies to stray from agenda items and to go off on irrelevant tangents. A polite but prompt statement, such as "I don't mean to interrupt, but I think we should refocus on the topic we started talking about," usually is suf­ ficient. At times, when patients seem to "stray" to even more impor­ tant issues (e.g., a discussion of the patient's marriage leads into hints that the patient is contemplating suicide), it is advisable for thera­ pists to switch gears to accommodate and follow up on these impor­ tant topics by revising the agenda. In general, topics such as the patient's active drug use, suicidality, or hopelessness about therapy will supersede most other agenda items. Third, therapists need to be somewhat conscious of time in the session so that the various topics are covered in sufficient breadth and depth, and so that transitions from one agenda item to the next can be made in a timely manner. At times, therapists may choose to inter­ ject the following question in order to facilitate this process: "We're about halfway through the session, and we have a decision to make. Should we keep talking about our current topic a while longer, or would it make sense to wrap this up and go on to our next item?" This is a collaborative, flexible way to stay focused on meaningful therapeutic material, and to be as efficient as possible in making the best use of valuable therapy time. Fourth, therapists need not be stymied by patients who say "1 don't know" when asked what topics should be discussed as part of the agenda. (In fact, good cognitive therapists almost never take "I don't know" for an answer They persist nicely, find alternative ways to ask the question, or ask the patient to deliberate further.) Instead, thera­ pists can explain that one of the patient's responsibilities in therapy is to think about what he or she would like to talk about in session. At first, the therapist may assist the patient by suggesting some agenda items, asking, "Which of these is most important to you?" The thera­ pist may also ask, "What has been on your mind lately? What's on your mind right now?" Later, if the patient continues to be unwill- Structure of Therapy Session 103 ing or unable to generate topics for discussion, this problem in a itself can become an important agenda item. For example, the therapist may say, "Let's discuss your difficulty in thinking of things to talk about in session. Let's try to understand where the problem is, and how to overcome it." In doing so, the therapist avoids falling into the trap of accepting the patient's helplessness or resistance as an unchangeable fact. In addition, the patient learns that saying "I don't know" will not be reinforced, and that this strategy will fail as an intended means of escape from the work of therapy. S O C R A T I C Q U E S T I O N I N G Overholser (1987, 1988) defines Socratic questioning as a method of intervening that encourages the patient to contem­ plate, evaluate, and synthesize diverse sources of information. This type of questioning, also referred to as "guided discovery," is utilized over the entire span of the session. In contrast to questions typically designed for the therapist to gather information regarding the frequency, intensity, and duration of the substance abuse problem, Socratic questioning is used to bring information into the awareness of the patient. Therefore, Socratic questions are designed to promote insight and better rational decision­ making. Questions should be phrased in such a way that they stimu­ late thought and increase awareness, rather than requiring a correct answer. The proper choice, phrasing, and ordering of questions has a strong impact on the organization of thought in the patient. Further, we have found that most of our drug-abusing patients respond more favorably to exploratory questioning than to didactic "lecturing." Socratic questioning is a powerful technique to use while discuss­ ing the various agenda items. Therapist asks questions in such a way as to help patients to examine their thinking, to reflect on erroneous conclusions, and, at times, to come up with better solutions to prob­ lems. This often leads to patients' questioning, and thereby gaining greater objectivity from, their own thoughts, motives, and behaviors. Also, Socratic questioning establishes a nonjudgmental atmosphere and thus facilitates collaboration between patients and therapists. This can help patients come to their own conclusions about the serious­ ness of their drug abuse problem. As a rule of thumb, therapists should start utilizing Socratic ques­ tioning from the beginning of treatment. This helps to orient patients to an active thinking mode. If therapists find that Socratic question­ ing appears to be overwhelming patients more than helping, then the 104 COGNITIVE THERAPY OF SUBSTANCE ABUSE therapists may choose to be more direct, such as pointing out inco sistencies and errors in thinking and asking if the patients agree with and follow this logic. While it is important to use questioning to explore problems and to help patients draw their own conclusions, there should be a bal­ ance between questioning and other more direct modes of interven­ tion, such as reflection, clarification, giving feedback, and educating the patient. The following dialogue illustrates such a balance, with the therapist starting with some basic assessment questions: TH: Charleen, have you used any drugs or alcohol this week? PT: No, none. It's been over a month now. TH: What about your pain medication from the dentist? PT: What about it? TH: Well, I have a number of questions. First, are you taking the amount that you're supposed to take, and not more than that? Are you taking it when you're supposed to take it, and not more often than that? PT: I'm doing just what I'm supposed to do, so don't worry. TH: Do you know why I'm asking? Do you know why it matters? PT: Yeh, because you told m e that pain medication is like a dmg. TH: Not like a drug. It is a drug. It's a mild narcotic. PT: And I could get addicted to it. TH: Right. And do you know why I'm concerned about the amount and the frequency with which you're taking it? PT: No. TH: Think about it for a minute. W h y do you think we should be concerned about it? PT: I don't know. TH: Well, I realize that you might not know exactly why, but could you try to guess some possible reasons. I'll be happy to tell you m y reasons after you give m e your theory. Note that the therapist is asking a number of open-ended questions in the hope that the patient will begin to do some active thinking in the session. The fact that the patient does not respond to the latter question does not deter the therapist. Instead, he finds a tactftil, col­ laborative way to encourage the patient to apply some cognitive effort. Later, he plans to "reward" the patient for her effort by giving her some additional information in order to educate her about the dangers structure of Therapy Session 105 of pain medications in the hands of a recovering addict. First, how­ ever, he continues with some Socratic questioning. PT: I guess if I took more than I'm supposed to, I could get addicted faster. TH: That's right. What else? PT: I could get high on the pain medication and lose control and go out and use other drugs. TH: Absolutely right. Excellent answer. See, you do understand. Any­ thing else you can think of? PT: No. Not really. TH: Well, consider this. What would happen if you ran out of the pain medication before you were supposed to run out? PT: I'd have to get more. TH: Yes, but if the dentist knows that you're supposed to stiU have some medication left, and you're already asking for more, what would happen? PT: He might say no. TH: What might you do then? PT: I might have to find some other way to kill the pain. TH: Such as? PT: Such as whiskey, {laughs) TH: W h y would that be a problem? PT: Because then I would blow m y streak of staying off stuff I shouldn't take. TH: And would you just drink whiskey? PT: I might also use crack if I had the chance. TH: Right. Now, you've worked very hard to get to this point. It would be a crying shame if you set yourself back by taking too much pain medication. PT: I agree. TH: So, Charieen, have you been taking the medication as pre­ scribed? PT: Yes, but I still have pain, so I've been taking the Advils and the Tylenols too. At this point, the therapist is satisfied that the patient has arrived at her own conclusion that she could be at risk for a lapse or a full­ blown relapse if she misuses her prescribed medications in any way. 106 COGNITFVE THERAPY OF SUBSTANCE ABUSE At the same time, he has just heard something a bit disturbing; the fore he will ask for clarification before proceeding with some non- Socratic, didactic education. TH: Uh oh. You're taking more medications? H o w much? PT: {Getting a little annoyed) Until I feel better, that's how much! TH: Do you read the instructions before taking the over-the-counter medications? PT: No, I just take it until I feel better. TH: Charleen, please bear with me for a few minutes. I can tell you're getting a little ticked off right now, and I don't mean to get you angry but this is important. Can you hear m e out? PT: Do I have a choice? TH: Well, yes. You could ignore m e if you wanted to, but I'm hop­ ing you'll give me a chance to make m y point before you decide whether to disregard it or not. PT: Go ahead. TH: Thanks, I appreciate your being a good sport. Charleen, there are good reasons why medications have instructions. If people ignore the instructions, they can overdose. Or, they can cause something called "interactions" with other drugs. In your case, the over-the-counter medications could combine with the den­ tist's medication to create an effect in your body that's equal to many, many, many medications, which could be dangerous. Also—and I'm not sure that you knew this—every time a person takes a pain medication he lowers his body's own natural abil­ ity to kill pain. So, if you take too much of

anything, it can suppress your ability to feel well after you stop taking the medi­ cation. You see, if the medication runs out, and you've sup­ pressed your body's own natural abilities to kill pain, you're going to go into withdrawal and be in a lot of discomfort. Then, you won't be able to get a refill of the dentist's medication and you'll probably think that you have no choice but to drink whiskey or get some crack. That's why it's so important for you to take only what is prescribed, and nothing more, not even over- the-counter stuff. Do you get m y point? PT: You mean if I take these medications, m y body will never be able to kill pain by itself? TH: Not "never." It will just be suppressed for a few days. That's the withdrawal phase, just like for any drugs. But can you hold off on using drugs for a few days when you're in pain? structure of Therapy Session 107 PT: No way. TH: That's m y point. If you go on the way you're going on right now, you'll be in danger of using alcohol and crack, especially when you run out of the prescription. PT: I see. What should I do? TH: That's an excellent question. Can I turn it back to you? What do you think you should do? Now, the therapist shifts back into the mode of Socratic questioni PT: I guess I have to stop taking the Advils and the Tylenols. TH: And how about the dentist's medication? PT: I guess I have to make sure I read the instructions. TH: But what if you do exactly what you're supposed to do, and you're still in pain? PT: I don't know. TH What do you think I would do in your situation? PT You would call the dentist. TH I might do that, yes. What else? PT: You would try distracting yourself with activities, right? TH: Correct! Could you try that? PT: I could try. TH: What kinds of things could you do? The therapist continues to ask open-ended questions so that Charleen can generate her own interventions, the likes of which she is more likely to follow between sessions than those interventions simply directed toward her. Thus, the dialogue has demonstrated that a mix­ ture of interventions, including education, clarification, and Socratic questioning, can help patients to do meaningful work in session, and to elicit the maximum amount of information and cooperation. CAPSULE SUMMARIES Capsule summaries are an important part of the learn­ ing process in therapy sessions. As a general rule, therapists and patients should summarize what has been discussed in a session a minimum of three times. This provides opportunities to adjust agen­ das and to maintain the focus of the therapy session. The first cap­ sule summary typically is done after the agenda has been established. 108 COGNTTIVE THERAPY OF SUBSTANCE ABUSE the second one approximately halfway through the therapy session, and last, toward the conclusion of the therapy session. The first summary helps patients make a connection between the agenda of the present session and the long-term goals of therapy. The following represents a typical first capsule summary: TH: OK, let's summarize what we are going to focus on today. One thing is the situation when you had the strong urge to pick up on some crack. Second is your situation at work. You are anx­ ious about the fact that you might be laid off. Was there any­ thing I missed? PT: No, that's it. TH: Both of these issues fit very nicely with your long-term goals of treatment, one being coping with urges to use crack, finding other methods for coping with anxiety, and, last, your concerns about employment and saving money. Do you see how they connect? PT: Yeh, it all makes sense. The second summary helps the therapist to collect his own thoughts, to decide what to do next (such as advancing to the next item on the agenda), to convey understanding of the patient and provide an opportunity to correct any misunderstanding, and to make the therapy process more understandable to the patient. Initially in treatment the final summary is done by the therapist. However, as therapy progresses the therapist should move very quickly to get the patient to do end-of-session summaries. When patients summarize, it gives them responsibility for processing the session, and it lets therapists check on patients' understanding of what went on in the session. Further, patients improve their retention for the contents of the session when they actively review what has been dis­ cussed. H O M E W O R K ASSIGNMENTS The homework assignment is a collaborative enter­ prise generated and agreed on by the therapist and patient as a team. Its two main functions are to serve as a bridge between sessions, ensuring that the patient continues to work on his or her problems, and to provide an opportunity for the patient to collect information to test erroneous beliefs and to try new behaviors (Blackburn & David­ son, 1990). Structure of Therapy Session 109 Patients are encouraged to view homework as an integral and vital component of treatment (Burns & Auerbach, 1992; Burns & Nolen- Hoeksema, 1991; Persons, Burns, & Perioff, 1988). Since the therapy session is time-limited, normally less than an hour, homework assign­ ments become extremely important as they offer patients ongoing opportunities to practice various skills that they have been taught in the therapy session. It is best to assign homeworks that draw from the therapy ses­ sion, as homework is most effective when it is a logical extension of the therapy session (Newman, 1993). This can be done by reviewing what has happened in the therapy session and then focusing on how these points or lessons can be continued and reinforced outside treat­ ment. Ideally, such assignments ultimately lead to the continued use of new skills, even after the termination of formal treatment. It is generally advisable to review the previous week's homework as an early agenda item in each therapy session. By doing so, thera­ pists convey to patients that homework is an important part of the therapy process (Burns & Auerbach, 1992). Also, by reviewing home­ work from previous sessions, therapists can correct patients' mistakes early in freatment—for example, in completing a Daily Thought Record (DTR) (see Chapter 9, this volume). By making sure that the home­ work assignment is reviewed, therapists can make certain that patients are practicing new cognitive and behavioral skills correctly. Therapists who neglect to review the homework in each session create three problems. First, the patients usually begin to think that the homework is not important and, therefore, that treatment is some­ thing done to them rather than something they actively work on even in the absence of the therapist. Second, the therapists miss oppor­ tunities to correct mistakes such as the patients' inadequately respond­ ing rationally to their automatic thoughts. Third, the therapists lose the chance to draw helpful lessons from the homework and to rein­ force these lessons. The therapist can minimize patient noncompliance by being sure to explain the rationale for the assignment and by discussing with the patient any possible or expected difficulties (Newman, 1993). For example, the therapist might ask: "What are some things that could happen that might get in the way of completing the assignment?" and/or "What are the odds of your completing the assignment?" In addition, if the therapist has some doubt about the patient's under­ standing of the task, he or she should, if possible, rehearse the assign­ ment before the patient leaves the session. If a homework assignment is not carried out, therapists should address this issue. One method is to use the "Possible Reasons for Not 110 COGNTTIVE THERAPY OF SUBSTANCE ABUSE Doing Self-Help Assignment" Checklist (see Appendix 6, page 327). This checklist helps to identify those reasons why patients often do not do homework assignments. The therapist can pull out a copy of this list and ask the patient to select those items that apply to his/her non­ compliance. The following are some examples of items on this check­ list: "I don't have enough time, I'm too busy," "I feel helpless and 1 don't really believe that I can do anything that I choose to do," and "It seems that nothing can help m e so there is no point in trying." These beliefs become new targets for examination and testing. In summary, the homework assignment functions as a bridge between therapy sessions and provides an opportunity to test beliefs and prac­ tice skills learned in the session. The task should be a logical exten­ sion of the session and be relevant to the goals of therapy. The thera­ pist can minimize noncompliance by giving rationales for assignments and discussing possible difficulties with the patient. To facilitate patients' understanding, homework assignments can be rehearsed in session. Therapists should explain the importance of homework, and are advised to review assignments at each session. Incomplete assign­ ments should be discussed as an agenda item in the session. The rea­ sons that patients cite for not doing the homework can be ascertained through questioning or a checklist, and these reasons are treated as beliefs to be tested. F E E D B A C K IN T H E T H E R A P Y SESSION Therapists and patients regularly exchange feedback during therapy sessions. Throughout the session, the therapist asks questions to be sure that the patient understands what the therapist has said and where the therapist is heading. For example, the thera­ pist might ask, "Can you tell me what point I'm trying to make with these questions?" Sometimes patients misunderstand what therapists are trying to accomplish. Asking questions at these points gives patient and therapist an opportunity to clarify miscommunications in the therapy session. At the end of the session, the therapist should try to get feedback from the patient regarding (1) what was learned in the session, (2) how the patient felt during the therapy session, and (3) how the patient feels about the therapy in general. For example, the therapist might ask the following questions: "What did you get out of today's session?" "Was there anything that I said or did that rubbed you the wrong way during today's session?" "Do you feel we are accomplishing something useful?" Other ways of eliciting feedback include responding to nonverbal Stmcture of Therapy Session 111 behavior in the therapy session. For example, if the therapist not that the patient is frowning, the therapist might say, "I noticed you just had a frown on your face. What thoughts were going through your mind right then?" This will often result in eliciting valuable feed­ back. The key points to remember are that the therapist should endeavor to become adept at eliciting and responding to verbal and nonverbal feedback throughout the therapy session, that the thera­ pist should regularly check for the patient's understanding of what is going on in the therapy session, and that key points should be sum­ marized periodically throughout the therapy session. This, in turn, helps to build a strong collaborative relationship. SUMMARY In this chapter the importance of session structure and its eight components are discussed. Setting agendas helps to make maximum use of time, keeps the sessions focused, sets the tone for a working atmosphere, and counters therapist drift. Repeated mood checks identify changes in mood that might lead to relapse. Bridging sessions provides continuity across sessions and keeps therapy ses­ sions focused on goals of treatment. In discussing the list of agenda items, therapists help their patients to prioritize the list, to stay focused on important material, to make the most efficient use of time, and to contribute actively to the discussion. Also, therapists use skillful Socratic questioning as often as possible, which helps patients make their own discoveries. Capsule summaries should occur at least three times in a session. The importance of homework must be conveyed to the patient, and the appropriate steps for minimizing noncompli­ ance should be taken. Therapists provide and elicit feedback to clear up possible misunderstanding and/or misinterpretation of what is happening in the session. C H A P T E R 7 E d u c

a t i n g P a t i e n t s i n the Cognitive Model A J. ̂ s the cognitive therapy of substance abuse is a collaborative enterprise between therapist and patient, it is essential that patients gain a conceptual grasp of the key components in the model, such as understanding the associations and causal relation­ ships between cognition, affect, behavior, craving, and using. Patients need to learn about the phenomenon of automatic thoughts and the key elements for testing hypotheses. Some therapists start educating drug abuse patients in the treat­ ment model before they themselves have gained an adequate under­ standing about their patients' formulations of the various problems. In doing so, therapists may miss an opportunity to foster an atmo­ sphere of teamwork that is so important to nurture early in freatment. Asking patients for their views helps to nurture the collaboration. In some cases, patients are quite aware of the specifics of their problems; they just feel stuck and are not sure what steps they need to take to arrive at functional solutions. While gathering the patients' formula­ tions, therapists can begin to educate patients in the cognitive therapy model by focusing on the beliefs that are inherent in their interpreta­ tions of their drug problems. ELICIT PATIENTS' F O R M U L A T I O N S OF THE PROBLEM Substance abuse patients generally have explanations for their drug problems, such as "I have a high-stress job," "Today everybody uses drugs," "It's this marriage; if she would only change," and so on. By beginning to explore these "reasons," the therapist starts to understand the patient's "internal reality" and to establish a col­ laborative set for therapy. 112 Educating Patients 113 Therapists ask patients how they believe their drug problem devel­ oped, and how they would explain their current difficulties with work, relationships, the law, and other important life areas. In addition, therapists inquire about what the patients think they must do to solve their drug problem. Similarly, clinicians ask why patients believe that they have not been willing or able to solve their drug and general life problems on their own to this point. Although patients may present what appear to be understandable reasons for their drug abuse, they usually have some degree of doubt (as do their skeptical therapists!). H o w much they believe their own explanation can be assessed by asking them to rate it on a scale of 0 to 100, with 0 meaning they do not believe it at all and 100 meaning they believe it completely. This subtie tactic begins to teach patients that their beliefs are not the same as facts and will be subject to evaluation. For example, one patient explained to the therapist during the ini­ tial therapy session that he believed his alcohol and cocaine use were the direct result of where he lived. He stated that the conditions were miserable: "There's high unemployment, poor housing, and drugs all over the place." He believed that anyone with these types of hard­ ships would also be drinking and using cocaine. When the therapist asked how much he believed in his own explanation, the patient re­ plied "85%." The patient stated that there were indeed some people in the area who did not use drugs, but they were "religious." However, on closer review, the patient noted that there were two members of his own family who were using neither drugs nor alcohol—his sister and father. The patient was given an assignment to list all of the people on his street that he believed used and those who he believed did not use. Although there were a large number of users, a clear majority of people on his street did not use drugs or abuse alcohol. The patient was quite surprised with these findings. Therapist and patient then agreed that looking at other explanations for his cocaine and alcohol abuse would be worth pursuing. DEMONSTRATE THE RELATIONSHIP BETWEEN SITUATIONS, COGNITIONS, AFFECT, CRAVING, BEHAVIOR, AND DRUG USE The following is an example of a didactic presenta­ tion: "An automatic thought is a spontaneous thought or picture in your mind. Right now you might not pay much attention to these 114 COGNITIVE THERAPY OF SUBSTANCE ABUSE thoughts or pictures or make any connection between them and how you feel, but they do in fact affect your emotions and cravings for drugs. Automatic thoughts can be related to past, present, or future events, such as 'I knew I should not have gone in that bar,' 'I can't stand this craving,' and 'Oh hell, I'm never going to kick this prob­ lem.' Furthermore, these thoughts seem completely believable when they occur; therefore, they are accepted as fact without question. Further, they seem to make sense in spite of evidence to the contrary." A powerful method for teaching patients how to recognize auto­ matic thoughts is to have them relate their ongoing thoughts live in the therapy sessions. Therapists might say, "I want you to remember when you were in the waiting room just prior to this session. How were you feeling?" Patients sometimes will respond by saying "anx­ ious," "nervous," "unsure of myself," "bored," "angry," and other emotions. Therapists can then ask, "What was going through your mind right then as you were sitting out there?" Some typical responses are, "I hope no one sees me here," "1 wonder what this is going to be like," "Is the therapist going to like me?" "Am 1 going to be able to do this?" "What is this therapy all about?" "What am I doing here?" "I won't be able to stop using," and "I don't need to see a shrink." Patients then are told that these are examples of automatic thoughts and that they have direct bearing on the aforementioned emotions. For home­ work, patients may be instructed to self-monitor some of their auto­ matic thoughts between therapy sessions. They are asked, for example, to write down their thoughts while feeling depressed, bored, anxious, angry, and especially when having cravings or urges to use drugs. The next phase entails demonstrating the relationship between situations, emotions, cognitions, behaviors, and cravings. This may be accomplished by using examples patients bring to the therapy sessions. Therapists use the patients' examples to show how the patients' thoughts played a role in their negative feelings, their urges to use drugs, and their resultant drug-related actions. For example, "Walter" stated that he was extremely angry because the therapist had implied that the patient's failure to attend a recent therapy session was drug-related. He added, "1 was so pissed off that 1 thought about going out and getting bombed." The therapist, rather than becoming defensive, seized this opportunity to teach Walter about the connections between situations, thoughts, emotions, and drug urges. Specifically, he helped Walter to realize that his thoughts about "getting bombed" did not arise spontaneously, nor did his urges to use result purely from having a chemical addiction. Rather, Walter's thought that the therapist distrusted him triggered an angry reaction Educating Patients 115 (a thought led to an emotion), and the anger in turn sparked though about reasserting control in the therapeutic relationship through using drags (an emotion led to a drug-related belief), and this finally stimu­ lated an urge to use (a drug-related belief led to a drug urge). Thus, a potentially destructive interaction between patient and therapist was turned into an opportunity to learn about the cognitive model of drug abuse. As patients become more skillful at making their own connec­ tions between situations, affect, cognitions, and craving, the thera­ pist can begin to discuss with them the concept of beliefs. The therapist explains that the way we interpret events is largely determined by our belief systems. Beliefs tend to lie in a dormant state out of awareness until they are activated by specific situations. Patients who have difficulty understanding the notion of beliefs within a drug use context may be given the following nonclinical example: "A person has the belief that 'all people are created equal.' This is a belief that usually is dormant; it is not a statement that he goes through life thinking to himself. However, under certain circum­ stances, this belief is activated, such as when the person sees an injustice occur (e.g., someone who is guilty of a serious crime is set free because he is wealthy and influential). In these examples, the belief 'all people are created equal' is activated because circumstances occur that have to do with the belief. This, in turn, leads to a series of automatic thoughts, such as 'This shouldn't happen,' 'This is unfair,' and 'Why is this happening?' At this point, when the belief is triggered, the automatic thoughts are brought to awareness for that person and he becomes righteously angry." Therapists explain that while the above belief is adaptive, many drag-related beliefs are not, and the thoughts and feelings they lead to may make matters worse by triggering drag cravings and urges. Dysfunctional beliefs lead people to misinterpret situations, to over- generalize, to exaggerate, to see things in all-or-none terms, and to engage in other errors of thinking. Drug-abusing patients often make the mistake of assuming that their dysfunctional beliefs are valid and, therefore, that their interpretations are correct. One way to illustrate the notion of accurate/inaccurate beliefs is to remind patients of the story of Christopher Columbus. At one time, many people in the Western world held the belief that the world was flat. However, this did not make it so. It took a bold expedition to test the accuracy of this belief. One might say that when Columbus proved that the worid was not flat, many people updated their information or belief about the surface of the worid. However, there were still a few skeptics who 116 COGNTTIVE THERAPY OF SUBSTANCE ABUSE held on rigidly to the idea that the world was flat. In the same wa people may believe that drags are the only way to feel good, even though drags have time and time again been proven to cause more misery than joy. As pointed out earlier (Chapter 2, this volume), addictive beliefs are an essential component in the sequence leading to compulsive using. Patients often start off with the belief that their drag of choice is not harmful. They may also have the belief that they function bet­ ter with other people when under the influence of drugs such as cocaine. This belief can lie dormant until the patient faces a situa­ tion such as a social event. Being informed of an upcoming party may activate this belief and thus lead to craving, followed by certain auto­ matic thoughts that give permission to use the cocaine. This in tum leads to a series of habitual behaviors that facilitate finding the cocaine. Patients also have beliefs that develop over time. For example, a patient may start off with the belief that it is O K to use cocaine, that "it's not addictive." He may also entertain the belief that using cocaine makes him more sociable. However, over time, he might also develop a new set of beliefs regarding the cocaine, such as "I can't be social without it" and "I must have the cocaine in order to function." In this scenario the patient has moved from being a recreational user to substance dependence. In educating drag-abusing patients about the cognitive therapy model, it is helpful to teach them to identify drag-related beliefs. As stated earlier, drag-related beliefs can take different forms. They may be (1) beliefs about the drug itself, such as "Cocaine is not addictive," (2) beliefs about what is expected from the drug, such as "Coke will help to chill me out," and (3) permission-giving beliefs, such as "1 deserve to feel good." Mr. C, a 34-year-old polysubstance abuser, had the initial belief that he could not become addicted to using cocaine. He started off using cocaine socially-"only" at parties. Later he developed the belief that he could work better using cocaine. This, in turn, led to his use of cocaine at work when he was under pressure to meet deadlines. He had the illusion that he was much more productive at work when using coke. However, he overlooked the large amount

of money he was spending on cocaine. Furthermore, he was not as productive because he began to miss days at work after cocaine binges. Later, when he tried to stop and he began to experience strong urges and cravings, Mr. C's beliefs centered on the cravings themselves. Some of these were, "I can't stand the craving," "These feelings won't go away," and "The urges make m e use." Educating Patients 117 In order to assist therapists in the process of identifying patien beliefs about drags, we have developed the Beliefs About Substance Use questionnaire (see Appendix 1, page 311). This questionnaire, clinically generated, lists 29 common beliefs that patients report about substance use. W e have found that patients who are otherwise un­ skilled in reporting their thoughts can recognize beliefs that they main­ tain regarding drag use when they utilize this inventory. A noteworthy feature of the Beliefs About Substance Use questionnaire is that it allows patients to endorse beliefs that are contradictory to one another. This can be important in helping patients understand that they may hold conflicting beliefs about their drag-taking behavior. Thus, both their ambivalence and the dysfunctional nature of their thinking styles may be highlighted. Another useful method for identifying beliefs is via inductive questioning (also known as the "downward arrow technique"; cf. Burns, 1980). The substance-abusing patient first recognizes an auto­ matic thought; then the patient and therapist attempt to understand underlying meanings of the thoughts. This technique is illustrated by the following example: Mr. C. reported that during the week he was feeling extremely angry and anxious. The therapist then asked the patient to describe the specific situation. Mr. C. reported that while at a party, he had seen other people using and also saw some of his drug buddies, and he started having urges to use. TH: What thoughts were going through your mind right then? PT: It's not fair; they can use and I can't. TH: Let's presume for the moment this thought is accurate. What about it is important—what does it mean to you? PT: I'll never be able to use again. TH: And if you'll never be able to use again, what will be the sig­ nificance of thatl PT: I'll always have these urges and feel anxious. TH: And what are the implications for your life? PT: There's no escape. I'm trapped and helpless. As one can see, an important core belief ultimately was uncov­ ered through using the downward arrow technique (see Figure 7.1), and the patient came to understand the role of beliefs in his prob­ lems a bit more clearly. 118 COGNTTIVE THERAPY OF SUBSTANCE ABUSE "It's not fair. They can use and I can't." Automatic Thoughts I'll never be able to use again." "I'll always have these urges and feel anxious." Deeper core beliefs "There's no escape. I'm trapped and helpless." FIGURE 7.1. The downward arrow technique. THE "CRAVING SCENARIO" Therapists can teach their patients a great deal about the patients' substance abuse as seen within a cognitive therapy per­ spective by diagramming a "craving scenario." Essentially, this entails spelling out the cognitive m o d e l of substance abuse in the form of a flow chart, complete with examples that pertain directly to the patient's subjective experiences with drags. For example, M s . L. reported a cocaine lapse to her therapist, w h o proceeded to m a p out the patient's "craving scenario" (see Figure 7.2), w h i c h highlighted the sequence of events a n d beliefs that led u p to the actual episode of drag use. PROBLEMS IN EDUCATING PATIENTS IN THE COGNITIVE MODEL Sometimes patients initially fail to identify their auto­ matic thoughts. They report, "I don't have any thoughts." In order to overcome this problem, therapists may wait for the patients to dem­ onstrate affective shifts in the therapy session and then ask, "What is going through your mind right now?" W h e n aroused in this man­ ner, patients often have access to their thoughts. Patients are also asked, "If you don't have any thoughts, can you report what you are feeling?" Oftentimes, they report feelings in the form of cognitions; for example, "I feel like I don't want to be here today." Initially, thera­ pists may choose to accept these responses as feelings, but, at a later point, it will be important to educate patients to make a distinction Educating Patients 119 between cognitions, such as "I don't feel like being here today," and feelings, such as anxiety, anger, sadness, shame, and guilt. S o m e patients have difficulty labeling the particular feelings that they are experiencing. They say such things as "I feel like shit" or "I feel awful." O n e m e t h o d to help patients label feelings is to encour­ age them to use the simplest terms possible in describing their feel­ ings, for example, m a d , sad, or glad. Also, if a patient says, "I'm upset," the therapist could ask, "And where in your body d o you experience this feeling of being upset?" T h e patients m a y then report s o m e type of physiological indicator such as tightness in the stomach, tightness in the chest, stiff neck, and so on. Patients can be taught to use these bodily sensation cues to ask themselves the important question: "What's going through m y m i n d right n o w ? " With repetition, patients eventually c o m e to understand that it is important to notice and to modify their thoughts and beliefs. stimulus Circumstances—External Ms. L was at a party, met up with some of her former drug buddies. Stimulus Circumstances—Internal Had a sudden feeling of euphoria. Later became tired; felt bored, sad. Drug Beliefs Activated "Using Is a lot of fun." "I can't stand the boredom." "My life is screwed up anyway so why not use?" Core Beliefs "I'm a failure." "My life is hopeless.' Automatic Thoughts "Go for It." "This will be great." "They're having a blast." Focus on Short-Term Solution Ms. L joins the group and snorts a few lines. FIGURE 7.2. The craving scenario. 120 COGNITIVE THERAPY OF SUBSTANCE ABUSE SUMMARY An important part of the early stages of therapy involves educating patients about the cognitive model of drag addic­ tion and its treatment. Most fundamental to this process is the therapist's explication of the causal and correlational connections between stimulus situations, thoughts, beliefs, emotions, drag urges, and drag taking. Therapists can achieve this important goal by highlighting natu­ rally occurring sequences of events in the patients' lives, as well as in session. In this manner, patients learn that therapy entails much more than simply venting about problems and/or being persuaded to give up their drag use. Rather, patients learn that their drag prob­ lems involve an understandable series of external and internal events that, left undiscovered and unmanaged, "automatically" lead to drag use. They learn that these same events, once understood, offer a num­ ber of choice points for patients to minimize the chance that they will experience opportunities, urges, and actions that will perpetuate drug use. Most important in this process is the patients' understand­ ing that their automatic thoughts, triggered by core beliefs and beliefs about drugs, play an important role in their addiction. As a result, they learn that by modifying these thoughts and beliefs, they assist themselves in the process of recovery. The "craving scenario" is one useful method for illustrating the series of external and internal events outlined above. Another useful tool is questionnaires, such as the Beliefs About Substance Use inven­ tory, which helps patients to recognize some of the implicit beliefs that fuel their drag use. In addition, skillful questioning by therapists can help patients to illuminate the cenfral role that their thinking plays in any situation that is pertinent to their risk for using drags. Ulti­ mately, the patients themselves become adept at modifying their thinking styles, a vital therapeutic step. C H A P T E R 8 S e t t i n g G o a l s T X here is an old saying that maintains, "If you don't know where you're going, you won't know when you get there." This statement rings especially trae for therapy with addicted indi­ viduals. In this chapter, we examine the reasons it is important to establish goals for therapy. Setting goals creates a therapy map that helps to give a sense of direction to patients and therapists. Generally, patients enter treatment wanting to feel better—to get rid of the depression, anxiety, panic, and other negative affect states. W h e n the patient and therapist agree on a set of goals, they collaboratively focus on change in the patients' behavior, for example, being abstinent from cocaine and finding bet­ ter ways of solving real-life problems. In the absence of clearly defined goals, therapy sessions often appear fragmented or disjointed. In one case, a patient came in with a long histoty of cocaine use. However, her presenting problem was wanting to "feel better" about herself. Through careful questioning, the therapist was able to conclude that this might be achieved by her going back to school, finishing school, and pursuing a career. Since her use of cocaine was interfering with these goals to a large degree, the therapist assumed that one of her goals was to become totally abstinent. It was not until they were halfway through the first therapy session that it became apparent that the patient planned to continue her cocaine use, "but only on the weekends," and wanted to work only on the goal of going back to school. She saw no contradiction between these goals. Formulating goals tends to make explicit what patients can expect from treatment. Sometimes patients' expectations of therapy are unrealistic. By initially discussing the expected outcome of therapy and defining it in concrete behavioral terms, patients know where therapy is headed and, through understanding the cognitive therapy 121 122 COGNITIVE THERAPY OF SUBSTANCE ABUSE model, have an idea as to how the goals will be obtained. In sum, a alluded to at the beginning of the chapter, patients will know where they are going and how they are going to get there. Focusing on the expected outcome of therapy tends to make patients feel hopeful about the possibility of change. Many substance abusers have made numerous unsuccessful attempts in the past to stop on their own and feel hopeless about kicking their habit. Clear goals direct their attention to the possibilities for change. For example, "Jake" entered treatment and, at the vety first therapy session, stated that he could not imagine himself being off of cocaine, even though he had recently finished a detoxification program and had not used cocaine for several weeks. It was a difficult (but not impossible) task to get this patient to focus on the possibility of change and to try to imagine himself being cocaine free and coping with many of the other concerns that he brought into therapy—excessive debt and family dis­ cord. Setting goals helps to prevent therapy drift. Many substance abus­ ers enter therapy only after accumulating many problems such as the loss of a job, marital problems, poor health, depression, and anxiety. With so many presenting concerns, it is quite easy to shift haphaz­ ardly from one topic to another in each session. Knowing specifically the long-term goals of therapy and the priority order in which they will be addressed helps to prevent drift from taking place. The thera­ pist and patient can focus on one or two of the most immediate and pressing problems, yet still fully realize that there are additional issues that will be dealt with as therapy progresses. Specific goals tend to act as anchors and thus make it more obvious to the therapist when therapy has taken a turn in a new direction. For example, consider the case of a patient who came into treatment for help with his anxiety about abstinence from cocaine. He had not used cocaine for over a year, but in the past few weeks he noticed that he was becoming more and more anxious about the possibility of using again.

The initial goal in therapy was to help the patient develop better ways of coping with his anxiety about some of the urges and cravings that were reappearing. Although this was the primaty focus of therapy, it became obvious after several sessions (when the patient was less anxious about relapse) that he was also experiencing severe marital discord. He disclosed that his wife was also abusing diet pills and alcohol and that this was causing a great deal of strife between them. Knowing the original goal of therapy, which was to help him deal with the anxiety about a possible relapse, the therapist and patient were able to see that focusing on marital concerns was going to be a change in the original treatment plan. It Setting Goals 123 would have been vety easy to drift automatically into working on t marital discord at the expense of a discussion about managing anxiety and cravings for drags. Instead, patient and therapist put both topics on the therapeutic agenda, allotted a certain proportion of session time for each, and decided that future sessions would explore the causal connection between his renewed drag cravings and his wife's substance abuse. The setting of mutually established goals reinforces the therapeu­ tic alliance and the spirit of collaboration between patient and thera­ pist. It also gives the patient a sense of active participation in his or her treatment. This is especially important for substance abusers who often see their lives in disarray and feel out of control and at the mercy of their dependency. Collaboratively setting goals aids in fostering the patient's sense of efficacy and confidence to overcome drag depen­ dence and other problems. For example, a young cocaine addict reported the following after a goal-setting session: For the first time since he had tried stopping on his own he had some sense of control over his life and it was clear what he wanted to get from therapy—to learn techniques for coping with cravings and to learn better ways of finding a job. He felt as if he was part of the therapeutic process, and that therapy was not something that was "being done" to him. To define positive therapeutic outcomes in concrete terms is an important part of the structure of the cognitive therapy session. Goal setting, along with other elements of the structure of the therapy session, such as agenda setting, helps to avert the common trap whereby each session is reduced to a series of crisis interventions. Therefore, patient and therapist gain a sense of the long-term goals of therapy along with the short-term goals of the session at hand. Understanding the goals of therapy also is important for evaluat­ ing therapeutic progress and outcome. Oftentimes, patients become dis­ couraged in freatment because of a lack of progress or setbacks, such as lapses in drag use. This, in turn, often stimulates black-and-white thinking about therapy: "Therapy is not working at all." By referring back to the original goals of treatment, and by reviewing the patient's progress throughout, the therapist can undermine some of the patient's hopelessness about treatment. For example, one patient and his therapist had documented the following goals at the beginning of treatment: to abstain from cocaine and alcohol, to gain more confidence in social situations, and to obtain and maintain a steady job. Over a period of about 6 months, the patient did remain abstinent from cocaine and alcohol. However, he was unable to obtain any type of employment. This was vety dis­ couraging for the patient and he began reporting negative automatic 124 COGNITIVE THERAPY OF SUBSTANCE ABUSE thoughts about the therapy. The therapist then was able to point o that, although he had not found employment, the patient was feel­ ing much better and had a strong sense of pride about being able to stay away from drags and alcohol. Thus, an important goal of treat­ ment was being met. In addition, the therapist questioned the patient about the specifics of the original goal of employment. In order to achieve this goal, the patient and therapist had agreed on the short- term goal of developing job-seeking skills, such as how to conduct himself at an interview, where to look for a job, and how to prepare a resume. Indeed, the patient had made gains in these areas. After their discussion, the patient was able to see the progress he had made and was able to challenge his negatively biased thinking about the thera­ peutic "failure" of not finding a job. The patient felt a bit more hopeful about therapy and more motivated to continue in treatment. Conversely, a patient who is discouraged because she has not completely quit her smoking and drinking may be cheered somewhat on realizing that some of her more general goals for therapy are being met, thus giving her momentum to tackle further her alcohol and nicotine addictions. This brings up an important point; namely, that goals for therapy do not simply entail cessation of problematic drag use. Criteria for success in therapy must be assessed across a number of important life concerns, including family relationships, social func­ tioning, and work productivity, to name but a few (Covi et al., 1990; McLellan et al., 1992). There are numerous issues that can be brought up and discussed in any one particular session. With clear, concrete goals, the thera­ pist and patient can make maximum use of the therapy time, and can address problems in an organized and systematic fashion. G E N E R A L RULES F O R SETTING G O A L S Therapists should collaborate with their patients in establishing goals for treatment. When patients enter treatment they frequently are ambivalent about abstinence from drugs and alcohol (Carroll, Rounsaville, & Keller, 1991; Havassy et al., 1991; Miller & Rollnick, 1991). It is inadvisable for therapists simply to proclaim that their patients must strive for abstinence as a condition of being in treatment. Instead, it is important for the therapist to explore collaboratively with the patient the benefits of total abstinence from drags such as cocaine. The act of collaboration will help the patient to feel that he or she traly is a part of the process of change. In setting goals, therapists try to highlight the relationship Setting Goals 125 between abstinence and problem-solving. For example, therapists dis cuss with patients how being drug free can contribute to keeping a job and to having better relationships and more money for other things such as clothes, vacations, and a car. Nevertheless, it must be explained that while abstinence increases the chances of obtaining the desired outcome, it does not guarantee it. As a case in point, Ms. F. presented as her primaty goal the wish to stop using crack. The thera­ pist then asked her what the benefits of not using crack would be. She stated that by not using she would be able to save money, that she would be able to pay her bills, and also that she would feel like going to work each day. The therapist then summarized, "Being drag- free is your primaty goal and other goals will be to save money, to be able to pay your bills, and to be able to keep your job. It is impor­ tant to note that abstinence alone will not insure achieving these other goals. It will help you to be in a better position to learn how to get what you want in these other areas of your life. Perhaps we'll work on these skills as well." Goals are best stated in concrete, specific terms. Often, at the beginning of therapy, patients present vague, nonspecific goals for treatment, such as "I just want to get m y life in order," "I just want to be m y old self again," or "I just want this anxiety to go away." Therapists assist patients in defining treatment goals in more circum­ scribed behavioral terms, such as finding a job; staying away from people, places, and things associated with drugs; being able to go out and have a good time without using drags; or reestablishing a bro­ ken relationship. For example, Mr. R., a 42-year-old cocaine addict, stated that he wanted "his world to stop falling apart." In order to concretize the goals, the therapist asked what he would like to be doing differently at the end of treatment. Mr. R. then presented more focused objectives: "First of all, I would like to get a chance to see my children more often. I'm separated from m y wife right now and she doesn't allow m e to see the kids. I would like to stop using coke. 1 want to get involved with the church again. I used to be really into it. I would like to have a regular job. I'm tired of doing odd jobs. I want more excitement in m y life. I'm bored most of the time except when using drags." The therapist facilitated this process by periodi­ cally asking, "And what else would you like to be doing differently?" As a result, Mr. R.'s goals were translated from a vague statement of his "world to stop falling apart" to much more concrete, behavioral, measurable events. The therapist summarized Mr. R.'s goals as follows: 1. See children more often. 2. Stop using coke. 126 COGNITIVE THERAPY OF SUBSTANCE ABUSE 3. Get involved with the church. 4. Have a regular job. 5. Have more excitement, but stay drag free. Once the patient's goals are concretized, the therapist can start to think of the necessaty operations to achieve them, and the criteria on which to assess treatment outcome. An example of goal attainment was Mr. R.'s finding a permanent job with a construction company. Another goal was reached when, after getting a job, his wife allowed him to see the children each weekend. Further, through urine test­ ing, the therapist was able to establish that Mr. R. was not using cocaine. Finally, therapist and patient worked on developing sources of nondrug positive reinforcement, such as hobbies and physical rec­ reation (cf. Stitzer, Grabowski, & Henningfield, 1984). Having these specific goals in the forefront helped to keep the therapist and patient from drifting in each therapy session. Also, hav­ ing these goals written down at the beginning of treatment proved to be a powerful motivator for Mr. R., as the patient was able to com­ pare his situation at the beginning of treatment with his functioning at later stages in treatment, and thereby to recognize his progress in therapy. In setting goals, it is important to remember the following: 1. Be collaborative in setting goals. 2. Establish goals in positive terms as they relate to abstinence. 3. Be concrete and define goals in measurable behavioral terms. STANDARD GOALS OF TREATMENT Two standard goals of treatment are (1) to reduce drag dependency, with the cornerstone being to help the patient develop techniques for coping with urges and cravings, and (2) to help patients learn more adaptive methods for coping with life problems. When substance abusers enter therapy, they often are ambivalent about their desire to stop using. Increasing their motivation to reduce drag dependency becomes an important early focus in therapy. In the first phase of treatment, it is imperative to facilitate the patient's understanding of the various advantages and disadvantages of using or not using drugs and alcohol. The following is a transcript of a therapist discussing with his patient the advantages and disadvantages of using cocaine. Setting Goals 127 TH: One thing that we said that we would go through are the ad­ vantages and disadvantages of using drags. What are some of the advantages to using cocaine? W h y is it good to use? PT: It ain't good. It ain't good but it makes m e feel good. "TH: OK. It makes you feel good. PT: Yeah, thaf s an advantage of it. It makes m e feel good for awhile. TH: What is another advantage? PT: I see evetybody else doing it, so I want to do it too. TH: So, are you saying that it makes you fit in? PT: Yeah, it makes m e fit in the crowd. W h e n I see somebody else doing it, I want

to be part of the crowd. People to talk to when I'm doing it. It seems like I have friends, but they are not friends, you know. TH: OK, so you have more friends, but they are not real friends. Maybe we can consider this as a disadvantage to using? What do you think? PT: Yeah. It seems like you have more, but you don't really have no friends. TH: OK. N o w let's focus on certain advantages for not using. W h y is it good not to use cocaine? PT: You save money. TH: "You save money." {Therapist writes this down) PT: You can think clearly. Your brain ain't all messed up. You can think clearly. You can function better and work. TH: Some people say that they can function better at work when they have cocaine. What do you think about that? PT: Oh, I can't. It just makes m e want to take days off. I don't feel like working. TH: So another advantage to not using is that you feel like going to work? PT: Yeah, I can go to work. I can work. I can maintain m y bills. Yeah, because when I used I was taking days off. You just don't have the motivation to do nothing but smoke. TH: So, some advantages for not using is that you can save money, think more clearly, feel like going to work, and pay your bills on time. PT: Yeah, and I feel better about me. 128 COGNITIVE THERAPY OF SUBSTANCE ABUSE TH: Are you saying that sometimes when you don't use coke you feel better about yourself? In other words, you feel proud of yourself when not using? Is that right? PT: Yeah, that's the feeling I'm talking about. Yeah, and when I use, later I feel depressed and guilty that I gave in. TH: Well, yeah. That's something we can look at. Something we will put under the categoty of disadvantages for using and, that is, we could say that after using cocaine—how would you say it? You feel bad about yourself? PT: Yeah. You feel real bad about yourself for picking up. Then it's like you are on a merty-go-round again. You just want to keep on using once you start. TH: Now, can you think of any other advantages for not using? Any good reason for not using? PT: M y kids, m y family, I have more time for them. TH: Good. OK, let's switch tracks now. Let's look at the disadvan­ tages for not using it. In other words, right now you are not using it. Are there any problems when you are not using coke? What's the cost of not using? PT: 'Cause I'm not using it? TH: Yeah, you are not using it. Do any thoughts go through your mind? PT: A little voice saying, "Go ahead, one time ain't going to hurt" [a permission-giving belief]. TH: One time won't hurt? PT: Yeah, I can handle it. One time ain't going to hurt you. TH: Yeah, that thought crosses your mind often? PT: Yeah, sometimes the thought does come, "Yeah, go ahead and take one. It ain't going to hurt you." TH: So what is the price you pay for not using? PT: The only one 1 can think of is this voice saying, "OK you can go tty." This urge to use. TH: So, are you saying that the disadvantage when you are not us­ ing is that sometimes you are troubled by these thoughts tell­ ing you to use? PT: Yeah, just go ahead and use, just once. TH: OK. I get your drift now. Setting Goals 129 PT: Saying, "Go ahead, it's good to use it." It makes me uncomfort­ able. I start getting that urge again. TH: So, in other words, when you are not using coke, the thought makes you uncomfortable and you start getting the urge to use. Having these urges can certainly be the price you pay for not using, and these urges certainly are uncomfortable. N o w what are the disadvantages for using? PT: For picking up? I spent m y money on it. It is something I don't want to do. And then I say, "All right then, you already did it. You might as well continue" [permission-giving belief; absti­ nence violation effect]. TH: So the disadvantage is that once you start using it, you give yourself permission to keep using it and later you feel bad about yourself? PT: Right, I give myself permission to keep on using it and feel depressed and guilty later. I let myself down. And then I use all of that money. It's an awful lot of money used. And also I've gotten into legal trouble for using it. That's certainly a disad­ vantage. And also m y life is a lie. I end up lying to some of m y best friends. TH: OK. These things that we just went over—the advantages of us­ ing, the advantages of not using, the disadvantages of using, and the disadvantages of not using—are some things that I think we need to review in therapy over and over again. First, let's write them down on some index cards for you to carty around with you as reminders. In this example, one sees that by reviewing the advantages for using and the advantages for not using cocaine, the therapist has elu­ cidated some important goals for treatment. For example, under the "advantages for not using" categoty, there are some concrete, posi­ tive goals to be obtained: having more money, being able to think more clearly, being able to pay bills, and so on. However, there is another set of goals (that is a bit less obvious) that was highlighted as a result of discussing the "advantages for using"; that is, the patient viewed the cocaine as making her feel good, fitting in with the crowd, and having more friends. A set of goals can be derived from these statements, with the therapist saying, "If we could work on helping you to feel good, to be able to fit in with the crowd, and being able to have friends, but without using cocaine, would these be important goals for us to tty to achieve in therapy?" By using this strategy, the 130 COGNITIVE THERAPY OF SUBSTANCE ABUSE therapist focuses on the positive aspects of abstaining from cocai and presents the goals in a positive manner, while still empathizing with the patient's desire for the drug. This is important since some patients view abstinence from drags as a form of deprivation in the sense that it is something that is taken away from them (Jennings, 1991). The therapist collaboratively helps the patient to reframe the goal in a more positive way. Therefore, the patient can work on attain­ ing the perceived positive aspects of using cocaine but without incurring the disadvantages involved in acmally using the drag. As previously mentioned, the two standard long-term goals of treatment are the reduction of cocaine dependency and the learning of more adaptive methods for coping with real-life problems. Regard­ ing the latter goal, substance abusers tend to have poor problem-solv­ ing skills. They tend to blame others for their problems, to be impul­ sive in making decisions, to ruminate about their problems without actively taking steps to solve them, and to withdraw and avoid instead of thinking about their problems and coming up with practical solu­ tions. This withdrawal and avoidance often is achieved through the use of drags. For example, one patient blamed his current situation—being unemployed and being on parole—on society. He claimed that given his current situation, anyone would be using cocaine. For example, even after he had been off of cocaine for awhile, he impulsively decided that he would make some extra money by "bagging cocaine." He also tended to raminate about his problems and to spend a great deal of time fantasizing about how he would get out of his current dismal situation—unemployed and living with his parents. Yet, when questioned by the therapist, the patient was able to see that he was taking no active steps to solve this problem. In addition, he tended to withdraw from others and his problems by daydreaming and by using alcohol and cocaine. The therapist was able to help this patient with his problem- solving strategies first by encouraging him to define his problems in clear, specific terms; for example, he was unable to find a job because he was not actively looking for a job and, in addition, the patient had poor job-hunting skills. The therapist also helped the patient iden­ tify errors in his thinking that interfered with looking for solutions. For example, the patient was under the assumption that since he was on parole, no one would hire him. The reality, though, is that there are firms that hire people who are on parole, and many parolees are able to find jobs in spite of their criminal records. In addition, this patient valued his autonomy and therefore had a great deal of diffi­ culty reaching out to others. He believed that it was a sign of weak- Setting Goals 131 ness to do so when it was really in his best interest to make maxi­ m u m use of the social support systems in his area, such as public assistance, food stamps, support group meetings, and therapy. A D D R E S S I N G T H E PATIENT'S A M B I V A L E N C E DIRECTLY As noted earlier, many patients are ambivalent about being in therapy and about giving up their drag use. These mixed feelings and attitudes can be addressed as part of the early process of establishing therapeutic goals, as illustrated by the following dialogue: TH: One thing that we said we would do today is continue working on goals. I would like to start with that. Is that O K with you? PT: Yeah, I guess so. TH: At the last session you seemed a bit uncertain about totally giv­ ing up cocaine. PT: Yeah. And I'm still not sure. Sometimes it seems like a good idea but then I feel like it would sure be nice to pick up evety now and then. You know what I mean? Sort of control m y use like when I first started. TH: So sometimes you think that you want to go for total abstinence then at other times you feel you still want to use but be able to control it. PT: Yeah. TH: OK, what do you think would happen if you tried to stop com­ pletely? PT: I'm not sure . it would be hard . I would miss it. TH: It would be hard and you would feel a sense of loss . {patient nods in agreement). that would be the down side, but what about the up side? Are there any benefits to stopping totally? PT: I think I would feel better about myself. TH: So you would feel better about yourself. H o w is that? PT: I feel terrible about how far down I have fallen the past year. I've tried to quit several times . and each time I fail. maybe if I could stop this I could feel good about myself, the way I used to. TH: That would certainly be a benefit. Remember in the last session we talked about some specific advantages for not using. Maybe 132 COGNITIVE THERAPY OF SUBSTANCE ABUSE this would be a good time to take another look at that list and also to talk about how hard it is to give up cocaine and that you will miss it. Does that sound O K to you? PT: OK. Often patients feel overwhelmed because, through errors in their thinking, they exaggerate their difficulties and minimize the pos­ sibility of corrective action. This, in turn, leads them to believe that there are no solutions and that drag use provides their only respite. In response, the therapist can help the patient to reframe his or her problems in a more hopeful way. Reframing involves getting the patient to collect objective data about situations, to generate alterna­ tive ways of

looking at the situation, and to begin to brainstorm solutions. The process of searching for an alternative in order to com­ bat the patient's hopelessness is illustrated by the following: TH: Let's discuss this problem of your girlfriend calling you when she is high. PT: No need to talk about that. there's nothing I can do about it. she's m y son's mother. TH: So there is nothing that can be done about it. sounds like you feel it's pretty hopeless. PT: You're right. TH: Can you tell me more about what happens? . I'll jot down some of the details of this problem. PT: She goes out and gets ripped on crack. Then when she is crash­ ing, she calls m e . she's ctying. complaining . wants me to come over and that's what I usually do, you know TH: She gets high, calls you, ctying and complaining, she asks you to come over and you do? PT: Yeah. TH: How do you end up feeling? PT: Like hell. I get angty with her . I can't stand to see her that way . I feel sorty for her, kind of sad. TH: What thoughts go through your mind? PT: Here we go again . I'm tired of this . she lied again [girifriend told patient several times she would stop using and get help] . when 1 get real angty I want to just go out and get drank . get high thinking about coke . sometimes I do just that, you know, just chill out. Setting Goals 133 TH: So, she calls, you get angty, feel sad, you go over to her hous you want to get high to deal with the anger and sadness? PT: That's exactly it. TH: You said earlier there is nothing you can do about it. What would you like to see happen? PT: For her to stop calling m e when she's high or crashing. TH: Let's think about this for a few minutes. Her calling you, un­ less you take your phone out, is for the most part out of your confrol. I was wondering, are there things that are still within your control? PT: I don't have to talk with her . I don't have to go over. TH: Trae. But, what would it mean if you didn't talk with her and you didn't go over? PT: She's the mother of m y son . it would mean that I'm not help­ ing her. TH: So you believe, at this point, that by talking to her and going over you are helping her? Is that really trae? PT: Not really. I keep doing the same thing over and over again . she still doesn't stop and she won't get any help. TH: So, maybe an alternative way of looking at this is that it's best if you decide to steer clear of her when she's using. You believe you are helping her by talking to her and going over to her place. But, when you look back, you are really not helping her situation and you set yourself up possibly to use cocaine to deal with the anger. PT: That's right. TH: Would your not talking to her and not going to her house be part of a solution to this? PT: Trae. TH: I believe that when she calls, this incorrect belief within you gets activated, fired up, and you behave as if it were trae. PT: That's right. It's only afterwards that I see I'm not really help­ ing and it's the same thing over and over again. TH: I think this gives us something to work on to help you solve this problem. First thing we'll do is to help you deal with her calling and the second is to explore other things you might do to help her. 134 COGNTTIVE THERAPY OF SUBSTANCE ABUSE SUMMARY This chapter examined some reasons why it is impor­ tant to establish goals for therapy: (1) to foster a sense of direction, (2) to help patients feel more hopeful, (3) to prevent therapist drift, (4) to reinforce collaboration, and (5) to evaluate therapeutic progress and outcome. The following general rules for setting goals also were covered: (1) be collaborative, (2) highlight the relationship between abstinence and problem solving in positive terms, and (3) state goals in concrete, specific terms. W e discussed in detail two standard goals of treatment: to reduce drag dependency, and to learn better prob­ lem-solving skills, as well as presented methods of addressing the patient's ambivalence and negativity about getting help. C H A P T E R 9 T e c h n i q u e s o f Cognitive Therapy F M . or optimal results, the vicious cycles associated with substance abuse are best addressed with a combination of cog­ nitive and behavioral techniques. Cognitive techniques address drag- related beliefs and automatic thoughts that contribute to urges and cravings, while behavioral techniques focus on the actions that caus­ ally interact with cognitive processes. Behavioral techniques help the patient test the accuracy of drug-related beliefs that trigger and per­ petuate drag use, and are also used for teaching the patients skills (e.g., assertiveness and relaxation) in order to deal with high-risk situ­ ations, urges, and cravings. In this chapter we describe some of the most common, widely used techniques of cognitive therapy. Although some of these techniques are adapted for specific use with substance abusers, most are applicable to patients across the diagnostic spectram. BASIC PRINCIPLES The Therapeutic Relationship The efficacy of cognitive and behavioral techniques is dependent, to a large degree, on the relationship between therapist and patient. Beck et al. (1979) explain that the relationship requires therapist warmth, accurate empathy, and genuineness. Without these, the therapy becomes "gimmick oriented." The Cognitive Case Conceptualization Effective treatment requires a comprehensive and accurate cognitive case conceptualization. The case conceptualization 135 136 COGNTTIVE THERAPY OF SUBSTANCE ABUSE (Chapter 5, this volume) is defined as the collection, synthesis, integration of data about the patient so that testable hypotheses about the etiology and treatment of the patients' various maladaptive beliefs and other symptoms can be formulated and tested. These data include demographic information, presenting problem, DSM-III-R diagnosis, developmental profile, and cognitive profile of the patient. Without an adequate case conceptualization, the choice of specific techniques may be arbitraty and even inappropriate for a particular patient. This is seen in the case of a patient who uses cocaine ostensibly in order to give him more "energy" to work late hours at the office. Such a patient would not be receptive to the therapist's blind application of relaxation techniques. The Socratic Method In cognitive therapy, effective interaction between therapist and patient is best accomplished by frequent use of the Socratic method (i.e., guided discovety). Through the Socratic method, patients are guided through a process of discovering their distorted patterns of thinking and behaving. Despite the fact that cognitive therapy involves learning new beliefs and behaviors, these are not taught through lectures or preaching. Instead, the cognitive therapist uses probing questions, reflections, summaries, and hypotheses to elicit, examine, and test patients' basic beliefs and automatic thoughts. Overholser (1987) provides an excellent description of the Socra­ tic method. He explains that "the Socratic method of interviewing encourages the client to contemplate, evaluate, and synthesize diverse sources of information ." (p. 258). This process, when done properly, should reduce "subjective distress" and reduce "acute symptomatol­ ogy." Overholser further explains that Socratic questioning promotes insight and rational decision-making by making the patient aware of important information. Most important, this process shapes thinking through active questioning and selective reflecting. The goal of the Socratic method is for the patient to learn to think independently (i.e., autonomously) and rationally. Homework Assignments To a large degree, success in therapy is facilitated by the completion of formal (assigned) and informal (spontaneous) homework assignments (Burns & Auerbach, 1992; Persons et al., 1988). Formal homework assignments involve the practice of cognitive and behavioral techniques between sessions, where change is most impor- Techniques of Cognitive Therapy 137 tant. For optimal compliance with homework, assignments should be jointly formulated whenever possible. Further, the therapist should check to see if the patient understands the specifics of the assignment and its rationale, perhaps by practicing in advance in the session. The therapist and patient can put their heads together to anticipate poten­ tial barriers to completing assignments, and backup plans can be for­ mulated for times when homework cannot be completed (e.g., the patient is instracted to list the automatic thoughts that inhibited fac­ ing the issues inherent in the assignment). Homework compliance will be further reinforced if the therapist regularly checks on the status of previous homework assignments at each session. C O G N I T I V E T E C H N I Q U E S Advantages-Disadvantages Analysis The person who uses drags typically maintains beliefs that minimize the disadvantages and maximize the advantages of doing so. Hence, the advantages-disadvantages (A-D) analysis is an exfremely useful cognitive therapy technique. In the A-D analysis, the patient is guided through the process of listing and reevaluating the advantages and disadvantages of drag use. Typically, a four-cell matrix is drawn for patients and they are asked to fill each cell with the con­ sequences of using versus not using drugs. An illusfration of the A-D analysis is provided here. "Jill" is a 34- year-old woman who was seen in therapy for her cocaine addiction. As she had had an extended abstinence from cocaine, she expressed an interest in cigarette smoking cessation. Jill explained that she did not know if she "really" wanted to quit. The therapist engaged the patient in the A-D analysis as follows (the matrix they completed is presented in Figure 9.1: TH: You say you're not sure whether you really want to quit. PT: Yes, that's right. TH: OK, let's look at the potential advantages and disadvantages of quitting smoking. I will draw a window like this {draws matrix) so that we can keep track of your thoughts. PT: All right. TH: O n the vertical axis we write "advantages" here and "disadvan­ tages" here. O n the horizontal axis we write "quitting" versus "not quitting." PT: OK. 138 COGNTTIVE THERAPY OF SUBSTANCE ABUSE Quitting Smol<ing Not Quitting • breathe easier • continued stress Advantages • smell better relief • live longer • avoid withdrawal • save money • less hassle • withdrawal • self-esteem will symptoms eventually suffer • no way to deal with from not taking Disadvantages stress control and boredom • probably die from • giving up a smol<lng "friend" • still have this dirty, disgusting. nasty habit F I G U R E 9.1. Advantages-disadvantages analysis. TH: N o w what are the advantages of quitting? PT: I will breathe easier. TH: What else? PT: I will smell better. TH: What else? PT: I will live longer. TH: What else? PT: Aren't these enough reasons to quit? TH: They might be, but let's tty to exhaust the possibilities for each cell of the matrix before we stop. PT: OK, then there is the money. TH: You will save money. Any more? PT: I can't think of any. TH: OK. What about the advantages of smoking? PT: I can't think of any right now. TH: You must see advantages of smoking or else you wouldn't be a smoker today. PT: Well, 1 guess I can. Smoking seems to relieve m y stress at times. TH: What else? [This discussion continued until all cells of the A - D analysis were hill.] Techniques of Cognitive Therapy 139 When the A-D analysis is successful, the patient should have a more accurate, objective, balanced view of substance use than previ­ ously held. As stated earlier, those who abuse drags otherwise tend to minimize their drag-related problems and maximize (i.e., roman­ ticize) the benefits of drug use. Identifying and Modifying Drug-Related Beliefs In previous chapters, the cognitive therapy model of substance abuse has been presented. It has been explained that the patient who abuses substances is likely to have such drug-related beliefs as the following: "I work hard. I deserve to party." "Smoking relaxes me." "Drugs make m e more creative." "I have a successful career,

so I can't possibly have a drinking problem." "My life's a mess anyway, so drags couldn't make it worse." "If I stop using, I'll get depressed." Individuals who abuse drugs are typically not attentive to their drag-related beliefs, often viewing their drug use as a function of extrinsic factors. For example, they attribute cigarette smoking to "stress" rather than to their attitudes about smoking. Therefore, it is essential to help patients monitor and identify their beliefs about drags and drag use. In cognitive therapy the drag user is taught about these beliefs as they apply to his or her drag-use patterns. Specifically, the thera­ pist explains and illustrates the "cognitive model of substance abuse" (see Figure 3.5, page 47) to the patient, and together they fill in each box of the flow chart with examples of basic beliefs, automatic thoughts, feelings, and behaviors that are pertinent to the patient's life. For example, consider the case of "Mack," who reported to his therapist, "I went on a binge on Saturday night." The following dia­ logue ensued. TH: Tell me about your binge. PT: What's there to tell? I just felt pretty good and I decided to drink. TH: Let's look at the cognitive model together. [The therapist took out a printed copy of the cognitive model of substance abuse 140 COGNITIVE THERAPY OF SUBSTANCE ABUSE and showed it to the patient.] So the initial stimulus was inter­ nal; you "felt pretty good." PT: Yeh. TH: In response to feeling good, what was going through your head that contributed to your drinking? PT: I guess I was thinking "Gee, a drink would make m e feel even better." TH: And what automatic thought went through your mind? PT: "What the hell! I might as well." TH: And by that time you were beginning to crave? PT: Big time! When patients are systematically taught to monitor their basic drag-related beliefs and automatic thoughts, and when these cogni­ tive processes are shown to be related to their subsequent drag use, patients tend to report an increased understanding of why they use, and a better sense about how better not to use. D o w n w a r d Arrow Technique It is common for drag-using patients to have cata­ strophic (all-or-none or overgeneralized) thoughts not only about their substance use but about themselves, their life, and their future (the cog­ nitive friad; Beck, 1976). Such tiioughts might include tiie following: "My life is going to cramble." "I'll fall apart if I can't get m y fix." "I can't do anything right." "Nobody gives a damn about me." "I am totally out of control." The downward arrow technique is quite useful for addressing such beliefs as these. Many patients are unable to articulate these underly­ ing beliefs until they have been asked to consider the personal mean­ ing thdt their more manifest thoughts have for them. Therefore, when patients exhibit strong negative emotions that seem to be far more intense than their automatic thoughts alone would cause, therapists can ask patients to probe a bit deeper by asking successive variations of the question "What does that mean to you?" Oftentimes, the end result of the question is the elicitation of an underlying or core belief. The following is an illustration: Techniques of Cognitive Therapy 141 TH: Phil, you seem to be having a vety strong reaction against the idea of ttying to steer clear of drinking alcohol at your upcom­ ing office party. What is your concern about being sober at the party? PT: I wouldn't be any fun at parties if I didn't drink. TH: And if you weren't fun at parties, what would the implica­ tions fee? PT: People wouldn't hang around me. TH: And if people didn't hang around you, what would that mean? PT: It would mean they didn't like me. TH: And assuming that all of the above is trae, what would the con­ sequences be? PT: It might mean that m y career would suffer since I am a sales­ man, and I depend on people liking m e for m e to succeed. TH: And if your career suffered, what would the ultimate conse­ quences be? PT: I could lose m y house and m y family and evetything I've worked for! TH: And all this would happen because you weren't drinking alco­ hol at social events? PT: Well, when you put it that way, I guess it's pretty unlikely. TH: I agree, but do you see how a chain of progressively more prob­ lematic beliefs leads you to assume that catastrophe would result if you followed through with the assignment of being "dty" at the party? PT: Yes, I never realized that before. It does seem like it's do or die, but maybe it isn't. TH: We'll have to stay alert to similar chains of beliefs. For now, let's write down what we've just learned on paper [See Figure 9.2.] The downward arrow technique (so-called because of the way it is illusfrated on paper, with each successive belief pointing an arrow downward to the next underlying belief) is effective because it helps a patient to "decatastrophize" (i.e., to reevaluate and modify cata­ strophic thoughts). In the above example, the downward arrow tech­ nique helped Phil to articulate the catastrophic thought that he would lose his career, family, and house if he stopped drinking. O n doing so, Phil was able to see the distortion in his thinking. As a result, he 142 COGNITIVE THERAPY OF SUBSTANCE ABUSE Automatic Thought = "I can't not drinic at this party!" "I wouldn't be any fun." i "People wouldn't hang around me." •X' "They wouldn't like me." I "My career would suffer." Underlying Beliefs = "I could lose everything." FIGURE 9.2. Downward arrow illustration. was in a better position to modify this thought. In fact, the irony of Phil's catastrophic thinking traly came to light w h e n he did an A-D analysis and determined that he could "lose evetything" if he did not stop drinking. Reattribution of Responsibility Those who use drags will often attribute their use to extrinsic factors. For example, the alcoholic m a y attribute drinking to a bad marriage, a stressful job, and drinking buddies exerting pres­ sure to be "one of the guys." The therapist can help individuals to reattribute responsibility for their drag use to themselves so that they m a y take initiative to modify drag-using behaviors. Reattribution of responsibility requires the skillful application of the Socratic method, so that patients do not feel that their therapists are being judgmental or accusatoty. The following is an example of this process: TH: You say that you've been drinking again. What are your thoughts about w h y this is happening? PT: Well, m y wife has really been hassling m e lately. I might be able to stay sober if she would get off m y back once in a while. TH So you see your wife as causing your drinking? PT: In a way, yes . but it's not that simple. TH OK. Tell m e more about some of the complexities involved here. Exactly what role does your wife play, and what role your beliefs and actions play. PT: She criticizes m e , and I start thinking that I can't get any peace and that I'm trapped. Techniques of Cognitive Therapy 143 TH: And then? PT: And then I think that m y only escape in life is to get bombed and forget about m y miserable marriage. TH: So when you focus on the misety in your marriage, you deter­ mine that there is only one remedy—to drink until you go "blotto." A m I on target? PT: Yes. TH: Would it be fair to say that you decide to drink, rather than choosing some other way of resolving your problems with her? PT: Yes. I guess it's m y decision, but it's easier to blame her. {chuck­ les) TH: It may be easier to blame her, but does that help you to reach your goal of dealing with your problem with alcohol? FT: No. TH: What would help? PT: If I take charge of m y own life and m y own decisions, regard­ less of how pissed off I am at m y wife. TH: Not easy, I admit, but a worthy goal. In this example, the patient's focus shifted from external to inter­ nal factors. Initially, he blamed his wife for his drinking. At the end of this dialogue he had begun to see that he had some responsibility for his drinking. As a result, he may begin to take some responsible actions toward changing his drinking. Daily Thought Record The Daily Thought Record (DTR) is a ftindamental strategy in cognitive therapy, which has been useful in the freatment of depression, anxiety, and other problematic mood states (Beck et al., 1979; Burns, 1980). The standard DTR is a five-column form that is completed by the patient (see Figure 9.3). Those who abuse substances tend to do so as a result of their beliefs (often maladaptive) about drags. For example, the alcohol abuser, prior to going to the corner tavern, may have the belief "I need a drink." By using the DTR, the patient is able to examine this belief and consider its validity in a more systematic, objective fash­ ion. In addition, the DTR provides a time lag after the initial urge during which the patient may choose not to drink (or use other drags), and may experience a natural diminution of the craving. Addition- 144 COGNITIVE THERAPY OF SUBSTANCE ABUSE ally, the DTR provides a method for coping with negative mood stat so that they are not as likely to trigger drag use. Consider the case of Mack, who reported that he was most tempted to drink when alone on weekends. For homework his thera­ pist asked him to complete a DTR based on the experience of being alone on a Saturday night (see Figure 9.3). Mack initially described himself as being lonely and angty as a result of not having a date. He rated these emotions as quite high: 80 and 75, respectively. These feelings were based on his beliefs: "No one cares about me" and "It's unbearable to be alone." Using the DTR as a guide. Mack's therapist helped him to consider alternative rational responses, such as "My friends and family care about me" and "I CAN bear to be alone." As a result of doing so. Mack reported feeling sufficient relief that he held off on having a drink. This result boosted his sense of self-efficacy markedly. A useful method for teaching patients to generate objective rational responses involves the application of a series of open-ended questions (see the bottom of Figure 9.3). These questions include the following: 1. What concrete, factual evidence supports or refutes my auto­ matic thoughts and beliefs? 2. Are there other ways I could view this situation? Is there a blessing in disguise here? 3. What is the worst thing that could happen? What is the best thing? What is most likely to realistically happen? 4. What constractive action can I take to deal with the situation? 5. What are the pros and cons of m y changing the way I view this situation? 6. What helpful advice would I give m y best friend if he/she were in this situation? Any or all of these questions can help stimulate patients to think of rational responses. W e have found that the regular application of these questions makes for an excellent ongoing homework assignment and helps patients learn to use DTRs to their maximum benefit. Imagery Imagety techniques can be used with dmg users to help them visualize "self-control" and avoid drag use. Imagety can be a useful technique for focusing patients on drag-related beliefs and automatic thoughts, or distracting them from their cravings and urges. Directions: W h e n you notice your mood getting worse, ask yourself, "What's going through m y mind right now?" and as soon as possible jot down the thought or mental image in the Automatic Thought column. SITUATION AUTOMATIC THOUGHT(S) EMOTION(S) RATIONAL RESPONSE O U T C O M E Describe: 1. Write automatic thought(s) 1. Specify

sad, 1. Write rational response 1. Re-rate belief 1. Actual event leading to preceded emotion(s) anxious/angry automatic thought(s) in automatic unpleasant emotion, or 2. Rate tielief in automatic etc. 2. Rate belief in rational thought(s) 2. Stream of thoughts, 0-100%. 2. Rate degree 0-100%. 0-100%. daydreams or recollection, of emotion 2. Specify and leading to unpleasant 0-100% rate subsequent DATE/ emotion, or emotions TIME 3. Distressing physical 0-100% sensations 4x Questions to help formulate the rational response: (1) What is the evidence that the automatic thought is true? Not true? (2) Is there an alternative explanation? (3) What's the worst that could happen?Could I live through it? What's the best that could happen? What's the most realistic outcome? (4) What should I do about it? (5) What's the effect of my believing the automatic thought? What couW be the effect of changing my thinking? (6) If was in this situation and had this thought, what would I tell him/her? (friend's name) F I G U R E 9.3. Daily T h o u g h t Record (blank). 146 COGNITIVE THERAPY OF SUBSTANCE ABUSE It can also serve as a method for changing drag-related beliefs an thoughts. Examples of imagety used in this fashion include imagin­ ing assertive, direct methods for "saying no" to others who offer drags; imagining positive, enjoyable activities as alternatives to drag use; and imagining a healthy, productive life as a result of freedom from drags. The following example demonstrates the use of imagety in smoking cessation. PT: I don't know how I'll survive without my first cigarette of th TH: What are your thoughts just before you smoke that cigarette? PT: I usually don't think. I just go to m y pack, take one out, and light up. TH: Perhaps your thoughts are so automatic that you don't pay at­ tention to them. I'd like to help you recall thoughts that lead to smoking that first cigarette of the day. Close your eyes for a moment and imagine what happens when you first wake up in the morning. What do you see? Smell? Hear? H o w do you feel? Now, what thoughts are going through your mind? What are you telling yourself? PT: Well, first I'm just kind of groggy. When m y mind starts to clear, I lie in bed thinking about what I have to do that day. I feel myself getting a little nervous and I think "Oh just relax. Go to the kitchen for a cup of coffee and a cigarette." TH: What happens next? PT: Well, to be honest, I usually go the bathroom first, but after that, I go to the kitchen and have a cigarette and coffee. TH: As you head to the kitchen can you recall what you are think­ ing? PT: Sure! I am thinking about the lift I'll soon get from the ciga­ rettes and coffee. TH: So you think "I'm going to get a lift from that first cigarette. Quick, go smoke!" What do you feel with that image and what happens next? PT: I feel an urge to smoke and 1 indulge myself. TH: OK, let's tty something. The images of smoking and drinking coffee are quite positive. Can you replace these with an alterna­ tive image of what could happen in the morning? PT: 1 guess so. Last time I quit smoking I would wake up and go jogging. TH: What were your thoughts prior to going jogging? Techniques of Cognitive Therapy 147 PT: They were sort of tike the smoking thoughts, but instead I thought that the run would give m e a lift. TH: OK, let's tty to imagine jogging in the morning. What do you see? Smell? Hear? Feel? Make it as attractive and tempting as possible. PT: I see the soft light of the morning sun as it shines on the trees, the house, and the landscape. The morning air smells fresh and clean. I hear lots of birds chirping because it's early morning. 1 feel healthy and alive. TH: What happens when you produce that new image? PT: 1 lose some of m y interest in the cigarette. TH: Great! So now you have an alternative image to the smoking image when you wake up in the morning. Can you tty to vol­ untarily "call up" this image to your awareness in the morn­ ing? PT: I'll fry. TH: Let's also make sure your family physician agrees that it is safe for you to take up a regimen of jogging again before you start, OK? BEHAVIORAL TECHNIQUES Activity Monitoring and Scheduling Patients who abuse drags tend to engage in activities and behaviors that support their drag abuse and may concurrently fail to take part in activities that promote prosocial life goals, such as work, hobbies, community service, and stable relationships. Activity monitoring and scheduling can be useful basic strategies for under­ standing and modifying drug-related behaviors and for increasing productive behaviors. The process of activity monitoring and scheduling is simple and straightforward. The patient receives a blank grid (the Daily Activity Schedule) which contains the 7 days of the week divided into 1-hour blocks (see Figure 9.4). For a period of 1 week the patient records daily activities and the degree to which he or she felt a sense of pleasure or mastety from participating in each activity. Pleasure and mastety, recorded on a scale from zero (none) to ten (extreme), provide an indication of the patient's mood and the level of reward or satisfac­ tion derived from each activity. The Daily Activity Schedule can be used for at least three pur- NOTE: Grade Activities M for Mastery and P for Pleasure 0-10 M T W Th F S Su 6-7 7-8 8-9 9-10 10-11 11-12 12-1 1-2 2-3 3-4 00 4-5 5-6 6-7 7-8 8-9 9-10 10-11 11-12 12-6 REIVIARKS: FIGURE 9.4. Daily Activity Schedule (blank). Techniques of Cognitive Therapy 149 poses. First, it serves as a journal of present activities. By revi completed schedule, therapist and patient gain a baseline understand­ ing of the patient's activities and how they relate to drag use. Sec­ ond, the Daily Activity Schedule can serve as a prospective guide for future activities. That is, patient and therapist can use a blank form to schedule alternative activities that are less conducive to drug use. Furthermore, to the degree that the patient lacks satisfaction and a sense of accomplishment in life, the therapist may choose to exam­ ine the patient's core beliefs about his or her lovability and adequacy, respectively. And finally, the Daily Activity Schedule can be used to evaluate the extent to which the patient has been following his or her proposed schedule successfully. That is, after a weekly plan has been completed, patients may take home a blank form to monitor actual behaviors. Frequently, a failure to follow through with planned activities comes about as a result of drag-related behaviors, along with their concomitant beliefs, such as "I can't do anything right" or "I never reach m y goals." W h e n this happens, therapists must remain upbeat, helping patients to see that useful information has been obtained, and that goals can still be achieved in spite of early setbacks. When patients succeed in planning and completing nondrug activities that give them satisfaction and build their self-efficacy, they begin to view themselves as less helpless, less out of control, and less dependent on chemical "fixes." Behavioral Experiments Behavioral experiments are used to test the validity of patients' drag-related beliefs and core beliefs. For example, con­ sider the patient who believes "I would lose all m y friends if I didn't smoke pot." A behavioral experiment might involve having this patient participate in "usual activities" with friends, without using marijuana. (The patient would be encouraged to fully participate in all non-drag- related activities.) Thus, the "independent variable" in this behavioral experiment would be the patient's use of marijuana. The "dependent variable" would be maintenance of friendships. The patient would be encouraged to avoid any "extraneous variance" by maintaining con­ sistency in all other aspects of his or her behavior. Regardless of the results of this experiment, the patient is likely to learn some impor­ tant lessons. Specifically, if he loses friends, he will be encouraged by the therapist to examine the meaning of his pre-abstinence friend­ ships. If he maintains his friendships, he will, it is hoped, modify his original distorted belief: "I will lose all m y friends if I don't smoke marijuana." 150 COGNTTIVE THERAPY OF SUBSTANCE ABUSE Another form of behavioral experimentation is the "as if" tech­ nique. Using this technique, the therapist encourages the patient to act as if a desired behavior or set of circumstances were trae for him. For example, the patient who wishes to quit smoking might spend a week acting "as if" he were a nonsmoker. For example, he might ask others not to smoke around him, he might exercise, or he might sit in the nonsmoking sections of restaurants. Such activities are designed to modify the patient's drag-related beliefs as well as behaviors. Behavioral Rehearsal (Role Play and Reverse Role Play) Many patients with substance abuse problems have concurrent problems with interpersonal communication (e.g., assertiveness, self-disclosure, and active listening) (Piatt & Hermalin, 1989). As a result, they often feel frastrated and overwhelmed in inter­ personal situations, resulting in a vulnerability to drag use. Hence, the therapist may initiate role-playing to teach the patient effective interpersonal skills. The following is an example: PT: I feel like getting wasted evety time my wife nags me. TH: What do you mean when you say she "nags" you? PT: I mean when she asks me to do more than m y share of the work. TH: What do you do when you think she's nagging? PT: Well, typically I go to another room or I just leave. That's when I'm most likely to drink. TH: So you withdraw. PT Yeh. TH How else could you handle the situation? PT I have no idea. TH OK, let's tty some different options. I will play the role of your wife, and I would like you to discuss your feelings with me as honestiy as possible, without attacking or being aggressive. PT: I don't understand. What should I do? TH: Simply pretend that I am your wife and practice talking to me in a constractive fashion about m y nagging. PT: OK, who starts? TH: 1 will, {acting as patient's wife, sounding annoyed at patient) I want you to take care of the yard this weekend. It's been three weeks since you promised to plant grass and soon it will be too late to even tty. I'm sick and tired of waiting for you to do things Techniques of Cognitive Therapy 151 around here! {silence; patient looks puzzled) [The therapist momentarily stopped role play to encourage patient.] N o w you respond to m e as your wife. PT: Man, that sounded too much like her! TH: OK, now talk to m e as you would to her. PT: {Another pause, then role play continues) Maty, I'm pretty sick of you nagging me! TH: It's the only way anything gets done around here! PT: I do a lot around here! {in raised voice) You're so busy complain­ ing that you never notice! TH: [Again, role play stopped. Therapist talked to patient.] Now, let's look at what has happened. What are your thoughts about this role play? It became apparent that this patient lacked effective conflict reso lution skills. Thus, the therapist must begin by teaching the behav­ ioral skills of active listening, assertiveness (vs. aggressiveness), and compromise. The teaching process involves some didactic training, along with frequent role-playing, to learn and practice more effective interpersonal behaviors. One way to gain a reluctant patient's active participation in role playing is to volunteer to take the patient's role while the patient portrays the "problematic other" (e.g., an employer, a spouse, or an old drag associate who is ttying to convince the patient to get high). In this manner, the patient can show the therapist just how difficult the situation is to manage, while the therapist can model some responses that the patient might not have thought of before. A more demanding variation of this procedure

has been described by Moorey (1989), who suggests that drag abusers can learn to empa­ thize with important people in their lives by role-playing the part of a significant other who has been hurt by the patients' drag use. This exercise also serves to highlight the destruction that the drag abuse has wrought on the patients' personal lives. On the plus side, repeated role playing helps patients develop new, mature, effective repertoires of social behavior in a safe envi­ ronment where errors can be corrected without actual consequences. Relaxation Training There is often a component of anxiety to drag use (see Chapter 15, this volume). For example, cigarette smokers and heavy alcohol users often report that they smoke or drink to relax. Hence, drag use may be a form of self-medication for people who have dif- 152 COGNTTIVE THERAPY OF SUBSTANCE ABUSE ficulty relaxing (Castaneda et al., 1989; Khantzian, 1985). Even co users, who consume cocaine for its stimulating effects, may feel anx­ ious or tense in anticipation of using, especially if there is some delay between the time they crave and when they actually use. Thus, relaxation training may be a useful technique in that it provides the patient with a safe (drag-free) method of relaxing. Sec­ ond, it provides the patient with a time lag after the initial craving experience, during which the craving may subside (Carroll, Roun­ saville, & Keller, 1991; Horvath, 1988). Ultimately, relaxation train­ ing may be useful in building the patient's new belief that he or she is in control of and responsible for his or her coping responses (see Chapter 15, this volume, for additional information). Graded Task Assignments Quite often patients must make dramatic behavioral changes in order to facilitate a drag-free (or drag-reduced) life. For example, the patient whose only friends are other crack users will have to restracture his or her social life almost entirely in order to mini­ mize the chances of relapse. C o m m o n sense and experience tell us that this is no easy task. Hence, the patient is encouraged to engage in approximations of the desired behaviors in order to build toward the end goals. For example, the patient who needs to modify her friendships might be encouraged to begin by spending drag-free time with a non-drag-using acquaintance (e.g., a new friend from a sup­ port group meeting), such as going to lunch or to a movie. On suc­ cessful completion of this exercise, the patient would choose another (more challenging) assignment until he or she had built up a new drug-free network of cohorts. Problem Solving Drag users who frequently demonstrate impulsivity often are vety poor problem solvers. In fact, in advanced stages of drag abuse, many patients either ignore their problems (denial, avoid­ ance) and/or respond to their problems by anesthetizing themselves with drags. For those patients with a long histoty of drag use, it is strikingly apparent that they have precious littie accumulated experi­ ence in recognizing and solving life's problems constractively. For example, one of our drag-abusing patients was troubled by her husband's ongoing drag abuse. One day she found a stash of his crack cocaine. Rather than confront him with this finding, or flush the drags down the toilet, she smoked evety cap until the stash was Techniques of Cognitive Therapy 153 used up. When she reported this to her therapist, he shook his head in disbelief and asked her what her rationale was for such a self- defeating act. She replied, "I didn't want him to use, so I figured if I smoked it all, he wouldn't be able to use." The therapist noted that this was an example of a "permission-giving" belief, and that it reflected a failure to think the problem through carefully (to say the least). Another patient reported a scheduling conflict between his therapy sessions and his job. His immediate response was to quit the job, rather than wait a week to work out a new schedule with the therapist. The upshot of these illustrations is that drag-abusing patients must be taught the principles of problem-solving (Nezu, Nezu, & Perri, 1989). The steps of problem solving include the following: 1. Defining the problem in clear specific terms 2. Brainstorming a number of possible solutions 3. Examining the pros and cons of each brainstormed solution (for the present, for the future, and for significant others as well) 4. Choosing the best hypothesized solution 5. Implementing the behavior after some planning, preparation, and practice 6. Evaluating the outcome and assessing for more problems to solve This is a long, gradual process that is fraught with frustration along the way. Therapists must remain supportive, patient, and encouraging if patients are to persevere in learning these skills. Exercise Most substance abuse is incompatible with physical health and sustained exercise. For example, cigarette smoking and regular aerobic exercise (e.g., jogging) would seem to be incongra- ous. Hence, regular aerobic activity is likely to heighten a person's awareness of the disadvantages of substance use and the advantages of quitting. The therapist may encourage the patient to engage in physical exercise as part of the treatment program (of course, only with a physician's medical approval). Such activity may help the patient to redefine him- or herself as a healthy, physically fit person. This image should cause cognitive dissonance for the patient and may motivate him or her to modify the pattern of substance abuse. [A notable exception to the above involves athletes who abuse 154 COGNFTTVE THERAPY OF SUBSTANCE ABUSE anabolic steroids, thinking that it is very much compatible with a letic achievement. In such cases, therapists would not want to focus on exercise as an intervention. Instead, anger control, interpersonal conflict resolution, and focusing on the unappealing side effects of steroids (e.g., balding, acne, reduced sexual responsivity, and myriad serious medical consequences) should be the central focus.] Stimulus Control At first glance it would seem that an effective strat­ egy for reducing substance abuse would be to eliminate all stimuli that trigger drag use. However, it quickly becomes apparent that doing so is not practically possible: all people will have episodes of feeling sad, lonely, anxious, bored, frastrated, and other internal sources of high risk. Ex-smokers inevitably find themselves in places where others are smoking, alcohol-dependent individuals eventually face enticing advertisements, and many users of illicit drags have to come in contact with relatives who abuse such drags. In order to minimize contact with drug triggers, patients are encouraged to identify those stimuli (internal and external) that put them at high risk for the activation of drag-related beliefs that trig­ ger drag use (Carroll, Rounsaville, & Keller, 1991). For example, some people are vulnerable to negative moods (boredom, anxiety, sadness, etc.) while others are vulnerable to positive moods (joy, happiness, excitement, etc.). Still others are vulnerable to extrinsic cues (meals, other users, time of day, geographic location, etc.). Patients are encouraged to plan ways to avoid these cues whenever possible. How­ ever, more importantly, patients are encouraged to prepare methods for dealing with these cues when the cues are encountered (see Chap­ ter 10, this volume). C O M M O N OBSTACLES IN TREATMENT When a patient does not appear to be responding favorably to cognitive therapy, it is possible that there is a problem in the therapeutic relationship. The patient who does not trast the therapist or feel comfortable in therapy is likely to be guarded in sessions; therefore, he or she might avoid important self-disclosures for fear of judgment or retribution. Without these admissions it is unlikely that the patient will objectively examine or acknowledge biased thinking patterns. Such examination is central to the success Techniques of Cognitive Therapy 155 of cognitive therapy, and can be fostered via an accepting, warm, collaborative therapeutic approach. When the therapeutic relationship is judged to be sound, but the techniques appear to be ineffective, it is important to review the case conceptualization for missed diagnoses, overlooked beliefs, and impor­ tant unassessed historical events. For example, many substance-abus­ ing patients have a coexisting personality disorder (borderline, anti­ social, avoidant personality disorders, etc.). These patients require careful attention simultaneously to their chronic maladaptive person­ ality (i.e., belief) patterns and to their substance abuse problems. Patients may also have problems with anxiety and depression, and they may be attempting to treat these problems with psychoactive sub­ stances (i.e., to self-medicate). Therapists must keep in mind that such a patient's "resistance" to treatment simply may reflect an unspoken fear that without drags his or her anxieties or dysphoria will become overwhelming. Also, taking an updated review of the patient's his­ toty can stimulate a breakthrough in treatment. For example, one therapist did not realize until many months into treatment that his patient had gone through humiliating failure experiences in grade school and that memories of this had led the patient to resist any­ thing called "homework," for fear that it would make him look stu­ pid. Once this was understood, the therapist was able to help the patient to generate rational responses to combat these negative expec­ tations and fears. The topic of homework is important enough to merit its own separate discussion. Patient nonparticipation in homework assign­ ments can hinder the therapeutic learning process. It is tempting in any medical or psychological intervention to simply tell the patient to "go home and do. ." However, for homework to be maximally effective it should have certain qualities. First, it should be collabo­ ratively determined. Second, the therapist should check for the patient's understanding of the exact nature of the assignment, as well as the patient's understanding of the underlying rationale for the assignment. Third, the therapist and patient should consider any potential barriers to completing homework assignments and prepare contingency plans. Finally, the patient should have an opportunity to practice the homework with the therapist in order to test his or her understanding of and ability to do the assignment. A final problem in applying the techniques of cognitive therapy to substance abuse might be in the therapist's therapeutic style. It is essential that the therapist stimulate the patient's thinking process with sensitively worded open-ended questions, rather than by lectur- 156 COGNTTIVE THERAPY OF SUBSTANCE ABUSE ing or preaching to the patient. When the cognitive therapy techni described here are presented in a dictatorial fashion, the therapist's words are likely to "go in one ear and out the other." Generous appli­ cation of the Socratic method often is an antidote to this problem. SUMMARY In this chapter, we presented many of the most widely used techniques of the cognitive therapy of substance abuse. Most of the techniques that have been successfully applied in the treatment of other psychiatric syndromes are useful in the freatment of substance abuse. It is important that these techniques be applied with careful attention paid to the therapeutic relationship, the patient's individual case conceptualization, the patient's application of these techniques in the form of homework assignments, and the therapist's use of open- ended questioning. The techniques that we described do not represent an exhaus­ tive list. In fact, we encourage therapists to make use of their creativ- ify and their patients' unique individual needs and strengths to devise new variations of cognitive therapy techniques and assignments. As long as the technique serves a logical purpose, fits within the case conceptualization, adheres to ethical guidelines, and focuses on changes in beliefs as well as drag-related behaviors per se, there is no limit to what may be applied successfully. C H A P T E R 1 0 D e a l i n g w / i t h C r a v i n g / U r g e s B 'ecause of their resurgence during and after treat­ ment, uncontrolled cravings and urges to use are major factors con- ttibuting to treatment dropout and often lead to relapse even after long periods of abstinence. Teaching patients to cope with craving is therefore one of the most important goals of treatment (Annis, 1986; Carroll, Rounsaville, & Keller, 1991; Childress et al., 1990; Covi et al., 1990; Horvath, 1988, in press; Shulman, 1989; Tiffany, 1990; Washton, 1988). The therapist initially assesses the patient's idiosyncratic per­ ception of craving. Then, over the course of treatment, the therapist helps the

patient to understand the various factors that contribute to craving, to reframe the experience, and to develop better ways to deal with this problem. Horvath (1988) has distinguished the phenomenon of cravings from urges, describing the former as the subjective sense (e.g., physi­ cal arousal, emotional arousal, "need," and "desire") of wishing to attain the psychological state induced by drags. In contrast, urges are described as the behavioral impulse to seek and use the drugs. Although these are useful theoretical distinctions, in practice we have used the terms "cravings" and "urges" interchangeably, as we will in the remainder of this chapter. TYPES OF CRAVING We have identified four major types of craving, each with its own unique characteristics (although there is some overlap from one type to another). 157 158 COGNTTIVE THERAPY OF SUBSTANCE ABUSE 1. Response to withdrawal symptoms. Heavy users of drags such as cocaine and heroin often come to experience a diminishing sense of gratification from the use of the drag, but an increasing sense of inter­ nal discomfort on cessation of the use of the drag. In such cases, the craving takes on the form of a "need to feel well again." This is espe­ cially trae for the heroin user who experiences severe, flu-like symp­ toms during withdrawal, and the cocaine user who becomes deeply depressed during a "crash." Therapists who treat patients who are going through this type of craving will need to be empathic to the patients' acute sense of pain and suffering as a result of abstinence. It is most important to inform such patients that this discomfort is tem- poraty (although in extreme cases medical supervision may be nec­ essaty). 2. Response to lack of pleasure. Another type of craving involves patients' attempts to improve their moods in the quickest and most extreme way possible. This phenomenon is most likely to occur when patients are bored, are unskilled in finding prosocial means of enjoy­ ment, and wish to "self-medicate" (Castaneda et al., 1989; Khantzian, 1988) in order to blot out unpleasant thoughts or feelings. Here, thera­ pists must be aware that the therapy sessions themselves may be suf­ ficiently upsetting to patients that they may experience a craving for drags in order to forget their froubles. Therefore, therapists are advised to assess their patients' moods and degrees of craving at the end of particularly stressful (i.e., productive and meaningful) sessions. 3. "Conditioned" response to drug cues. This type of craving requires no particular dysphoric mood, stressor, or hedonic urge on the part of the patient. Patients who have abused drags have learned to asso­ ciate many otherwise neutral stimuli (a particular sfreet comer, a given person, a telephone number, a certain time of day, etc.) with the acute gratification obtained from the use of drags. These neufral stimuli therefore become "charged" with meaning and can induce automatic cravings even in the absence of stressors. Therapists must help their patients to become aware of, and cope with, the cravings that arise simply as a result of their association with these evetyday stimuli. 4. Response to hedonic desires. Patients sometimes experience the onset of drag cravings when they wish to enhance a positive experi­ ence. For example, some patients have made a habit of combining drags and sex as a way to magnify the sexual experience. Others, for example, seek drags as a way to make their social interactions more "enjoyable and spontaneous." Unfortunately, the high that is achieved by such practices is difficult to match (in the short term) in a drug- free life. Therefore, these are particularly difficult types of cravings to combat in therapy. Therapists have the most leverage when patients' Craving/Urges 159 drag use has progressed to such a degree that their life problems overwhelmed their isolated moments of drag-induced hedonic joy. Under these conditions, patients typically are more willing to work to find other means of achieving gratification in life. Still, there will be an ongoing battle with these cravings whenever the patient expe­ riences a natural good mood. CRAVINGS: UNDERSTANDING THE PATIENT'S EXPERIENCE A therapist can begin to understand the patient's crav­ ing experience first by identifying automatic thoughts (ATs) associ­ ated with the experience. Cravings can be triggered in the therapist's office by having patients simply describe the last time they used drags. Induced imagety is a more powerful method for evoking these crav­ ings. As a word of caution, it is important that the patient understand the rationale for this induction, namely, to learn to identify and cope with cravings and cues to craving. Also, therapists must be prepared to help reduce the strong feelings of craving prior to the end of a session (Childress et al., 1990). If not, patients may leave the therapy session highly aroused and without the skills necessaty to cope with their cravings. Thus, a lapse may ensue. Craving induction techniques should not be implemented until after patients have had practice with general cognitive therapy skills and coping techniques (see Chapter 9, this volume). In a typical craving induction, patients are asked to imagine the last time they used cocaine, and then to describe the image. They are instracted to give as much detail as possible. The aim is to have patients relive the experience as vividly as possible, and therefore gain access to the "hot" cognitions that accompany the craving. A typical way to introduce a craving experience is the following: "Jim, today I want to tty to understand your experience of craving so that I can help you to develop better strategies for coping. Therefore, I'm going to ask you to do a short exercise with me." "I want you to think back to the last time that you used cocaine [or another drag relevant to the patient's problem]. [Wait a minute or two for the patient to get into the image.] N o w I want you to think about the events that led up to your using. I would like you to tty to picture it in your mind, describe the setting, tell m e the sequence of events, and relate what you are feeling. As soon as you notice that you are beginning to have a craving, please indicate this by lifting your hand." {Patient indicates he's having an image) "Describe what 160 COGNITIVE THERAPY OF SUBSTANCE ABUSE you are feeling and what thoughts are going through your mind just now." Therapists should ask patients to compare how similar the crav­ ings experienced in the office are to those they experienced outside. In addition, patients can be asked to come up with their own meth­ ods to help induce the craving. For example, some cocaine abusers report that one of the strongest cues for craving is remembering a particular sex partner that they had while using cocaine. The thought of that person and the image of having sex serve as powerful cues for eliciting strong desires to use cocaine. COPING WITH CRAVINGS Patients can be helped to reduce the aroused cravings by a number of techniques, including (1) distraction, (2) flashcards, (3) imagety, (4) rational responding to urge-related automatic thoughts, (5) activity scheduling, and (6) relaxation training. These techniques should be demonsfrated and taught early in treatment. To develop a durable sfrategy for handling cravings, of course, patients must also learn to deal with the dysfunctional beliefs that facilitate using. Distraction Techniques The key goal of distraction techniques is to get patients to change their focus of attention from internal (e.g., auto­ matic thoughts, memories, physical sensations) to external. Although some of these techniques seem quite simple, they do help to dimin­ ish strong cravings. The following are brief descriptions of commonly used distrac­ tion techniques: 1. Instruct patients to concentrate their attention on describing their surroundings, such as cars, people, trees, and storefronts. Ini­ tially, patients can practice in the office. The more that they can focus and give details about these external events, the more likely they are to focus less on the internal cravings. 2. Use talking to disfract. This can involve starting a conversation with a friend, a relative, a support group sponsor, or the therapist. 3. Patients can remove themselves from the cue-laden environ­ ment. They can take a brisk walk, visit a friend, or go for a drive. One of our patients found the public libraty an excellent place to escape in order to reduce cravings. Craving/Urges 161 4. Perform household chores as a positive distraction. If patients are at home and they notice these cravings and urges, something as simple as beginning to clean the house can distract them from the craving. In addition, this goal-directed activity also helps increase their self-esteem because they have accomplished something useful. (As a caveat, this activity may be ill-advised if drags and paraphernalia are scattered in hiding places throughout the house.) 5. Encourage patients to recite a favorite poem or prayer. For some patients, it is more helpful actually to write down the poem or prayer on a piece of paper. 6. Suggest that patients spend time involved in games, such as cards, video games, board games, and puzzles. These activities can be quite challenging and therefore require focused concentration. Fur­ ther, patients can do some of these activities even if they are alone. Flashcards W h e n cravings are strong, patients seem to lose the ability to reason objectively. Generating coping statements can be helpful in getting patients through this critical period. The usefulness of coping statements can be enhanced by asking patients to write these statements on flashcards (e.g., 3" x 5" index cards). Some examples include a flashcard with the list of advantages for not using drags and a list of things that could be bought with the money intended for cocaine. The following are examples of statements that one patient wrote on his flashcards: 1. You feel more sane when you don't use. 2. Things are going great with m y wife; keep it that way! 3. You look good physically; keep it that way! 4. Get the hell out of this situation nowl Imagery Techniques These techniques include (1) image refocusing, (2) negative image replacement, (3) positive image replacement, (4) image rehearsal, and (5) image mastety. Refocusing is essentially a disfraction technique. Patients direct their attention away from internal cravings by imagining external events. Refocusing can begin first by saying "Stop!" In order to accen- hiate this thought-stopping technique, patients may interject a visual image of a stop sign, a police officer, or a brick wall, to name a few. 162 COGNITIVE THERAPY OF SUBSTANCE ABUSE They then begin to describe to themselves what they see going on around them. For example, one patient was at a picnic where many people were drinking and having a good time. He began to have spontaneous memories of the last time he used cocaine, which led to a desire to use in the present. He said "Stop" to himself, pictured a stop sign, and then began focusing his attention on the people around him who were not drinking. He identified them by name, what they were wear­ ing, and what they were doing. In doing so, he was able to focus his attention away from the cocaine memories and he experienced sub­ sequent reduction in the craving. Another imagety technique is negative image replacement. Often­ times during the first few weeks of abstinence, patients report pictur­ ing themselves using, sometimes even having dreams about using. In these images they see the use of drags as a method for coping with their current distress, and the image takes on a positive glow. In response, it is helpful for patients to substitute a negative image regard­ ing the many unfortunate consequences of taking the drug, such as feeling helpless and hopeless (especially after a period of abstinence) or losing money, jobs, and relationships. For example, one patient, while at a nightclub, became quite angty that he could no longer drink alcohol. He saw other people around him drinking and this brought back nostalgic memories of some of his drag and alcohol days. In response, he replaced the image with one pertaining to the unpleas­ ant physical experiences that he would have when he crashed the day after using alcohol and cocaine. This image was strong enough to dissuade

him from taking the first drink. Positive image replacement is a related technique to help cope with cravings and urges. For example, one patient experienced vety strong negative images about his current situation, that almost his entire family was Strang out on drags. His father was about to lose the house where the patient was living. Consequently, the patient had images of losing his children, having to put them in a foster home, and having to live in a shelter. At that moment, in his sense of hope­ lessness, the patient began to have thoughts of giving up his absti­ nence from cocaine. However, he instead referred to a flashcard that described a positive scene. He imagined himself being back at work again, being in his own home, and able to take care of his chil­ dren. Also, a concomitant of this positive image was the self-satisfac­ tion that he would have after a long day of working. This technique diminished his hopelessness somewhat and, along with it, his crav­ ing. Imagety rehearsals should be used to prepare patients when it is Craving/Urges 163 known that they are going to be in cue-laden situations. One patien who had been abstinent from cocaine and alcohol for about one year, planned to go to a formal banquet where alcohol would be served. In the image rehearsal the therapist asked the patient to imagine going to the banquet and saying, "No thanks, I'll have a club soda," when he was offered a drink. The therapist told the patient to repeat the image several times and monitor his thoughts and feelings associated with the imagety rehearsal. The patient initially was quite anxious while doing this, but later developed a sense of mastety or confidence in being able to go to the banquet and still deal with alcohol being served all around him. Some patients fear that while experiencing vety strong cravings and urges to use drags they will not be able to tolerate the negative feelings that they are experiencing without giving in to the urge to use (Horvath, 1988; Washton, 1988). W e have found that it is help­ ful to teach these patients mastety imaging, seeing themselves as a vety strong and powerful person who is overcoming cravings and urges. One patient who was an intravenous cocaine user reported having repeated images of what he described as "the cocaine lady." In this image, he would be have the sensation of strong cravings for cocaine as he would picture a beautiful woman who was going to offer him cocaine. The patient was taught by his therapist to change the image so that he would have more control. A metaphor that was used was that of a director of a play; that is, the cocaine lady was one character in the play and the patient was the director, able to decide what she would look like and how she would act. He subsequently redirected the image so that "the cocaine lady" was a grotesque-looking person who was vety small, while the patient was a heavyweight boxer able to fight off the urges that he was experiencing. Rational Responding to Urge-Related Automatic Thoughts Therapists start by training patients to self-monitor automatic thoughts when they are having unpleasant emotions such as anger, anxiety, sadness, or boredom. Later, the patients are in­ stracted how to assess their automatic thoughts while experiencing cravings and urges. It is helpful to have patients carty a "therapy notepad" and a pen in order to write down these thoughts. Patients are told that anytime they experience strong cravings or unpleasant emotions, they should ask themselves "What thoughts are going through my mind right now?" They are also instructed to note any physiological distress and then 164 COGNTTIVE THERAPY OF SUBSTANCE ABUSE to ask themselves, "What am I feeling?" and "What thoughts are goi through m y mind?" They then write down the answers and bring their notepads to the next therapy sessions. The Daily Thought Record (DTR) is used to help patients exam­ ine negative automatic thoughts and to generate adaptive responses. DTRs can be completed before, during, and after episodes of craving. The use of DTRs can demonstrate to patients that they are not help­ less in the face of their cravings/urges, and a review of old DTRs can serve as a reminder of this key fact. Figure 10.1 depicts "Jim's" DTR. As can be seen under the Situa­ tion column, Jim was sitting at home. He had recently had an acci­ dent at a constraction site, resulting in a broken hand and wrist. Under the heading "situation" he wrote: "Sitting at home, m y hand is bro­ ken, and I can't go to work. There is plenty of money in m y pocket." Also, he started thinking about some of his old drag buddies and the last time that he used cocaine. Jim was also aware of having a strong craving for cocaine. He rated at 9 5 % the amount of boredom and anxiety that he was experiencing—an indication of sfrong negative feel­ ings. Some of the automatic thoughts he identified were "There is nothing to do" and "I can't stand this boredom." In examining their automatic thoughts, patients ask themselves five basic questions (see Chapter 9, this volume). The first question is "What is the evidence for and against m y automatic thoughts?" The second question is "Are there other ways of looking at this situation?" The third question is "If it is trae, what are the realistic consequences?" The fourth question is "What are the drawbacks to m y continuing to dwell on these thoughts?" The final question asks, "What construc­ tive action can I take to solve this problem?" Jim began examining the automatic thought, "There is nothing to do," by asking himself, "What's the evidence against this?" He responded to this question by saying, "Actually, there are plenty of things that I could do; for example, go to a meeting, watch a game, or call m y therapist." Next, he asked himself, "Are there other ways of looking at this? Do 1 really mean there is nothing to do?" His response was, "No, it is not trae that there is nothing to do, but the pain of boredom makes it difficult for m e to see other things that 1 might be able to do." He then asked, "If trae, what are the realistic consequences?" He responded, "Well, if it is trae that there is noth­ ing to do, then the consequences will be that I will feel bored, and, although the boredom is painftil, it's not the end of the world. The consequences are that I will feel bored and even that will go away." Jim's next question was, "If trae, what are the drawbacks to my con­ tinuing to dwell on these thoughts?" He responded, "The disadvan- DAIL Y THOUGHT RECORD Directions: W h e n you notice your mood getting worse, as(< yourself, "T/Vhat's going through m y mind right now" and as soon as possible jot down the thought or mental image in the Automatic Thought Column. SITUATION AUTOMATIC THOUGHT(S) EMOTION(S) RATIONAL RESPONSE OUTCOME Describe: 1 Write automatic thought(s) 1. Specify sad. 1. Write rational response to automatic ttiought(s). 1. Re-rate belief 1. Actual event leading to that preceded emotion(s). anxious/ 2. Rate belief in rational response 0-100%. In automatic unpleasant emotion, or 2. Rate belief in automatic angry, etc. thought(s) 2. Stream of thoughts, day­ thought(s) 0-100% 2. Rate degree 0-100% dreams or recollection. of emotion 2. Specify and leading to unpleasant 0-100%. rate emotion, or subsequent DATE/ 3. Distressing physical emotions TIME sensations 0-100%. sitting at home,my "There is nothing to do" Bored 'Actually, there are plenty of things I 10% hand broken, and I could do; for example, go to a meeting. can't go to work. "I can't stand this Anxious watch a game, or call my therapist." Bored There is money in boredom." (30%) my pocket. (95%) "It is not true that there is nothing to Thinking about some dfoi cublutt ftohre mpaei nt oo sfe eb oroetdhoemr mtahkiensg s itth adti f­ Anxious (20%) old drug buddies and I might be able to do." the last time I used cocaine. "If it is true that there is nothing to do, Start craving for btohreend ,t hae ndc onasletqhuoeungch est hwei lblo rebdeo mt haits pIa ifnefeull . cocaine. it's not the end of the world. The conse­ quences are that I will feel bored and even that will go away." "The disadvantage of continuing to dwell on these thoughts is that I feel helpless, which in tum, leads to the desire for cocaine." "I can go get a newspaper and read the sports page until it's time for a meeting." (90)% Questions to help formulate ttie rational response: (1) What is the evidence ttiat the automatic thought is true? Not true? (2) Is there an alternative explanation? (3) Whafs the worst that could happen? Could I live through it? What's the best that could happen? What's the most realistic outcome? (4) What should I do about it? (5) Whars the effect of my believing ttie automatic thought? What could be the effect of changing my thinking? (6) If (friend's name) was in this situation and had this thought, what would I tell him/her? FIGURE 10.1. Jim's Daily Thought Record. 166 COGNITIVE THERAPY OF SUBSTANCE ABUSE tage is that I feel helpless, which, in turn, leads to the desire cocaine." The patient's last question, "What constractive action can I take?" led to the response, "I can go get a newspaper and read the sports page until it's time for a meeting." Jim's belief in his rational response was 90%. In the last column, we see that Jim has re-rated his belief in the automatic thoughts at 10%. This indicates that the rational response has had a significant impact on modifying Jim's belief in that automatic thought. W e also see that his level of bore­ dom and anxiety has diminished, going from 9 5 % for each to 30% for boredom and 2 0 % for anxiety. This level of diminishment indi­ cates a reduction in the degree of intensity for these emotions, which, in turn, may help to reduce the likelihood of Jim's using cocaine to cope with the boredom and anxiety. In addition, by using a 0-100 rating scale on the standard DTR form (regarding the level of confidence about the thoughts), the patient understands that the automatic thoughts are not necessarily objective realities. Patients can learn to use the rating scale to gauge changes in their perceptions as they apply cognitive and behavioral techniques. The 0-100 rating scale serves therefore as a useful cogni­ tive barometer. Craving is an idiosyncratic experience made up of cognitive, affective, behavioral, and physiological components. Therefore, by identifying its various components patients can be more objective about the craving experience, and thus diminish the subjective in­ tensity. Later, through the use of subsequent DTRs, the therapist was able to help Jim to be more objective about craving. The trigger (e.g., a sense of extreme boredom or anxiety) activated the beliefs, "I can't cope without cocaine" and "The craving makes me do it," represented by the automatic thought, "I can't stand this." His physiological responses, tension, excess sweating, and urge to seek relief represented the sequence of events that Jim originally labeled "craving." The thera­ pist then helped Jim see that interventions could be made, for exam­ ple, becoming aware of the automatic thought and being able to respond rationally to it, thus diminishing the urge to use cocaine. In addition, it is important to help patients to cope with the crav­ ing by teaching them to test their idiosyncratic predictions about the duration and intensity, as well as the patients' mastety, of the crav­ ing phenomenon. This result can be achieved by teaching them to monitor the intensity, frequency, and duration of craving in order to attack their dichotomous or catastrophic view of the craving phenom­ enon (Horvath, 1988, in press; Tiffany, 1990). Examples of such catastrophic predictions are the following: Craving/Urges 167 "If I don't use something right now, I won't be able to face going to work; I'll lose m y job." "Without the drug,

I'll be a nervous wreck all day. Evetyone will think I'm having a breakdown." "I'll never have a normal life again. I'm a slave to the drag. I simply have to have it to get through the day." "If I resist taking the drag now, I'll just need twice as much later to feel normal later. I might even overdose if that hap­ pens." Activity Scheduling Patients who have a long histoty of drag abuse often engage only in activities that center around the use or the procure­ ment of drags. Oftentimes, their entire social network is drag related. When patients are ttying to control their substance use they often find that initially it is beneficial to stay away from the people, places, and things associated with their former lifestyle (O'Brien et al., 1992). As a result, recovering patients may be faced with a great deal of idle time on their hands. The boredom that accompanies this state can spell frouble for patients' abstinence unless new activities are substituted. Activity schedules are helpful in this regard. First, the activity schedule is used to gather baseline data on how patients actually spend their time. Activity schedules can also be used proactively to strac- ture the patients' day in a constructive way. Many drug-abusing patients have forgotten some of the activities they once enjoyed prior to their drag-using days. The scheduling of activities can revive some of these old, enjoyable, prosocial activities, the likes of which may assist the patient in rebuilding a drag-free life (Hall, Havassy, & Was­ serman, 1991). Such activities serve two purposes. Some of them help patients in the short term to deal with the immediate crisis of coping with urges. Other acti'̂ dties on this list are long-term alternatives to patients' previous drag-related behaviors. In general, the purpose of these sub­ stitute activities is to give patients something to do other than the short-lived and deceptively positive experience of using drags. This is not to say that these activities would be equal to the immediate, intense pleasure received from using such drags as cocaine; however, these activities do have many long-term advantages. While it is vital to teach drag-abusing patients to find alterna­ tive, nondrug sources of reinforcement, therapists must bear in mind that this may require a great deal of training and practice. The diffi­ culty lies in the fact that taking drags requires no particular skills. 168 COGNITIVE THERAPY OF SUBSTANCE ABUSE but the alternative nondrag activities may require considerable sk (Stitzer et al., 1984). Therefore, therapists must not take for granted that patients have the know-how to schedule positive activities and must be prepared to deal with patients' low self-confidence, high fras- tration, marked hopelessness, and passive avoidance surrounding this technique. Relaxation Training Another technique that we have also found to be use­ ful is relaxation training (Bernstein & Borkovec, 1973). Relaxation training gives patients a tool that they can use to help cope with such feelings as anxiety and anger, which, for some patients, can be trig­ gers for cravings (see Chapter 15, this volume). When introducing relaxation techniques to patients, it is impor­ tant to offer them a rationale for the use of this intervention. For example, relaxation training is a method for reducing tension that, left unchecked, might trigger cravings. Relaxation training also helps one to develop an improved general sense of well-being, and to lower one's sense of stress in (fey-to-day life. In addition, a relaxed individual is less likely to act in*pulsively and out of a sense of desperation. It is important that patients understand that relaxation is a skill that can be learned like any other skill. The more they practice their relaxation training, the better they will become at evoking a deep state of relaxation. W e recommend that the first relaxation exercise take place in the therapy session, under the therapist's supervision, in order to ensure that the patients are doing it properly. SUMMARY The three main goals of this chapter were: (1) to focus on the importance of dealing with urges and cravings, (2) to understand better the patient's subjective experience, and (3) to describe techniques that can help patients to cope better with urges and cravings. Uncontrolled urges and cravings are a major factor contributing to treatment failure. Therefore, it is imperative to teach patients early in treatment how to monitor and deal with urges and cravings. C H A P T E R 1 1 F o c u s o n B e l i e f s B eliefs are relatively rigid, enduring cognitive stractures that are not easily modified by experience. In cognitive therapy it is generally maintained that beliefs have a profound impact on feelings and behaviors. For example, depressed patients have global, negative views about themselves, the world, and the future that con­ tribute to their feelings of despair, guilt, and sadness (Beck et al., 1979). Negative beliefs also contribute to such depressive behaviors as isola­ tion and withdrawal. In cases of anxiety disorders, patients have nega­ tive, apprehensive beliefs about some future threat that contribute to avoidance, anxiety, and perhaps panic (Beck et al., 1985). There are at least three types of beliefs pertinent to the patients' addiction to drags: anticipatoty, relief-oriented, and facilitative or permissive. As described in Chapters 2 and 3 (this volume), anticipa­ toty beliefs involve some expectation of reward, such as "The party tonight will be great. I can't wait to go get high!" Relief-oriented beliefs are those that assume that using drags will remove an uncom­ fortable state, for example, "I can't stand withdrawal. I need a hit." And finally, facilitative or permissive beliefs are those that consider drag use acceptable, in spite of the potential consequences, for exam­ ple, "Only weak people have problems with drags. It won't happen to me." Permissive beliefs also have much in common with what are more commonly known as "rationalizations." Patients have thoughts that seem to "justify" their drag-using, such as "I have to use cocaine or I won't be able to concentrate on m y work." Such thinking is tanta­ mount to self-deception. The following examples illustrate the addictive beliefs of two individuals who are cocaine-dependent. (These case examples will be used throughout this chapter to illustrate important points.) 169 170 COGNTTIVE THERAPY OF SUBSTANCE ABUSE "Louise" is a 21-year-old unemployed, single parent who has been using cocaine for two years. Most people who encounter Louise can see that she has had a "rough life." W h e n Louise cannot afford to purchase cocaine, she turns to prostitution to acquire money. She holds the following addictive beliefs about cocaine and herself: "I need drags to numb the pain." "I might as well do drags since m y life won't ever improve any­ way." "Getting high is the only thing I look forward to." "I'm tough; I can handle drags." In contrast to Louise, "Bill" is a 39-year-oId successful sales execu­ tive who has been using cocaine for the past 3 years. He "loves to party" with his friends and coworkers. Bill holds the following addic­ tive beliefs: "I work like hell all week. I deserve to get high on the weekends." "I can't keep up the pace without an occasional 'pick-me-up' [cocaine]." "I've never failed at anything, so drags won't hurt me." "I'm basically a pretty decent guy." At first glance. Bill and Louise appear to be quite different from each other. However, as we examine them more closely we see that they each fall prey to anticipatoty, relief-oriented, and permissive beliefs that perpetuate their addictions. In conttast to addictive beliefs, individuals may have control behefs. Conttol beliefs are defined as beliefs that decrease the likelihood of dmg use and abuse. The following are examples of conttol beliefe: "Drags are dangerous to m y well-being." "I am capable of withstanding the urges." "If I tolerate this craving for awhile, it will go away." "If I resist the urges, 1 will feel stronger." "It is in m y best interest to stay drag-free." An addicted person may maintain contradictoty beliefs. For exam­ ple, a drag-dependent person may hold the addictive belief "I love the feeling of being high." Simultaneously, the same person may hold the control belief "This is killing me." As a result of these contradic­ toty beliefs, drag-dependent persons often feel a great deal of ambiva­ lence about their habit. They may find themselves, for example, awak­ ening in the morning and "swearing off" drugs. By noon they may Belief 171 be seeking treatment for their addiction, although by evening they may be using again. (Confradictoty beliefs are also common, of course, among people who have tried to diet or quit smoking.) When addictive beliefs are more salient than control beliefs, a drug-dependent person is more likely to use drugs. Of course, the opposite is trae: when a person's control beliefs predominate over addictive beliefs, that person is more likely to abstain from drags. An ideal goal for the cognitive therapist is to identify and eliminate the patient's addictive beliefs, replacing them with more adaptive con­ trol beliefs. More realistically, the goal of cognitive therapy is to facilitate a process whereby the patient's control beliefs become more salient than his or her addictive beliefs. The result, of course, will be that the patient abstains from, or at least diminishes, drag use. The following is a list of specific methods to address the drug-abusing patients' problematic belief systems: 1. Assess beliefs. 2. Orient the patient to the cognitive therapy model. 3. Examine and test addictive beliefs. 4. Develop control beliefs. 5. Practice activation of control beliefs. 6. Assign homework that addresses beliefs. In the remainder of this chapter, these methods are described in detail. ASSESS BELIEFS In order to modify addictive beliefs, the cognitive therapist must first have an accurate understanding of the role of these beliefs in the patient's life. Thus, a careful assessment must take place for each patient. This assessment may be accomplished in two ways: through therapist^atient interaction during psychotherapy sessions and standardized questionnaires. The following open-ended questions are examples of those use­ ful for eliciting information about patients' beliefs: "What are your thoughts about ?" "What was going on in your head when happened?" "How do you explain ?" "How do you interpret ?" "What does mean to you?" 172 COGNITIVE THERAPY OF SUBSTANCE ABUSE "What's your 'rale of thumb' here?" "How did you size up the situation?" As the patient responds to these questions, the therapist verbally reflects what the patient has said, with particular emphasis on the beliefs expressed by the patient. At various points in the interview, the therapist provides "capsule summaries" of what has been dis­ cussed, with strong emphasis placed on the patient's thoughts. To illustrate this process we present the following dialogue between a patient and her therapist, taken from their first session. Louise was referred for therapy by a primaty care physician who treated her at a county health clinic for gonorrhea. TH: Hello, Louise. What would you like to talk about today? PT: I don't really even know. I was sent here by that doctor at the clinic. I figured I had to be here. TH: You must have some concerns . some things that are bother­ ing you. PT: Yeh, I guess. But I don't know what good it will do to talk to you. TH You doubt that this will be helpful. PT Yeh, that's right. TH What other thoughts do you have about being here? PT Well I've been in treatment before, but as you can probably guess, I'm on the shit again. TH: What do you mean by "on the shit"? PT: O h come on, man! You know what that means! I'm doing drags! TH: Does "on the shit" mean that you are doing drags daily? weekly? monthly? PT: To me it means doing any drags at all! TH So any slip and you consider yourself "on the shit"? PT: Yeh! I was clean for a month and then last week 1 had a really bad time with my old man. I went right out on a two-day binge. TH: And what have you done since then? PT: If you mean drags, I have been clean since then, but I don't suppose it

will last. TH: So when you slip, even once, you see yourself as having a relapse. PT: Right. Beliefs 173 TH: And when you say "I don't suppose it will last" I get the impre sion that you don't feel fully capable of staying off drugs. PT: No, not really. Sometimes it seems pretty easy to stay clean and sometimes it's really impossible. TH: So from what you have said so far, you are skeptical about being here. You doubt that I can be helpful. You see yourself as having fully relapsed, based on a two-day binge. And generally you see yourself as being somewhat helpless to control your drag use. PT: Yeh, that's it in a nutshell! In just the first few minutes of the initial interview the patient revealed some of her addictive beliefs. She did not appear to possess salient control beliefs. The therapist continued to constract a data­ base of her addictive and control beliefs, which later played an exfremely important role in therapy. In addition to the interview process, several questionnaires are available to collect data about an individual's beliefs. Some are designed to evaluate general beliefs (e.g. Dysfunctional Attitude Scale; Weissman & Beck, 1978); some are designed to assess mood (e.g., Beck Depression Inventoty; Beck et al., 1961); while others (recently devel­ oped at the Center for Cognitive Therapy in Philadelphia) are designed specifically to assess drug-related beliefs (e.g., Craving Beliefs Ques­ tionnaire, Beliefs about Substance Use, and Automatic Thoughts about Substance Abuse). These questionnaires are given to the patient at the beginning of therapy to provide baseline information. They are also completed on subsequent visits to assess changes that may have occurred over the course of treatment. During the therapy process, these questionnaires help the therapist to understand the patient's "belief status" as it relates to problems and progress. For example, during her third visit, Louise stated that she wanted to start using cocaine again. O n examining her Craving Beliefs Questionnaire, the therapist saw an increase in Louise's addictive beliefs about craving. She indicated on the questionnaire that she strongly believed the following: "The craving is totally out of my control." "Craving can drive you crazy." "I'll always have cravings for cocaine." "The craving makes m e so nervous I can't stand it." "Since I'll have the craving the rest of m y life I might as well go ahead and use cocaine." 174 COGNTTIVE THERAPY OF SUBSTANCE ABUSE "If the craving gets too intense, cocaine is the only way to cope with the feeling." "I can't stand the panicky feeling when craving cocaine." "The craving frightens me." In addition to providing these data to her therapist, Louise also completed a Beck Depression Inventoty (BDI) prior to this session and her therapist noted that she had a BDI score of 20, suggesting mod­ erate depression. Louise endorsed the following items: "I feel sad." "I feel I have nothing to look forward to." "I am dissatisfied or bored with evetything." "I am disgusted with myself." "I blame myself all the time for m y faults." "I feel irritated all the time now." "I have lost all of m y interest in other people." "1 have to push myself vety hard to do anything." "I have lost interest in sex completely." Together, these questionnaires alerted the therapist to Louise's present state of dysphoria and its potential effect on her drag treat­ ment program. It became more apparent during the interview that Louise was straggling with a vicious cycle (see Figure 11.1): she was having strong urges to use cocaine; she believed that she could not control these urges; she believed that they would never go away; she further believed that there was nowhere to tum for support, since "all" her "friends" used cocaine; she believed that her lack of friends meant that she would never be happy again; she felt depressed; she believed that only cocaine could make her happy again, which led to further urges; and so forth. From this assessment of Louise's behefs, her thera­ pist was able to help her address and begin to modify these beliefs. ORIENT THE PATIENT T O THE COGNITIVE THERAPY M O D E L Many addicted individuals have an externalized view of their addiction. They may believe the following: "I have no con­ trol, whatsoever," "I just need to submit myself to the doctors. Maybe they will beat it this time," or "This treatment probably won't work since nothing else has." Thus, it is important that patients be oriented to the cognitive therapy model in the initial stages of therapy. Ori- Beliefs 175 Internal High- Basic Drug- Automatic Craving/ Risk Stimulus Related Belief Thought urges Depression "Only cocaine "Go get can make me highl" happy." Continued Instrumental Facilitating Belief use of Strategy cocaine There's nowhere to Seek friends who tum. I have no choice can supply cocaine. but to use." FIGURE 11.1. Cognitive model applied to Louise. enting patients involves modifying their beliefs about their addiction from an externalized orientation (e.g., "Control is beyond m e " ) to an internalized orientation (e.g., "I a m responsible for m y drag use and for m y recovety from addiction"). As part of the process of orienting the patient, key terms are defined, including "addictive beliefs," "control beliefs," "'automatic thoughts," "stimulus situations," "craving," "lapse," and "relapse." Next, the interrelationships between these p h e n o m e n a are explained, with special emphasis o n the role of beliefs in the addictive process. In the following dialogue. Bill's therapist introduced h i m to the cognitive therapy model. TH: Bill, let's talk about the development of your addiction. H o w do y o u think y o u b e c a m e addicted to cocaine? PT: W h e n I began to use cocaine with m y friends it was an inno­ cent thing. TH: What do you mean by "innocent"? PT: Well, when I began using cocaine I could control it. It would enhance a good time with m y friends. N o w it seems to control me. TH: What do you mean when you say "it controls me"? PT: Sometimes it just feels like I have no choice about whether or not I am going to use drags. TH: Are you saying that you have no control over the urges and craving; that they seem involuntaty and irresistible? PT: Yes, most of the time. TH: So perhaps you believe that the chemical properties are like a magnet, drawing you involuntarily towards continued use of drags. 176 COGNITIVE THERAPY OF SUBSTANCE ABUSE PT: Right. TH: OK, let's consider another perspective. What I am about to show you is the model I use to understand addiction. Let's start with a diagram, {therapist draws the diagram [presented in Chapter 3, this volume]) First, let's define the terms on this diagram. A stimulus is an internal or external circumstance that may stir up feelings and beliefs. A belief is an established idea you have about the stimulus or about how you might respond to the stimulus. Your belief, in turn, triggers some automatic thoughts, which themselves trigger urges and craving. Do you have any questions so far? PT: I'm not sure I know what you mean. TH: OK. The importance of this model is that it focuses on your thoughts and beliefs as playing a major role in your urges and craving. Previously, you believed that your urges were purely a result of a biological process over which you had no control. Alternatively, it is useful to think of urges as being influenced by your thoughts, which are ultimately under your control. PT: Then if I am in control of m y thoughts, and if m y thoughts control m y drag use, and if m y drag use is so bad for me, then why do I continue using? TH: That's a good question. Bill. When you do use cocaine it's partly because you believe that the immediate advantages of using outweigh the long-term disadvantages. PT: I just realized that another reason why I keep using is that I don't believe that bad things will ever happen to me. TH: Right. So, Bill, in cognitive therapy you can expect me to focus heavily on your thoughts and beliefs. Specifically, I will help you to modify your beliefs so that you are less vulnerable to drag use. What do you think of that? PT: It sounds pretty good to me. TH What "sounds pretty good" about this model? PT: Well, it gives me more hope about controlling m y urges and behaviors, rather than having them control me. EXAMINE A N D TEST ADDICTIVE BELIEFS Addictive beliefs develop over an extended period of time. As a result they become overlearned and extremely resistant to change. The drag abuser collects data supporting such beliefs as "drags Beliefs 177 are fun and vety exciting," "cocaine greatly enhances sex and many other activities," and "nothing is quite like using cocaine." Many drag abusers have tried to quit using drags at one time or another; how­ ever, their difficulty in doing so provides them with validation for the belief "It's useless to tty to control m y addiction." Given the resistant nature of addictive beliefs, the process of modifying them is quite a challenge. After the therapist has assessed the patient's beliefs and oriented the patient to the cognitive therapy model, an examination and testing of addictive beliefs should begin. Examination of addictive beliefs involves asking patients probing questions that test the validity of these beliefs. This process is known as the "Socratic method," or "guided discovety." The following are examples of questions appropriate for this process: "What is your evidence for that belief?" "How do you know that your belief is trae?" "Where is that written?" "Where did you learn that?" "How confident are you in that belief?" As the patient considers these questions, his or her addictive beliefs should begin to "loosen" slightly. That is, he or she should begin to consider the possibility that the addictive beliefs are not nec­ essarily trae. The following dialogue between Bill and his therapist illustrates this process. TH: Bill, let's talk about your beliefs about using cocaine. PT: You want to know the trath? It has been three weeks since m y last hit and . I have to be honest here . I really miss it. TH: What do you miss about using? PT: I miss it all: m y friends, the parties, the rash of it all. TH: So you associate cocaine with socializing and having fun. PT: Of course. There is nothing as much fun as sitting around with a bunch of friends getting high. TH: So you don't believe that anything is as much fun as getting high? PT: {thinking) H m m . {shaking his head vigorously, smiling). No! TH: Nothing? PT: {still smiling) Nothing I've ever done! TH: Let's look at that belief carefully. First of all, how confident are you that there is nothing as much fun as getting high? 178 COGNTTIVE THERAPY OF SUBSTANCE ABUSE PT: Maybe there is something more fun, but I don't know what it is. TH: Bill, prior to using cocaine, what would you do for fun? PT: H m m . {long pause). maybe that was partly why I began using cocaine. I remember being bored quite a bit. Actually, I was really in a rat. bored with m y job and m y life generally. TH: So you initially turned to cocaine to escape the boredom and the monotony of your life. PT: Yeh. TH: It sounds like you were in a fairly unsatisfying and even unhappy period in your life. PT: Definitely. TH: And you were looking for a simple, instant solution. PT: Maybe. TH: Maybe? PT: Well, I do think I have a tendency to seek quick and easy solu­ tions. TH: Let's go back to your original belief: "Nothing is as much fun as getting high." When you began to use cocaine back then, what other avenues had you explored for dealing with your boredom and stagnation? PT: Well, maybe I really didn't give much else a chance. TH: So, what evidence do you have that using

cocaine is really the only fun you can have with your friends? PT: Actually when you put it that way, and when we look at my life, 1 guess I got into it at a time when any escape would have looked good. At the beginning of this dialogue Bill was confident that noth­ ing was as rewarding as cocaine use. However, his therapist's ques­ tions led him to reconsider this belief. As the patient's confidence in his addictive beliefs began to wane, he could begin to replace these beliefs with more adaptive control beliefs. D E V E L O P C O N T R O L BELIEFS Generally, the Socratic method provides an excellent strategy for having patients examine their dysfunctional beliefs and replace them with more constractive, alternative beliefs. In the case of cocaine addiction, the Socratic method stimulates patients to Beliefs 179 examine their addictive beliefs and to replace them with control beliefs. Some specific questions that introduce control beliefs are the following: "What would you do if the drag weren't available?" "What are the disadvantages of using the drag?" "How else can you look at this situation?" "What else could you do to achieve the same end? What else?" The previous discussion with Bill illustrated how guided ques­ tioning can loosen previously held beliefs about the benefits of tak­ ing cocaine. In this section, we continue Bill's dialogue to illustrate how the therapist helped him to develop control beliefs. TH: Bill, you now seem less dead set in believing that nothing is a much fun as getting high. PT: I'm not sure what to believe now. TH: What do you mean? PT: Well, I still think that getting high with m y friends was lots of fun, but maybe it wasn't the perfect high I made it out to be. TH: Bill, what else could you have done with your friends that would have been fun? PT: Well, I don't know about these guys, but with other friends in the past I could have gone to a baseball game, or played racketball, or done something like sports or something. TH: What else? PT: I guess there are lots of things . but none seems as exciting as doing cocaine. TH: Let's tty to think of some more things. What gave you the big­ gest thrill before you began using cocaine? PT: Well, I was an adventurous guy. W h e n I was much younger I would go camping and hiking and rock climbing, but I'm in no shape for that now. TH: What do you mean when you say "I am in no shape for that"? PT: I guess I'm just skeptical that I would enjoy that kind of thing anymore. It's just been so long since I last did it. TH: What would it take for you to tty doing those things again? PT: I guess I'd just have to do them. TH: What were some of the feelings you had in the past when you would go camping or hiking or climbing? 180 COGNFTTVE THERAPY OF SUBSTANCE ABUSE PT: I felt great. really alive! TH: H o w did that feeling compare to the cocaine high? PT: {pause). I guess, in some ways it was better. TH: What do you mean? PT: Well, I really earned the high I got from those activities. There were no shortcuts then. It was a super feeling. TH: So perhaps you now have a control belief to replace the old addictive belief: "I can experience a super high without using cocaine." PT: Yes, I just need to remember that thought. Another strategy for examining and testing addictive beliefs is th Daily Thought Record (DTR; Chapter 9, this volume). The DTR is a standardized form for listing and modifying maladaptive thoughts. In the case of cocaine addiction, it is useful for modifying addictive beliefs that lead to urges and craving. Specifically, the DTR has five columns: situation, emotions, automatic thoughts, rational response, and outcome. When the patient experiences an urge or craving, he lists the addictive belief that precipitates or fuels this craving. Then, in the rational response column he lists alternative control beliefs. For example, if the addictive belief is "I can't stand the stress with­ out cocaine," the patient might list the alternative control response "Yes I can! In fact there are many days when I feel better because 1 didn't do drags." Another strategy for developing conttol beliefs is the advantages- disadvantages (A-D) analysis. People use drags because they view the advantages of doing so as outweighing the disadvantages. Thus, the purpose of the A-D analysis is to redirect the patient's attention to the disadvantages of using drags and the advantages of abstaining. The patient is helped to constract a four-cell matrix where the advan­ tages and disadvantages of two alternative decisions are compared. Regarding cocaine dependence, the two alternative decisions are using cocaine and abstaining from cocaine. Louise's therapist utilized this strategy as follows: TH: I would like to help you evaluate the advantages and disadvan­ tages of using versus abstaining from cocaine. As you can see, I am drawing a four-part box. {draws the matrix) Along the left side we write "advantages" and "disadvantages." Along the top we write "using" and "abstaining." Let's give this a tty. What are the advantages of using cocaine? PT: It's a break from the bullshit. and it's a good time. Beliefs 181 TH: {writing) So it's a break and it's a good time. What else? PT: It's a chance for m e to be with m y friends. TH: {writing) Time with friends. What else? PT: It makes sex a whole lot of fun. TH: {writing) Sex is more fun. Any other advantages? PT: I'm sure there are . I'll think of them. TH: OK, if you think of any more, let m e know. Let's move on to the disadvantages of abstaining. What comes to your mind? PT: Oh that's easy; I'll have to give up the things I just listed: the break, the fun, time with friends, great sex. TH: {writing) So you'll have to give up the "quick fix." PT: Yeh, that's another way to look at it. TH: What about the disadvantages of using cocaine? PT: 1 could get busted, I guess. TH: {writing) You could get busted. What else? PT: It's pretty dangerous out there. I've seen people get pretty badly hurt messing around with that shit. TH: {writing) Danger of getting hurt. PT: Yeh. There's also the crash. Sometimes I feel like dying would feel better. . {long pause) . . And when I really think about it, 1 get to feeling really out of control on the stuff. I guess another disadvantage is that I don't like being dependent on anyone or anything. TH: {writing) Let m e get that all: crashing after a high, feeling out of confrol, being dependent on people and on the drug . PT: It's hard admitting to these things, but they're all trae. TH: Any other disadvantages to using? PT: Yeh, I know you won't believe this, but I really love m y little girl. Each time I get high, I risk losing her. TH: {writing) So another disadvantage of using is that you might lose your daughter. Anything else? PT: Isn't that enough? TH: These all seem like pretty major risks. What about the advan­ tages of abstaining or quitting? PT: They go along with the disadvantages of using: I will avoid having the problems of getting busted, or hurt, or losing m y little girl, and on and on. 182 COGNITFVE T H E R A P Y O F SUBSTANCE A B U S E USING ABSTAINING Break from "bullshif Gains: It's a good time self-respect ADVANTAGES Time with friends respect of others Sex is more fun Avoids: 1. Getting busted 2. Getting hurt 3. Crashing 4. Loss of control 5. Being independent Danger of getting busted Danger of getting hurt DISADVANTAGES Crashing is av^ul No more quick fix Feeling out of control Dependency on others Danger of losing daughter FIGURE 11.2. Advantages-disadvantages analysis for Louise. TH: And what will you gain? PT: Self-respect. and the respect of others. TH: OK, that completes our analysis. Let's review what I have writ­ ten, {shows the matrix [Figure 11.2] to Louise) What do you see here? PT: I see a lot of things I don't like. TH: What do you mean? PT: This makes me uncomfortable. I didn't realize it, but I really don't like thinking about the problems with using cocaine. TH: And yet it is those thoughts, called "control" thoughts, that will help you to remain abstinent. PT: I understand that. It's just easier to ignore confrol thoughts when I am using cocaine. PRACTICE ACTIVATION O F C O N T R O L BELIEFS On completing the exercises (guided discovety, ratio­ nal responding via the DTR, and the A-D analysis), the patient was much more attentive to the disadvantages of using cocaine. She sue- Beliefs 183 cessfuUy developed control beliefs to strengthen resolve against f cocaine abuse. However, it is quite possible that she will not access these control beliefs when faced with "temptation," especially since she has overlearned her addictive beliefs. (This becomes especially evident in the Louise's last comment: "It's just easier to ignore con­ trol thoughts when I am using cocaine.") Hence, special attention must be paid to the activation of control beliefs as part of therapy. There are several methods that serve this purpose. Two methods pre­ sented in this section are flashcards and programmed practice in ses­ sions. In the final section of this chapter we introduce "homework" as the ideal opportunity to practice activating control beliefs. After the patient has developed control beliefs, flashcards can be used to reinforce and activate these newly developed beliefs. For example, on completing the A-D analysis the patient writes the disadvantages of using cocaine (i.e., control beliefs) on one or several 3" x 5" index cards. Louise's flashcards might list the follow­ ing confrol beliefs: "Getting high is fun but it has many disadvantages." "Getting high could get m e busted or killed." "When I use cocaine, I give up control of m y life." "When I use cocaine, I become dependent on the drag and on others." "When I use cocaine, I ran the risk of losing m y daughter." In using the flashcards, Louise was encouraged to review her con­ trol beliefs on a daily basis and access them whenever she has an urge to use cocaine. Programmed practice (or "covert rehearsal") in sessions, via imagety, is another tool for helping patients activate control beliefs. The patient is encouraged to imagine a tempting drag-related situa­ tion. As this situation evokes craving in patients, they activate con­ frol beliefs in the session in order to dampen the craving. The fol­ lowing dialogue between Louise and her therapist early in a session illustrates this technique: TH: Louise, at the end of our last session you said that it was easy to ignore control beliefs when you are using cocaine. Today I would like to help you practice activating control beliefs so that they come more naturally when you find yourself in high-risk situations. PT: That's a good idea, since those are the last thoughts on m y mind just before I take a hit. 184 COGNTTIVE THERAPY OF SUBSTANCE ABUSE TH: I'd like you to imagine and then describe a typical tempting situation where you would be likely to use cocaine. Be as detailed and as vivid as possible in your imagination and description. When this is done correctly it is common for people to start craving cocaine. Don't be afraid or surprised if this hap­ pens. Actually, it is desirable; I want you to crave cocaine for the purposes of this exercise. W h e n that happens we will prac­ tice activating your control beliefs, which should reduce the craving. PT: W o w , that's weird. If you insist. {long pause while Louise con­ centrates on images). OK, I've got it. A common scene is that I am at m y mother's house with m y daughter and m y mother is ragging on m e for not having a job.

She is calling m e all kinds of names: "lazy," "worthless," you know the list. Anyway, I feel this urge to ran, but I know there's nowhere to go. I want to hit her but of course I don't. I want to cty, but I wouldn't give her the satisfaction of seeing that she has hurt me. And finally I start thinking about going to Michelle's house. She always knows were to find some shit. I think: "That's the one thing that will get m e feeling better." I know that I can leave my daughter with m y mother while I go out to get high. I also think about what I'll do if I don't find Michelle. If she's not around, I'll just go downtown and tum a quick ttick. And then I get more intense feelings of wanting to get high . {attention returns to therapist). Well, you've succeeded in making m e crave the shit. N o w what are you going to do? TH You are craving cocaine now? PT: Damn straight! TH OK, now start reviewing your control beliefs out loud; you know what they are. PT: The disadvantages? TH Yes, but say it with feeling! Take out your flashcards if you like. PT: No, I don't need the flashcards. {she begins tentatively at first, but then builds her enthusiasm) I am not going to get high; my baby needs me. The stuff is killing me. It really doesn't make anything better. I'm better off without it. I can stay clean if I want to. I can make a life for myself and m y baby if I stay cleanl {she smiles) TH: What are you thinking right now as you smile? PT: That I can do it! TH: Great! Beliefs 185 In this dialogue, Louise succeeded in creating a strong urge to use cocaine, but she successfully countered that urge with control beliefs. This process was repeated several times over the next few ses­ sions with Louise. For homework, she was encouraged to practice this exercise in vivo, as drag temptations naturally arise. ASSIGN H O M E W O R K THAT ADDRESSES BELIEFS As in all other applications of cognitive therapy, homework involves applying the skills learned in therapy sessions. Thus, homework is a vital extension of therapy (Burns & Auerbach, 1992; Persons et al., 1988). As a long-term goal of homework in cog­ nitive therapy, patients should learn to use self-guided Socratic ques­ tioning spontaneously in their lives; for example, "What evidence do I have for that belief?" "How else can I look at this situation?" "What are the consequences of m y beliefs?" Homework is an opportunity to practice applying control beliefs in the "real world." It may involve having patients practice activat­ ing confrol beliefs in the face of tempting high-risk stimuli, since they will never succeed in avoiding all tempting stimuli. Louise, for exam­ ple, is unlikely to change her mother's behavior, although she can learn to cope more effectively with her. A specific homework assign­ ment given to Louise, therefore, might be to practice control beliefs in response to her addictive beliefs and automatic thoughts when in the presence of her mother. Homework may also involve testing addictive beliefs to evaluate their validity. For example. Bill might be challenged to tty various methods for having fun, in order to test his belief that "there is noth­ ing more fun than using cocaine." As explained in Chapter 6 (this volume), homework is assigned at the end of each session and it is reviewed at the beginning of each follow-up session. Initially, homework is quite stractured. For example, patients are instracted to complete DTRs on a daily basis. Later, how­ ever, homework can be less formal, as the patient develops new, more adaptive, patterns of thinking. SUMMARY The basic beliefs and automatic thoughts about drags may account for much of their use. There are at least three types of 186 COGNTTIVE THERAPY OF SUBSTANCE ABUSE drag-related beliefs that contribute to urges, craving, and ultimate use of drags: anticipatoty beliefs, relief-oriented beliefs, and permissive beliefs. The role of the cognitive therapist is to assess, examine, and test these beliefs with the patient, in order to ultimately replace them with control beliefs. There are m a n y cognitive strategies that facili­ tate this process, many of which were presented in this chapter. C H A P T E R 1 2 M a n a g i n g G e n e r a l L i f e P r o b l e m s P Aa.t ait ients rarely enter treatment for drag addiction or dependence on their own accord in the absence of general life prob­ lems (Carey, 1991). W h e n patients are in an early phase of their drug use, they are typically quite pleased with the effects of the drugs. This is so either because the drags produce a state of unmatched excite­ ment and euphoria or because they offer the abuser an artificial respite from the demands, pressures, ennui, and emotional pain that they may be suffering. At such times, patients operate under the assump­ tion that the use of mood-altering chemicals offers a workable, viable option to functioning in a drug-free state of mind. However, as the drag user becomes more regularly active in seek­ ing, achieving, and repeating the "high" experience, a number of problems surface. Such problems include, but are not limited to, (1) the realization that drug use does not help the actual demands, responsibilities, and troubles of evetyday life magically to go away; (2) the development of a physiological tolerance to the drags, and therefore the need to expend more time, energy, and money in the search for the ever-elusive "high"; (3) the exacerbation of neglected life concerns, thus increasing stress and the desire to escape through the use of psychoactive substances; and (4) fallout from worsening habits, in terms of damaged relationships, vocational and/or academic failure, and serious medical and legal complications. It is in this advanced state of psychosocial difficulties and life crisis that the individual may be regarded as a drug abuser and will most likely appear for psychological treatment. 187 188 COGNITIVE THERAPY OF SUBSTANCE ABUSE The therapist is faced with the daunting task of helping such patients not only to arrest and ameliorate their drag addictions, but also to deal with many serious real-life difficulties. While many of these problems are similar to those of any other diagnostic categoty of patient, there are many that are particularly salient to the drag- abusing population. It is imperative that therapists be aware of the typical life prob­ lems that the drug-abusing patient presents at the start (and during the course) of treatment. It is equally important that these problems be given adequate attention in therapy, in spite of the temptation to focus solely on the substance abuse disorder. With this in mind, the current chapter presents an overview of the most common life issues that the cognitive therapist will need to address in the treatment of this challenging population. "CHICKEN A N D EGG" C O N U N D R U M : W H I C H COMES FIRST, SUBSTANCE ABUSE OR ASSOCIATED LIFE PROBLEMS? An important assessment question concerns whether the patient's major life problems precede or postdate the onset of the substance abuse disorder. (Similarly, it is crucial to note whether the patient's antisocial behaviors are primaty or secondaty to the drug addiction. See Chapter 16, this volume, for more details.) Informa­ tion regarding the chronology of life problems and drag abuse pat­ terns can shed light on the "function" of the patient's use of psychoactive substances, as well as elucidating the factors that serve as triggers for the abuse of drags. For example, "Maria" presented with a crack addiction that had originally begun two years previously, in the aftermath of the vio­ lent death of her younger sister. After being arrested for possession, Maria spent the next three months in various inpatient rehabilitation facilities. When she was discharged, Maria was convinced that she would never "pick up" (resume using drugs) again, and that she was on the right track. However, shortly thereafter she was strack another blow when one of her best friends died. Almost immediately, she resumed her use of crack and once again found herself back in court. After a brief stay in jail she was released on parole, on the condition that she receive ongoing treatment. It was at this time that Maria entered cognitive therapy. In Maria's case, grief and loss were powerful triggers for drug abuse. Since she had no histoty of drug abuse prior to the death of Managing Life Problems 189 her sister, her prognosis was quite hopeful. It was clear that she had many years of experience as a well-functioning, responsible per­ son. Furthermore, her life was fairly well ordered, and her stressors ,/ere not out of the ordinaty realm of evetyday life. However, in order for therapy to be complete, it would be necessaty to help Maria come to terms with the deaths of her sister and friend and her concomi­ tant belief "I'm all alone." Additionally, the therapist would need to teach the patient to use cognitive therapy skills in a preparatoty fashion in anticipation of episodes associated with loss. For example, the illness of a significant other might be sufficient to induce Maria to have catastrophic expec­ tations of that person dying. Such an extreme worty would put Maria at risk for relapse, as her anxiety at the thought of losing someone (and feeling alone) might induce her to self-medicate with crack cocaine. Similarly, the calendar became a source of negative cues that had to be anticipated, and that served as a therapeutic call to action. Major holidays, birthdays, and anniversaries of the deaths of loved ones had become capable of arousing upsetting automatic thoughts and emotions, the likes of which could trigger a resumption of drug abuse. As it turned out, Maria learned the skills of rational responding, scheduling activities, and problem-solving quite well, and she survived the "anniversaty phenomenon" without incident. However, when she was "blind-sided" by her boyfriend's decision to leave her, she suf­ fered a temporaty drag lapse (a single binge episode). Another inter­ personal loss had triggered a need to blot out her emotional pain through the use of crack cocaine. Maria's case seems straightforward—life problems preceded the onset of substance abuse. O n the other hand, we see cases where the onset of serious life difficulties seems to occur as a result of the sub­ stance abuse. Until the time that "Roland" began using drugs in high school he seemed to have a fairly unremarkable life. He was an aver­ age student, came from an intact family free of substance abuse, and he had a circle of regular friends. After being introduced to marijuana, Roland began to skip classes and to disengage himself from his fam­ ily, many of his friends, and most of his normal recreational activi­ ties. As his drug use came to involve "harder" substances such as quaaludes and cocaine, he incurred more and more serious concomi­ tant life problems. For example, although he somehow managed to graduate from high school, Roland did not pursue further education or vocational training, nor did he seek employment. His sole source of income was through petty drag trafficking. His parents, recogniz- 190 COGNITIVE THERAPY OF SUBSTANCE ABUSE ing that something was dreadfully wrong, pressured Roland to "clea up his act" and to get a job. This frequently led to screaming and shoving matches between son and father. Finally, after Roland's par­ ents were frightened by two incidents when drag associates came to the door in the middle of the night, Roland was told to leave the house. Shortly thereafter, Roland was arrested for driving while intoxicated, as well as for possession of a controlled substance. Roland's steadily increasing problems with substance abuse led to academic and vocational stagnation, family conflicts, loss of his primaty domicile, and legal troubles. His main interests and activi­ ties were reduced to procuring, using, and selling illicit substances. His chief associates were drag users and dealers, and he had no friends who

led a drug-free lifestyle. Roland's drag use had led to numerous negative consequences in his life, yet his sense of helplessness in dealing with these mounting difficulties, coupled with his desire to "forget all his troubles" through the use of drags such as cocaine, perpetuated his drag-related lifestyle. These were problems that had to be addressed when Roland ultimately entered therapy, in addition to his problematic abuse of drags per se. Although the cases of Maria and Roland seem quite distinct in that the former suffered identifiable life troubles as a precipitating factor to the onset of her drag abuse, while the latter produced the majority of his own life problems as the result of his apparently "unprovoked" recreational use of drags, the two cases have at least one vety important similarity. Both patients eventually became trapped in a vicious cycle, where the dual problems of drug abuse and general life problems began to exacerbate each other. For example, Maria's use of crack cocaine, originally the result of her grief, became the cause of her arrest and incarceration. Aside from the obvious negative impact that this had on her life in its own right, Maria further suffered from an inability to find employment as a result of her criminal record. In her anger and frastration, she once again resorted to the use of crack cocaine. Renewed legal troubles soon ensued, and the vicious cycle was com­ plete. Roland's vicious cycle of substance abuse and life crises was even more entrenched and self-perpetuating than Maria's. His "druggie lifestyle" led to numerous personal, financial, and legal complications. He had no stable relationships, no sense of trast for others, no sense of self-esteem when he came off his high, no legal source of income, no healthy sources of stimulation and pleasure, no treatment for numerous medical problems, and a constant nagging fear of crimi- Managing Life Problems 191 nal apprehension. All these concerns were quickly "fixed" by using drags such as cocaine, thus keeping him firmly ensconced in his drag lifestyle. Drags were a major source of his chaos and crises, yet he continued to view them as his only "solution" to deal with these problems. Later, when Roland began treatment, he would not only have to overcome his addictions, he literally would have to "get a life" as well. (Roland's personality disorders also played an important role with regard to his drag use and general life problems. For more on this, see Chapter 16, this volume, on the interaction between sub­ stance abuse and personality disorders.) In either of these prototypical cases, the life problems represent broad "stimulus situations" that both trigger and are worsened by the patient's continuing abuse of substances. Figure 12.1 illustrates the beliefs and automatic thoughts that feed into this process. As depicted by Figure 12.1, the patient's chronic unemployment serves as a stimulus situation that sets off a chain of beliefs, automatic thoughts, and actions that lead to drug use. The patient's drag use then contributes to his or her becoming less employable (less moti­ vated, less reliable, etc.), and the cycle continues. This chapter focuses on the major areas of chronic life stress that plague so many substance abuse patients. (See Chapter 13, this vol­ ume, for examples of common acute crises and emergencies, many of which are related to the issues described later.) Some of these are more likely to be precursors to a drag problem, while some are more clearly the sequelae to drag abuse. In either case, it is important to bear in mind the way that these trouble spots become part of a vicious Life Beliefs Automatic Urges/ Problems Thoughts cravings "I'm a failure. (Chronic My life is "Might as unemploy­ hopeless, so well get ment) drugs can't high now." hurt me." :^ Lapse Instnjmentai Facilitating Beliefs episode drug-seeking (permission) behaviors "Using will make m e (action) feel better." F I G U R E 12.1. The vicious cycle of life problems and drag abuse. 192 COGNITIVE THERAPY OF SUBSTANCE ABUSE cycle that has spiraled out of control. The following life problem described in detail here: marital and family problems, socioeconomic problems, daily stressors, legal problems, and medical problems. MARITAL AND FAMILY PROBLEMS As noted earlier, it is vital for patients to be aware of the "people, places, and things" that they associate with the using of illicit substances. In the early stages of treatment, it is wise for the substance abuser who is ttying to remain drag-free to avoid needlessly coming into contact with stimuli that might provoke strong cravings or facilitate the obtaining of drags. (Later in treatment, however, it is important to teach patients to apply and practice self-help techniques in the face of those kinds of drag-related stimuli that may be unavoid­ able in their everyday lives.) W h e n the "people" and "places" are impersonal acquaintances and out-of-the-way locations, it is reason­ ably straightforward (under the proper motivational and coping con­ ditions) for the patient to steer clear of these stimuli. The picture is decidedly more difficult when the people and places are the patient's own family members, in the patient's own residence. Substance abuse amongst one's relatives poses a serious problem for the patient. In terms of etiology, a person whose parents or siblings abuse drags is at risk for modeling these behaviors (Gomberg & Nirenberg, 1991; Lang, 1992). The patient may have easy access to drag paraphernalia, and may have knowledge of family members' secret stashes. In terms of maintenance and relapse, the patient may have a particularly difficult time turning away from the continual lure of drugs when family members are high, when these family members encourage the patient to get high as well, and when drags and money are so blatantly available at all hours of the day. Furthermore, there may be strong social pressures to conform to the "drug subculture" in the household. One of our patients. Dee, was taunted unmercifully by her two substance-abusing brothers for her attempts to stay away from drugs and to attend therapy and support group meetings. They attempted to "bring her down" by ripping into her for her "holier- than-thou" attitude, hoping that she would succumb to their barbs by joining them in their smoking binges. Luckily for Dee, these broth­ ers lived a block away, so she did not have to deal with them on a constant basis. As it was, however, a great deal of time and energy in therapy was spent in learning how to assert herself effectively to her brothers, and to respond rationally to her own initial automatic thoughts. These thoughts included "If you can't beat 'em, join 'em," Managing Life Problems 193 "I have to get them off my back," and "I have to prove that I ain't stuck up." Rational responses that were generated in response to these automatic thoughts included the following: 1. "If they [the brothers] want to be losers, that's their business I'm doing the right thing by staying straight." 2. "I'd rather that m y brothers hate m e than go back to using and have m y kids hate me." M y kids are much more important." 3. "I'm not stuck up. I'm tiying to be humble and know m y limi­ tations. M y brothers are the ones who are being stuck up, only they're so stoned they don't see it." 4. "I can't change m y brothers, so why should I let them change me?" and, 5. "I've dealt with worse hassles before. I'll just remind myself that evetything they say is just bullshit, and I'll get back to m y own business." Dee was able to defend herself from her brothers' attempts at heavy-handed peer pressure, but the fact that her two "favorite" sib­ lings had drag problems was a considerable source of stress for her. Dee believed that her brothers' drag problems signified that she came from a family of "losers," each member of which (including herself) inevitably would have a life filled with troubles. Furthermore, she believed that she would need to stay away from her brothers as much as possible, thus depriving her of what had once been enjoyable and companionable sibling relationships. This exacerbated her sense of loneliness. It is generally unrealistic for patients to expect that they can solve the substance abuse problems of family members. It is generally wis­ est to focus on cognitive coping skills that enable patients to gain some distance from the problem, and to stay focused on their own recovety. Toward this end, support group meetings can be recom­ mended as an adjunct to cognitive therapy, especially when patients feel overly guilty for family members' drag problems. The negative experiences that these patients have had during their upbringing in alcohol and drag-using households can be discussed as part of treat­ ment as well. This builds rapport between patient and therapist and helps to elucidate implicit dysfunctional rales about substance abuse and family relationships that the patients may have learned. To have a mate who is self-absorbed in drag abuse entails tre­ mendous stress for a patient. Problems include the partner's (1) hav­ ing erratic mood swings, (2) being financially and sexually reckless 194 COGNTTIVE THERAPY OF SUBSTANCE ABUSE and irresponsible, (3) risking major medical and legal consequence (4) endangering the patient with regard to AIDS and other sexually transmitted diseases, and (5) seducing the patient into relapsing into substance abuse once again. When a drag-addicted mate refuses to acknowledge a problem or to get help, it is often necessaty for the patient either to leave the household or to induce the mate to leave. Such a strategy may be the best way to maintain a home environ­ ment that is conducive to recovety. In order to maximize the chances that patients will be willing be go along with such a strategy, therapists can emphasize that it may not be necessaty to leave the relationship permanently, but that such a move may be needed at present. The drawbacks to the above strategy, in the mind of the patient, may be compelling. The patient may be loath to confront a potentially violent partner, and may not have the resources to make a clean start in another domicile. Furthermore, the patient is forced to face the loss of a significant love relationship—a daunting realization, especially if the patient has dependent personality characteristics (see Chapter 16, this volume). When this is the case, the therapist may notice that the patient seems excessively emotionally attached to the substance-abus­ ing partner, no matter what the personal cost. In short, the patient may love the partner deeply, in spite of this person's drug abuse. The patient may go to great lengths to excuse or cover up the partner's transgressions, because the prospect of losing the partner (or even of hearing negative feedback about the partner) is too much to bear. Even worse, the patient may collude with the partner to use drags together in secret and to provide cover for each other. Such phenomena have been written about extensively in recent times under the rubric of "co-dependency" (cf. Lyon & Greenberg, 1991). In such cases, cognitive interventions must focus heavily on adaptive problem-solving (Piatt & Hermalin, 1989), and on the patient's exaggerated guift and fears of loneliness. For example, the patient may believe erroneously that the significant other would use more drugs if left alone, when in reality the significant other is dem­ onstrating an escalating drug problem whether the patient is there or not. Similariy, the patient may believe that he or she could not bear the loneliness of being without the drug-using partner, when in actijality the patient already is coping with being functionally alone, as the drag-using partner is emotionally absent. Additionally, it is vital to teach the patient to expand his or her social network of nonusers, so that the substance-abusing mate is no longer the dominant source of interpersonal reinforcement. At the same time, patient and therapist must be ever vigilant to the patient's own vulnerabilities to using drags. It is important to pay Managing Life Problems 195 close attention to the way that the patient's chronic life problem substance abuse feed into each other, rather than looking at each problem in isolation. For example, in the case of the

patient whose significant other is abusing drags, the belief that "if I stay off drugs I will have to give up the person I love and be all alone" may prime the patient to resume using drags. "Walter" had told his therapist many times that the love of his children was one of the only things he cared about in his life. There­ fore, the fact that he was now not permitted to see them was a source of fremendous distress. As a result, he escalated his drag bingeing— partly out of a belief that "a greater amount of drags is needed to blot out a greater amount of suffering," and partly out of a desire to make a suicidal gesture that would attract attention and care-and soon wound up in the hospital due to overdose-induced convulsions. His failure to handle his distress without the use of chemical substances led to an accentuation of his sense of loss (his children), which in turn brought about a life-threatening exacerbation of his drug abuse. Following his release from the hospital, and his resumption of outpatient cognitive therapy, a great deal of time in session was spent in reviewing the pros and cons of various strategies for coping with interpersonal loss. Among the most favored therapeutic suggestions were seeking the support of others, such as family, friends, and thera­ pist, and focusing on work-related activities, especially those that required a great deal of strenuous physical labor. Additionally, Walter was instructed to respond to his urges to buy and use drags by con­ juring up images of his children, the people he most wanted to be proud of him. These images were to serve as strong deterrents to his initiating the search for drags (however, they were less effective in stopping him from using once he had the drags and paraphernalia in his hands). Ongoing marital discord (or discord in any love relationship) can serve as a powerful stimulus for drag cravings and drug abuse. W e have seen patients use drugs in such cases for a variety of purposes. Such "functions" of the drag use include (1) reviving a chemically based, false and temporaty boost in self-esteem; (2) exerting control in the relationship by defying the spouse, and by inducing a self-pro­ tective state of apathy or invulnerability; (3) "soothing" the anger that is felt toward the spouse, especially if the patient has the belief that not using something will lead to an escalating physical confrontation; and (4) finding an emotional escape from marital unhappiness, espe­ cially if the drag-abusing spouse believes that there is no way to solve the marital problem or to leave the marriage. In general, unhappi­ ness and anger in a relationship feed into patients' feelings of help- 196 COGNITIVE THERAPY OF SUBSTANCE ABUSE lessness and loneliness, which in turn may lead to a wish for imme ate relief. The result may be a craving for drags, followed by their use. It is not surprising to note that the use of drags within the con­ text of a marriage will likely affect the relationship adversely. If the marriage is already disturbed, the substance abuse will exacerbate matters, thus contributing to yet another vicious cycle. The situation is perhaps most dire when the abuse of substances leads to physical, psychological, and/or sexual assault. In contrast to the oft-held belief (alluded to above) that the use of drags can "soothe" the angty spouse, drug use actually more often than not serves to disinhibit and to activate the potential for violence (Amaro, Fried, Cabral, & Zuckerman, 1990). Therefore, the therapist must be ever vigilant to possible signs of domestic violence in the life of the substance-abusing patient. Along with this vigilance, it is wise for the therapist to have ready access to information about crisis hotlines and shelters for victims of physical and sexual abuse. If the patient is primarily a perpetrator of such violence, the thera­ pist must do all that is possible to contract with the patient to deal with this problem as a number one priority in treatment. As discussed previously in Chapter 4 (this volume), the limits of confidentiality that exist when the patient is a threat to the well-being of others need to be spelled out. At the same time, great therapeutic skill must be employed to keep the patient positively engaged in the process of therapy and to keep the patient's trast. An examination of the patient's personal and family histoty may demonstrate that physical, psychological, and sexual abuse during the patient's childhood and adolescence played a significant role in the development of the patient's drag problem. (Note: In order to high­ light patterns and relational configurations in the patient's family, it is sometimes useful to map out a family tree on paper. Such a tree can indicate separations, divorces, deaths, abusive relationships, per­ sons who abused alcohol and drags, and the like.) This may be trae for any number of reasons, such as (1) the aversive conditions at home force patients to spend more and more time on the streets, thus exposing them more to the drug culture; (2) the perpetrators of vio­ lence in the family may be drug abusers themselves, thus modeling the behavior for the victims to emulate; (3) the use of drugs may be viewed as the only means of escape from an intolerable situation at home; and (4) the loss of self-esteem that is incurred over years of being abused creates an increased addictive vulnerability in victims, as they search for quick ways to produce good feelings and to obtain a crowd of associates who will validate them and do the same. These background factors produce such beliefs as "Using drugs Managing Life Problems 197 is a natural way of life," "Violence-particularly when under the influence-is acceptable," "Using is the only way of blotting out unpleasant feelings," and "I am weak and inferior and can feel good (and accepted) only by using." In treating such patients, self-esteem issues become a central component to the therapy. Therapists can help their patients begin to develop a stronger internal deterrent to drag abuse if they find (and work to build) evidence that dispels the patients' notions that they are worthless, deserving of a froubled life, and incapable of meeting their own needs through more socially acceptable and healthier means. SOCIOECONOMIC PROBLEMS Substance abuse disorders frequently occur against the backdrop of socioeconomic problems. For example, in the last decade we have witnessed a significant increase in the prevalence of cocaine abuse among the impoverished of our inner cities (Closser, 1992; O'Brien et al., 1992). Crack cocaine in particular has become more and more frequently abused within this milieu (Gawin & EUinwood, 1988; Smart, 1991). As the people of this segment of society grow more and more disillusioned with their chances of improving their lots in life through standard long-term means (e.g., finding quality educa­ tion, staying in school, and working one's way up a ladder of voca­ tional success), they may be more inclined to turn to nonstandard, short-term fixes (e.g., using drags for a boost in mood and selling drags for an increase in income). It has been argued that it is quite difficult to steer children, ado­ lescents, and adults alike away from drags when so few alternatives for finding enjoyment exist in the immediate environment. Addition­ ally, it is equally difficult to stay focused on the distant rewards of schooling, or the modest remuneration of low-level employment, when the distribution of drugs can produce staggering material rewards in a relatively short space of time. Furthermore, the risks of arrest and incarceration, overdose and poisoning, and violence are less of a deterrent against using drugs when there is a prevailing sense that the future holds no promise anyway. This is especially so for vulnerable individuals who have developed core beliefs of hopeless­ ness and helplessness. For these reasons and others, therapy with lower socioeconomic status substance abusers poses considerable challenges to the thera­ pist. Walter typified this type of patient. When the therapist made an attempt to appeal to Walter's sense of pride and self-worth (in order 198 COGNTTIVE THERAPY OF SUBSTANCE ABUSE to counteract his belief that he was a helpless victim) by asking could be "strong enough to be a man and walk away from his deal­ ing friends," Walter replied, "I don't feel strong when I walk away from drags. I feel like nothing, like I always do. I only feel like I'm worth something when I use a little something [usually cocaine or heroin]. That's the only time I feel like a big shot." In order to com­ bat this drag-abuse-fostering attitude, the therapist focused Walter's attention on how he felt after he came down off his high, which was lower, weaker, more helpless, and less adequate than ever. This fact was reviewed time and time again, so as to deromanticize the false sense of pride that the use of drags seemed to induce temporarily. Another critical component of treatment in this instance was to help Walter to recognize things in his life in which he could take pride while in a drug-free and alcohol-free state of mind. These included his skill as a longshoreman, his physical strength, and the love and pride of his children. Still, Walter had difficulty focusing on these factors, especially when he felt frustrated in reaching his goals. At times of despair and anger, he would lapse into all-or-none thinking, believing that he had nothing worth living for. Walter liked to make a point of this by quoting Bob Dylan's immortal line, "When you ain't got nothing, you ain't got nothing to lose." This saying activated the belief that "I have nothing and I am nothing," and fos­ tered his tendency to turn to drags when he would suffer a disap­ pointment. It therefore became critical to (1) discuss the precious things he did indeed have, such as the love and respect of his chil­ dren, and (2) how he would lose them if he were to indulge in drug abuse. It should be noted that one of the most important opportuni­ ties for producing changes in basic beliefs occurs when those beliefs have been activated, as by a disappointment or frustration. On the other end of the socioeconomic spectram we see afflu­ ent patients who have become substance abusers. Some common rationales proffered by more financially successfully substance abus­ ers resemble those of lower socioeconomic status patients, revolving around core beliefs of being ineffective or socially undesirable. One patient stated that he began his cocaine use at a time (ten years ear­ lier) when it was still considered "cool" to get high, and when cocaine was viewed as a drug of particularly high status amongst those on the fast track. He noted that tiie drag accentuated his feelings of power, attractiveness, and invulnerability-feelings that were not only pleas­ ing to him but also congraent with his view of what a corporate vice- president should be. Although he started as a social user, his contin­ ued usage led to physiological and psychological tolerance, which necessitated that he increase the quantity and frequency of his usage. As a result of his financial affluence he was able to continue his habit Managing Life Problems 199 unabated. In this sense, his wealth served as a contributoty causa factor in the development of his full-blown cocaine dependence. Ultimately, his performance at work deteriorated and he was unceremoniously fired. Following this event, he was unable to attain another position at the same level. The patient hypothesized that he had been blackballed within the local corporate community. At this point, he found himself in financial crisis, as he had not diminished his lavish life-style or cocaine usage, although he had ceased to have an income. As a result, he fell into a state of considerable crisis, with a serious cocaine dependence, and faced the threat of bankruptcy. It was only at this advanced stage of life difficulties and cocaine abuse that he sought therapy. At this time, he has succeeded in remaining free of cocaine for a number of months, although he is still moder­ ately depressed about his significant loss of status, money, and friends. Therapy continues to focus on (1) problem-solving with regard to earning

a livelihood, (2) dealing with continuing cravings for cocaine (although they have diminished somewhat over time), and (3) rebuild­ ing his self-esteem, which deflated when he lost his high-profile lifestyle and had to look at himself without the masked feelings pro­ vided by cocaine. Another high socioeconomic status patient reasoned that he began using cocaine in order to increase his energy and confidence. He came to believe that he would be unable to perform his job without the "boost" that he received from using the drug. He also enjoyed the temporaty sense of a release of pressure, and therefore was convinced that cocaine was a stress reducer. Predictably, as his habit grew, his perceptions of the quality of his work became distorted and inflated way beyond reality. He became less productive, and more and more interpersonally aversive due to his advanced symptoms of paranoia and impulsive anger outbursts. In similar fashion to the patient men­ tioned previously, he lost his job and incurred financial debts. Addi­ tionally, he was shunned by his friends and lover after he repeatedly rejected their suggestions that he receive help for his problems. A factor that both high and low socioeconomic status drug-abusing patients have in common is a vulnerability to peer pressure. Lower socio­ economic status patients are frequently confronted by friends and associates who urge them to use, share, and sell drugs. Such patients may come to believe that they will be deprived of meaningful social contact if they avoid evety substance abuser they know. As we wit­ nessed in the case of Dee, the razzing that her brothers gave her for not joining them in their smoking binges provided a strong tempta­ tion for her to use again. In this case, it was vital to help her to seek and develop contacts and friendships with people who were abstinent from drags and alcohol. 200 COGNTTIVE THERAPY OF SUBSTANCE ABUSE Other lower socioeconomic status patients may feel pressured by their associates to prove that they are "one of the gang," or that they have the "guts" to use drags heavily. Walter told his therapist that he was challenged to shoot up a powerful combination of cocaine and heroin by a couple of guys he knew at a junkyard where he often hung out. When the therapist suggested some typical "middle-class liberal" (patient's description) assertive comments that he could make in response to their challenge, Walter replied, "You can't talk that kind of intellectual crap in m y neighborhood. Maybe it works in your neighborhood, but not in mine." With this, the therapist adjusted the intervention by putting the responsibility for generating "proud, drag- free comebacks" onto Walter's shoulders. This episode highlights the role that socioeconomic characteristics play in conceptualizing prob­ lems and designing interventions. The peer pressure may take on a different form among the upper socioeconomic status patients, but it exists nonetheless. For example, a patient at an exclusive party may become convinced that he must join in with the "recreational" cocaine users in order to be consid­ ered one of the "beautiful people." Fortunately, this distorted, over- romanticized view of the wealthy cocaine user has more recently fallen into disfavor, as the extent and ramifications of the nation's cocaine problems have come to light since the latter half of the 1980s. In another vein, the more affluent cocaine user may be motivated by a need to gain even more money, more power, and more success as a way to gain acceptance by the perceived upper echelon in his or her profession or community. In this drive to succeed, the patient may resort to a chemical stimulant such as cocaine in order to give him or her a sense of increased productivity and sociability. When peer pressure (in any form) is a factor that contributes to substance abuse, it becomes necessaty to address the patient's exces­ sive need for social acceptance. In this regard, self-esteem issues come to the fore. Furthermore, therapist and patient must work together to help the patient learn more adaptive social problem-solving skills, so that drags are no longer considered part of the "solution." DAILY STRESSORS Mundane problems or stressors can serve as triggers for patients' drug use. The daily hassles that people face, such as working at a job that entails pressure and deadlines, or one in which they feel trapped for financial reasons, or dealing with two or three unraly toddlers on a continual basis without a respite, can create feel- Managing Life Problems 201 ings that exceed a person's tolerance for discomfort. An accumula­ tion of such stressful events and feelings, experienced day after day, can serve as factors that encourage a person to resort to drags in order to "get through the day." "Dee" was a patient for w h o m the management of evetyday con­ cerns was central to her maintaining abstinence. An important thera­ peutic priority for Dee entailed helping her cope with taking care of her infant son. As a single parent. Dee was confronted with a great deal of change in her daily life when her son was born. She had been happy working long hours as an assistant in a nursing home; now she had to curtail her hours considerably. She had also been used to coming and going as she pleased, as her older children were adoles­ cents who could be trasted to take care of themselves in their mother's absence. Now, Dee's freedom of movement was restricted, and she had to plan her activities with her baby's care in mind. In addition. Dee was vety troubled and annoyed by her son's nocturnal ctying spells. In sum, the evetyday demands of being responsible for the well- being of an infant reinforced in Dee a sense of inadequacy (as a mother), helplessness (in taking care of all her responsibilities), and hopelessness (in ever enjoying life again). These core beliefs were sources of marked anger, frustration, and sadness, the likes of which touched off thoughts and cravings to smoke crack as her "only" source of pleasure and "freedom." It was clear that keeping Dee away from the lure of drugs would necessitate lessons in coping with her new life as the primaty caregiver for a helpless child. Among other therapeutic strategies, problem- solving and the planning of daily activities (working a few hours, arranging baby-sitting for her child, attending a support group meet­ ing, spending time with her baby, reading, etc.) were reviewed and employed. In addition, much time was spent in using Daily Thought Records to counteract Dee's thoughts that suggested to her that her life would now be intolerably restricted. Indeed, she was encouraged to consider rational responses that focused on various potential bene­ fits that she would now receive as a result of her newborn's arrival. For example, she would have the opportunity to disprove all the crit­ ics who told her that she would not be able to raise this child due to her drag habit. Naturally, this rational response was a powerful posi­ tive motivator to engage in the process of cognitive therapy; however, it also gave rise to another automatic thought. Specifically, Dee wor­ ried that a lapse into drag use would lead to evetyone's giving up on her, judging her negatively, telling her "I told you so," and taking her baby away from her. In order to safeguard against this possible eventuality. Dee and 202 COGNITIVE THERAPY OF SUBSTANCE ABUSE her therapist worked on strengthening her reactions to her areas o greatest vulnerability. Specifically, Dee was taught how to better deal with her baby's ctying fits (which perturbed her vety much). In ses­ sion. Dee was instracted to close her eyes and to imagine being at home at a given time when her baby was ctying without letting up. When Dee indicated that she could indeed "hear" her baby Ctying, she was encouraged to express her automatic thoughts. Given Dee's aptitude for vivid imaging, her automatic thoughts traly represented her "hot" (i.e., affectively charged) cognitions. These included "I can't stand it anymore. I have to get out of here," and "I'm going to go out and pick up again [use drugs again], and then m y aunt will have to come and take care of m y son. Then I'll be free again." After recit­ ing these thoughts. Dee was then instracted to imagine what her life would be like in the aftermath of these events. With this, she would become remorseful, and would begin to express rational responses to override the hot cognitions elicited above. As the exercise continued. Dee spontaneously generated more automatic thoughts that further explained her negative emotionality in response to her baby's ctying. She thought, "My baby doesn't love me. M y baby doesn't want to be with me. He'd rather be with the sitter. He'd rather be with m y aunt." These thoughts fed into Dee's sense of rejection. In response. Dee was encouraged to consider alternative meanings to her son's ctying, such as "He's ttying to tell me he's uncomfortable—that he's hungty, or cold, or needing to be changed," and "He's just being a baby. He's not telling me he doesn't love me. He doesn't even understand stuff like that yet. He's just being a baby." Still keeping her eyes closed. Dee was then told to imagine the self-satisfaction she would feel if she resisted the temptation to use drags, and instead proved to herself and others that she was capable of taking care of this child. In addition. Dee was assisted in imagin­ ing the distant future, when her then grown-up son would love her and think highly of her, because she was always there for him and because he saw her as a positive role model. These techniques, repeated in different variations over the course of a number of ses­ sions, were highly efficacious in helping Dee to see herself as being a person worthy of love, and effective in dealing with the stressors of life. As her core beliefs of helplessness and unlovability diminished. Dee became more consistent in remaining abstinent from drugs and alcohol. In turn, her mothering skills improved. Stressors of daily living can include any events that frigger a sense of frustration, anxiety, anger, fatigue, and loneliness. When such events occur frequently, or involve chronic conditions such as living Managing Life Problems 203 in a noxious home environment or in an undesirable neighborhood, then the therapist needs to help drug-abusing patients to anticipate and adaptively respond to their maladaptive reactions to these situa­ tions. In this way, patients may learn to become adept at coping with (and solving) the commonplace triggers that put them at daily risk for substance abuse. LEGAL PROBLEMS Where there is illicit substance abuse, there is the threat of criminal apprehension. This is so not only because of the patient's drag use itself, but because drag use often leads to additional illegal activities as well. For example. Dee was first arrested when she was caught ttying to cash forged checks. Walter's criminal convic­ tion resulted from his hijacking and fencing stolen goods from the docks where he worked. "Charleen" was apprehended when she sold crack to an undercover officer. When a patient enters treatment as a condition of parole or pro­ bation, the therapist needs to be aware not only of the difficulties that the patient will have in trying to stay away from drugs, but also of the difficulties that the patient will have in coping with the constraints and stigma associated with being in legal limbo. Charleen often expressed her consternation at having to be monitored by both the therapist and the parole office. For her, almost evety therapy session and urinalysis served as a reminder that her life was not entirely her own. As she dwelled on all the drawbacks of this situation (e.g., loss of freedom), her anger grew, and with it her defiant desires to renew her drug use as well. Figure 12.2 represents one of the Daily Thought Records that Charleen worked on in order to quell the anger and cravings associated with such negative thoughts about her parolee status. Until she used the Daily Thought Record, Charieen had never considered the advantages that her legal and psychological monitor­ ing provided for her-namely, added support and incentive

to remain drag free. Walter also experienced a significant degree of dysphoria in reaction to automatic thoughts about his legal statiis. In particular, he was frastrated and angered by the limitations set on his traveling by the terms of his parole. He believed that most of his problems had to do with his family members and his neighborhood acquaintances who abused drags. He rationalized (not to be conhised with rationally responding!) that he would stand a better chance of staying away from drags if he could move upstate to a more raral area. In fact, he applied Directions: W h e n you notice your mood getting worse, ask yourself, 'What's going through my mind right now?" and as soon as possible jot down the thought or mental image in the Automatic Thought Column. SITUATION AUTOMATIC THOUGHT(S) EMOTION(S) RATIONAL RESPONSE OUTCOME Describe: 1 Write automatic thought(s) 1. Specify sad. 1. Write rational response to automatic thought(s). 1. Re-rate belief 1. Actual event leading to that preceded emotion(s). anxious/ 2. Rate belief in rational response 0-100%. in automatic unpleasant emotion, or 2 Rate belief in automatic angry, etc. thought(s) 2. Stream of thoughts, day­ thought(s) 0-100%. 2. Rate degree 0-100% dreams or recollection, of emotion 2. Specify and leading to unpleasant 0-100%. rate emotion, or subsequent DATE/ 3. Distressing physical emotions TIME sensations 0-100%. I'm on the bus going 1 I hate this, I hate 1. Hate I have to be watched like this so I won't 1. Hate to my therapy session. this, I hate this! (100%) go back on drugs again and mess up my life (50%) I have to go. I don't 2 Why do I have to be 2. Anger again. (80%) 2. Anger have a choice or I'll watched like this? (100%) I may hate it, but it's better than being (50%) mess up my parole and a crackhead and going to jail. (100%) I'll have to go back 3 I hate being monitored. 3. Frustration 3. Frustration to jail. I hate ruining my day (100%) Being monitored makes me more careful to (80%) to go see my parole stay off drugs, so I guess it's helping 4. Calmed officer and my ther­ me. (60%) down 4 apist. It makes me mad. My parole officer and my therapist want me (50%) I should be allowed to to be OK. I guess they care about me, even 5 live my own life. if they annoy me sometimes. (100% I'm being treated like I guess these meetings could have a good a criminal and a baby. reason. (50% 6 I want my freedom back I'll get my freedom soon enough! (100% now! ! (100% for all thoughts) Questions to help formulate the rational response: (1) What is the evidence that the automatic thought is true? Not true? (2) is there an alternative explanation? (3) What's the worst that could happen? Could I live through it? What's the best that could happen? What's the mosf realistic outcome? (4) What should I do about it? (5) What's the effect of my believing the automatic thought? What could be the effect of changing my thinking? (6) If was in this situation and had this thought, what would I tell him/her? (friend's name) F I G U R E 12.2. Cfiarleen's Daily Tfiought Record. Managing Life Problems 205 to the parole office for a change of venue, but was told that he wo have to wait a considerable length of time before this could be approved. Walter reacted with a sense of hopelessness, along with cynicism and anger. Now, every time he came into contact with the "problem people" he alluded to above, Walter would think that he was now justified in using drags. His rationalization was, "Hey, I tried to get away from these people, but the cops wouldn't let me. If I fuck up, it's on their heads." Naturally, the therapist in this case spent con­ siderable time in getting Walter to modify his views on this matter, and to find alternative methods for steering clear of these "people and places." Another legal concern that drug-abusing patients sometimes face is loss of custody of their children, either to an ex-spouse, a relative, or to child protection services. Dee was one such patient. Her aunt in Baltimore had taken care of Dee's baby son for two months while Dee went through an inpatient drag abuse rehabilitation program. Dee knew that her aunt was waiting in the wings to assume custody of the child if Dee were to relapse. In fact. Dee's aunt had stated that she would seek to become the child's legal guardian if Dee were to demonstrate that she were an unfit mother. Rather than viewing her aunt as a safety net, she saw her as a threat, and often got herself agitated over the possibility that she would lose her baby. Such a perception produced added pressure on Dee, which exacerbated her urges to resume her use of crack cocaine. In this case. Dee was confronted with the vety real possibility of losing custody of her child. The therapist aimed to help Dee to view this as a motivator to stay straight, rather than as a sword of Damocles hanging over her head. Furthermore, rather than suspiciously treat­ ing her aunt as an evil adversaty. Dee was taught to cooperate and work with the aunt. It was noted that they both shared a common concern—namely, the welfare of the baby. It should also be noted that therapists who treat drag-abusing populations are confronted with more legal and ethical questions than are those who freat most other groups. For example, the association between drag use and domestic violence means that therapists have to be especially vigilant to situations that would require a duty to warn an intended victim, or a duty to contact agencies that monitor child or spouse abuse cases. Managing such situations, while also maintain­ ing a constructive therapeutic relationship with the patient, requires considerable skill indeed. Another legal-ethical situation that we have encountered occurs when a patient attends a therapy session in an intoxicated state. Whether or not the therapist chooses to continue with the session is 206 COGNITIVE THERAPY OF SUBSTANCE ABUSE subject to personal choice and/or case-by-case decision-making. Ho ever, if the therapist chooses to interact with the patient, it is impera­ tive that the therapist assess whether the patient has driven a vehicle to the therapist's office. If the patient has in fact driven to session, the therapist should make evety effort to keep the patient off the highway until such time as he or she is sober. In one case, we required a patient to remain in the waiting room for two hours before permit­ ting him to leave the Center. Other alternatives include calling a cab, using public transportation, or contacting a relative who could give the patient a lift. MEDICAL PROBLEMS Drug abuse is associated with a myriad of chronic medical conditions (O'Connor, Chang, & Shi, 1992). Even when the patient has given up drugs altogether, the medical consequences of the abuse may linger indefinitely, causing pain, worry, hopelessness, and renewed urges to "self-medicate" via the use of illicit drags. This phenomenon is well illustrated by a scene in the film Bird, the story of the legendary jazz saxophonist Charlie Parker. Parker, whose hard- drinking, hard-dragging, and hard-driving lifestyle led to the devel­ opment of excruciating gastric ulcers, used heroin to deaden the pain. This habit only served to hasten his death at the age of 34. In one scene, he tearfully tells his drug-free friend, Dizzy Gillespie, "Ain't it a bitch . I go to the doctor and pay him $75, and it don't help m e . . . but 1 go to some 'cat' and pay him $10 for a bag of shit [heroin], and m y ulcers don't hurt, m y liver don't hurt, m y heart troubles is gone . . . and you tryin' to tell m e that this is the man I'm supposed to stay away from? Mr. Gillespie, m y comrade in arms, that is what I call a paradox." Therapists need to be aware of the medical issues involved in substance abuse, so as to be able to educate the patient about such matters, as well as to be able to detect physical signs that indicate that the patient may have relapsed. A patient who is actively abusing hard drags such as cocaine, heroin, or amphetamines, may be a malnourished and sleep-disturbed patient as well. Charieen had the misconception that the use of crack cocaine produced a beneficial weight loss. She lamented her weight gain during her recovery and treatment period, and talked about "the good old days" when she was using and was thin. The therapist taught her that her weight loss reflected a dysfunctional dependence on a drug that in no way substituted for nutrition. He emphasized that Managing Life Problems 207 weight loss needed to be achieved through exercise and sensible ea ing habits, not through drag-induced loss of appetite. It is common for patients who go on drag binges to be awake all night (while they are using), and to sleep most of the day. Another variation of sleep disturbance involves the patient's remaining awake for days at a time, and then crashing for a number of days. In either case, the body's natural sleep cycle has been badly disrupted, and normal vocational and social functioning ceases to be possible. It is noteworthy when a patient misses an afternoon therapy ses­ sion due to "oversleeping," or sounds groggy on the phone in the middle of the day. These are some of the telltale signs of substance abuse (Gawin & Kleber, 1988). In fact, a number of high-profile ath­ letes who were discovered to be cocaine abusers were first suspected as a result of oversleeping for important team practices, meetings, or travel obligations. Whenever practically feasible, we like to schedule our most dif­ ficult patients for the earliest appointments. A 9:00 a.m. appointment minimizes the likelihood that a patient will be able to mask the fact he or she used drugs the day before. At times when an early therapy session cannot be arranged, early-morning phone checks can be uti­ lized. For example, a patient may be instructed (as part of his home­ work assignment) to call the therapist each day at a specified midmoming time, just for a minute. When a patient complains that a session or a telephone call is too early to comply with, we respond by saying, "If you can't attend a therapy meeting at 9:00 a.m., will you be able to keep a job that requires you to be there at 9:00 a.m.?" In the same way that drag-abusing patients are often less than maximally compliant with therapy, they too are frequently noncom- pliant with medical advice. W h e n the patient has a steady physician, it is important to obtain the necessaty releases so as to have ongoing contact with the doctor. When the patient is on public assistance, and therefore may not see the same doctor with each medical visit, the situation is a bit more convoluted. Nevertheless, it is important to make evety effort to keep apprised of the patient's medical conditions and treatments. One of our most stubborn cases of medical noncompliance was "Ray," who suffered from a serious case of diabetes and was insulin- dependent. His maladaptive approach to his condition was a continual cause for concern in treatment. During one period in the course of therapy, he refused to inject himself with his required daily dosage of insulin, saying that he could control his blood-glucose level sim­ ply by watching his diet carefully. W h e n this was questioned, Ray added that the use of a needle (to inject insulin) would be a power- 208 COGNTTIVE THERAPY OF SUBSTANCE ABUSE ful inducement for him to shoot up "something a little harder than insulin." Needless to say, this posed quite a dilemma. To make matters worse, Ray refused to consult with his physi­ cian on this matter. The therapist attempted to appeal to the patient's sense of reason, and expressed a great deal of personal concern for Ray's life, all to no avail.

It was only after Ray began to experience significant physical malaise that he finally relented and contacted his doctor. Once there was open communication between patient, therapist, and physician, the next phase of treatment could begin. This entailed having Ray bring his insulin and needles to session, so that intensive rational responding could be practiced in the presence of the stimuli that elicited his most severe hot cognitions and cravings. Although this intervention involved a degree of risk for relapse, it was deemed by all parties to be less risky than the possibility of diabetic coma. Before long, Ray was successfully administering his own insulin shots, albeit sporadically. Ray's insulin compliance would need to be checked throughout the course of cognitive therapy. One of the most serious medical problems associated with the abuse of cocaine is the increase in prevalence of expectant mothers who are regular users. W e have witnessed a rise in the number of cases where babies are born prematurely, with life-threatening complica­ tions, and with physiological addictions to cocaine, as a result of their mother's habits during pregnancy (Closser, 1992; Grossman & Schottenfeld, 1992; Smart, 1991; Stimmel, 1991). (Additionally, there is recent preliminary evidence that traces of cocaine bind to sperm, thus also implicating fathers in transmitting the harmful effects of cocaine to their unborn children.) Again, education plays an important role in treatment. The thera­ pist can explain to pregnant patients the risks of drag use (and alco­ hol use, as well as cigarette smoking) to their unborn children. Such patients also need to be encouraged to receive regular prenatal medi­ cal attention. Imagety work can help these patients focus on mental pictures of healthy babies versus those who are seriously ill, so as to help sway the patients away from using drugs when cravings arise. One of our pregnant patients learned to recite a standard rational response to herself when she had an urge to go out and purchase crack cocaine. She would imagine a healthy, happy baby, and she would say to herself, "I'm going to start being a good mother right now. I'm going to start taking care of m y baby right now. I'm going to choose health for both of us. I'm not going to go out and use." Another medical problem related to substance abuse concerns communicable diseases, either by sexual contact or via the sharing Managing Life Problems 209 of needles. Substance abusers are notoriously reckless in their se behavior (e.g. Goldsmith, 1988; Watkins, Metzger, Woody, & McLel­ lan, 1991). For example, they are prone to ignore simple measures of protection, such as the use of condoms. Remember (as stated in Chap­ ter 4, this volume) that Walt stated flippantly that it was against his religion to wear a condom. In extreme cases, people who are addicted to hard-core drugs will trade sex for drags. This translates to many people having indiscriminate sexual relations with many other people over time. The risks of contracting a wide range of venereal diseases, hepatitis, and the AIDS viras are substantially increased within this population (Chiasson et al., 1989; Fullilove, Fullilove, Bowser, & Gross, 1990; Stimmel, 1991). Given the fact that many of these people are intravenous drug users who use and share unsterile needles (Metzger et al., 1991), the risk of acquiring AIDS escalates even more. Once again, education is a crucial component of therapy. Three steps toward the goal of safety from transmittable diseases include (1) abstinence from intravenous drug use, (2) practicing safe sex, and (3) remaining monogamous with a trasted partner. W e have found that patients are fairly compliant with point (1), considerably less com­ pliant with point (2), and very rarely compliant with point (3), espe­ cially if they continue to abuse drags. It is extremely difficult to help a patient who is actively abusing substances to monitor his or her sexual behaviors. It is far more realistic to get patients to be sexually safer once they become abstinent from drug use. Nevertheless, every effort must be made to address this medical issue, whether or not the patient is using (see Appendix, page 329, for more information on managing patients who are HIV positive, as adapted from Fishman, 1992). Finally, a most basic and obvious area of medical complication associated with drug use involves the deleterious effects of the drugs themselves (Frances & Miller, 1991). Dangers include damage to the central nervous system, cardiac and respiratoty abnormalities, liver atrophy, and death by overdose. Yet another hazard is encountered when the drag is adulterated by foreign substances. In one notorious case in the Philadelphia area, three men were killed when they smoked the poison-laced crack that was smuggled into their prison cells. SUMMARY In this chapter we presented an overview of the life problems that typically plague substance-abusing populations. W e noted the vicious cycles that occur when such life problems trigger 210 COGNITIVE THERAPY OF SUBSTANCE ABUSE the abuse of substances, which in turn exacerbates the patients' ne tive life situations. C o m m o n problem areas include family and relationship dysfunc­ tion and discord, socioeconomic hardships, chronic, cumulative daily stressors at home and at work, difficulties associated with legal apprehension, and medical conditions and complications. W e dis­ cussed the roles that these problems play in the course of cognitive therapy, and provided case illustrations that highlight methods of addressing such life crises in the context of a comprehensive out­ patient treatment for substance abuse. W e would like to add that we have been strack by the way that some patients are able to make broad-sweeping changes in their lives as a result of their steadfast commitment to the treatment regimen. When positive life changes follow the patient's success in achieving and maintaining a drug-free existence, it behooves the therapist to make certain that the patient understands the nature of this positive feedback loop. In the same way that the therapist teaches the patient to recognize the dangers of the vicious cycles that drag abuse fosters, the therapist reminds the patient to take stock of the beneficial changes that take place as a result of abstinence. When patients fully come to realize how much they can improve their overall life situations, they gain even more motivation to make the most out of therapy and to work at preventing relapse. C H A P T E R 1 3 C r i s i s I n t e r v e n t i o n A crisis is an unplanned, sudden, and often un- desired change in a person's life that typically is associated with emotional distress. The Chinese symbol for "crisis" consists of the combined characters for "danger" and "opportunity." Similarly, in the cognitive therapy of substance abuse, a crisis is viewed as a stressor that simultaneously presents a danger of relapse and an opportunity for learning. To the extent that patients successfully cope with a cri­ sis without using drags, they increase self-confidence and furare cop­ ing skills. The individual who does not cope effectively with crises decreases self-confidence, resulting in weakened coping skills and increased potential for future relapse. Being available to patients in times of crisis is one of the therapist's most important responsibilities. For example, when a patient is acutely suicidal or otherwise in a potentially harmful situ­ ation, it is vital that the therapist be accessible for emergency con­ sultation. Furthermore, it is advisable that the therapist be highly skilled in managing such crises. Patients who abuse drags are espe­ cially prone to get into serious trouble, and a tĵ ical course of therapy with such patients often involves having to handle a number of criti­ cal incidents (Newman & Wright, in press). For example, it is not uncommon to see a patient who seems to be making therapeutic progress, only to have that patient suddenly stop showing up for therapy sessions, and fail to return the therapist's telephone calls. Sometime later, the patient calls the therapist in a highly agitated state, and it becomes clear that the patient has begun to abuse drags once again. Typical crises involve (but are not limited to) renewed drug use, breakups and/or violence in significant relationships, loss of employ- 211 212 COGNITIVE THERAPY OF SUBSTANCE ABUSE ment, depletion of finances, recurring legal difficulties, crimina involvement, medical emergencies, and overdose and suicidality. This chapter serves as a blueprint for the therapist in the han­ dling of the acute crises of drag-abusing patients. W e review and dis­ cuss the most common types of critical incidents, and we explicate some of the therapist's options in dealing with these difficult clinical situations. First, we examine some of the warning signs that should alert the therapist to the possibility of imminent or current crisis in the patient's life. W A R N I N G SIGNS Even when patients are not voluntarily forthcoming about serious difficulties that they are encountering, there are a num­ ber of common telltale signs that indicate that they may be in crisis. Such "crises" may or may not entail drag use. However, more often than not, a crisis that starts out as a non-drug-related event, left unmanaged, turns into an episode of drug use, thus compounding the cri­ sis (Kosten et al., 1986). One common sign is that the patient is habitually late for therapy sessions, or does not show up at all. When a patient misses a session, especially when he or she has not called to cancel officially, it often spells trouble. W e have witnessed many instances when patients not only missed sessions, but literally seemed to disappear for long stretches at a time. When the patient is incommunicado in this man­ ner, the chances are high that he or she is actively using drags, or is embroiled in other serious difficulties. After a patient has failed to show up for a session, the therapist should attempt to contact that patient as soon as possible. If the patient is easily reached by telephone, the therapist can ask the patient directly what is happening (e.g., "Do you know why I'm calling? Did you know that we were scheduled to meet a half hour ago? Can you tell me what's going on right now?"). A more problematic scenario occurs when the patient cannot be reached following a missed session. This scenario is typified by the patient's (1) telephone ringing at all hours of the day and night with­ out being picked up, (2) not returning the therapist's telephone mes­ sages, and (3) relatives or housemates sounding hostile, giving cryp­ tic answers in response to queries about the patient's whereabouts, or giving lip service to their willingness to pass on messages to a patient who ultimately does not return the call. Crisis Intervention 213 In a high percentage of cases in which the patient drops out of sight for more than a few days at a time, drug use has been involved. As such, missed sessions provide the therapist with a conspicuous red flag. Another warning sign that the patient may be in crisis is the patient's demonstrating a marked change in mood or behavior. Examples include (1) a patient who ordinarily speaks clearly and articulates his thoughts well sounds oddly incoherent or otherwise cognitively disorganized during a telephone contact; (2) a patient who almost routinely scores zero (i.e., no self-reported pathology) on such questionnaires as the Beck Depression Inventoty suddenly endorses the most extreme symptom items (e.g., "I would like to kill myself"); (3) a patient who has generally been cooperative and amicable evi­ dences hostility toward the therapist; (4) a patient evidences labile affect in session, such as shifts between agitation, ctying, and "silli­ ness"; and (5) a relative of the patient telephones to say that the patient is acting "out of control" and pleads for the therapist to intervene immediately. Although these examples are the most typical, they by no means represent an exhaustive list. Whenever possible, pronounced changes in patients' functioning should be addressed as soon as possible. A skilled mixture of accurate empathy and frank confrontation is called for in such instances. In this manner, the therapist may strengthen the therapeutic relation­ ship while also making strides to stabilize the patient and begin to deal with the sources of the

crisis in a constractive manner. Yet another red flag for the therapist to notice and address is the patient's sounding or looking abnormally groggy, on the telephone or in person, especially during the middle of the day. One of our patients used the excuse that she had worked "the late shift" the day before a session in which she appeared extremely fatigued and sub­ dued. The excuse seemed plausible at first but began to lose credibil­ ity when she began to miss sessions and then answered the therapist's telephone calls in similar states of retardation, regardless of the time of day that she was called. Furthermore, when asked to schedule her sessions in such a manner that she would not have to arrive after working "the late shift," this patient was unable to produce a work schedule of any sort. At this point, the therapist told her point blank that he believed that her drowsiness was drag or alcohol related, and that this was a vety serious problem indeed. Patients rarely are eager and enthusiastic to report on renewed drug episodes or their concomitant crises, but they may be more willing to discuss "close calls." W h e n a patient spontaneously reports 214 COGNITIVE THERAPY OF SUBSTANCE ABUSE that he "almost used drags this past week", it is a sure-fire bet he will have at least another close call this week. More than likely, he has actually already used drugs during the past week, and will probably use even more drags in the coming week. When this topic comes to light in session, the therapist must be alert to make it the number-one priority item for the session. The rest of the session must involve a concentrated effort to plan an emergency strategy to ward off drag use once the patient leaves the office. When the patient does not mention near-miss drag episodes on his or her own, the therapist may choose occasionally to ask, "Have there been any times this past week when you were tempted to use drugs? What's the closest that you came to using?" Such questioning may lead to the discussion of problems and potential crises that the patient may not have volunteered to discuss. When therapists are aware of the warning signs of renewed drug use and other crises, they stand a much better chance of keeping their drag-abusing patients in treatment. In doing so, they may also suc­ ceed in nipping major problems in the bud, and dealing with full­ blown emergencies before they lead to harm or incarceration (Newman & Wright, in press). CRISIS SITUATIONS In the sections that follow, we discuss some common crises that are often directly related to the use of alcohol and illicit drugs. These crises include overdose and suicidality, loss of domicile, disappearance, loss of employment, loss of close personal relation­ ships, medical emergencies, criminal involvement, and violent con­ frontation with the therapist. Overdose and Suicidality Whether by accident or in a deliberate attempt to harm one's self, an overdose of illicit drags (perhaps in combination with alcohol or legal controlled substances) represents a potentially life-threatening situation. In many instances, the therapist of a patient who overdoses will not know about the episode until after the damage is done. For example. Dee called her therapist from her hospital bed, saying that she would not be able to keep her therapy appointment due to her hospitalization for a severe asthma attack. Later, when the therapist consulted with the physician on her case, it was learned that her attack Crisis Intervention 2 1 5 was induced by cocaine intoxication, and that Dee had nearly asphyx ated. On rarer occasions, a patient will call the therapist to inform him or her of a drug overdose. W h e n the overdose is an accident, the patient will likely be in a state of panic and confusion. An attempt should be made to confirm the patient's location, and to explain that the therapist will be calling "911" in order to have an ambulance sent. If a friend or relative is on hand, that person may be asked to do the same. In cases in which the patient is alone and is too incoherent to provide an address, the therapist will need to have handy such basic information about the patient. A simple solution is for the therapist to keep copies of all patient telephone numbers and addresses both at work and at home. When the overdose is a suicidal gesture or attempt, the same need for an ambulance exists. (Needless to say, under such conditions the therapist does not have an obligation to protect the patient's anonym­ ity; therefore it is appropriate to break confidentiality in order to save the patient's life.) However, if possible, it is important to keep the patient on the line. This is particularly necessaty when the patient is unwilling to reveal his or her whereabouts. When Ray called his thera­ pist at home (and reversed the charges) on Thanksgiving Day, he claimed that he had taken enough heroin and cocaine "to kill an elephant." He refused to say where he was, save to note that he was at a telephone booth. Luckily, the therapist had two telephone lines at home and was able to write a message to his wife, signaling her to call an operator from the other line in order to trace Ray's call. Although the therapist kept the patient on the line for 50 minutes, the trace was unsuccessful. The therapist proceeded to call the police directly, giving a description of the patient and recommending places that he could most likely be located. Fortunately, Ray's claim was exaggerated, and the "suicide attempt" merely made him sleep for most of the next 24 hours. When the suicide call comes directly to the therapist's office, it may be possible to contact a colleague in the same manner that the therapist in the above example contacted his spouse. In sum, the therapist should (1) determine the patient's location, (2) keep the patient on the telephone, or in the office as the case may be, (3) assess the degree of severity of the suicidal behaviors, and (4) contact the police, an ambulance, or another person in the vicinity who can do this for the therapist while the therapist gives the patient undivided attention. In the case of a suicidal emergency where drugs have not already been ingested, but rather the patient is making threats that have not 216 COGNITIVE THERAPY OF SUBSTANCE ABUSE yet been carried through, the therapist can afford to respond a bi cautiously and methodically. If a patient is feeling hopeless as a result of renewed drag use, or has suffered a loss as a result of the abuse of substances, the suicidal wishes may be reduced by attacking the hope­ lessness directly. If successful, the therapist may not have to contact the police or an ambulance. Instead, a face-to-face therapy appoint­ ment should be arranged as soon as possible (e.g., same day or first thing the next morning). The situation becomes a bit more cloudy when the patient is suicidal while under the influence of drags or alcohol. Even when the patient has not taken an overdose the intoxication still may result in an irrational exacerbation of the patient's intentions to self-harm by other means (Marzuk et al., 1992). Under these conditions, the patient may not be capable of following the therapist's instractions, or of understanding the therapist's attempts to help. If the therapist senses that this is the case, it is necessary to take the safest course of action. This may entail contacting and instracting a relative of the patient to admit the patient to hospital or the therapist's calling for an emergency vehicle directly. Loss of Domicile Another drug-related crisis entails the patient's being expelled from his or her household, usually by a spouse, parent, housemate, or landlord who has gone beyond the limits of toleration for the substance abuser's extremely maladaptive behaviors. In some instances the patient has an alternative place to go, such as to another relative or a friend. Unfortunately, unless the patient changes his or her behavior, the same sequence of events may recur. Ultimately, such patients may find themselves with no place to go but out on the streets, in shelters for the homeless, in drug houses, or (if they are lucky) an inpatient facility. When a therapist becomes aware that a patient has been forced out of his or her domicile, it is advisable that the therapist elicit per­ mission from the patient to consult with the patient's parole officer or with a social worker. This allows the therapist to improve the patient's chances of gaining admission to an inpatient drug abuse rehabilitation program. Although the inpatient setting may provide only a short-term solution to a long-term problem (Cummings, 1993), it is far better for patients to be receiving medical supervision than to be languishing on the streets. Furtherniore, the patient's participa­ tion in an inpatient program may help him or her to regain favor Crisis Intervention 217 with family members, as well as to reestablish a program of outpati cognitive therapy after discharge. Disappearance At times, crises emerge not when patients are forced to leave their homes, but instead when they suddenly disappear from their residences. As noted earlier, this usually indicates that the patient is on a drag binge, and may be taking shelter with others who are also "on a ran." This type of crisis is one of a variety about which patients do not contact their therapist. Although patients who "dis­ appear" to places such as crack houses (for days at a time) may be losing money, jobs, family ties, physical health, and other important facets of life, they typically do not realize their own states of crisis until after the ran is over. At this point, the patients are forced to face the devastation that they have wrought. They have to face their lack of money; their now accentuated drug urges; their poor physical hygiene and condition; their irate relatives, employers, and landlords; and possible legal consequences, especially if their parole officers track them down. When patients leave their homes to go out on a drag run they may be almost impossible to locate. Still, it is important for thera­ pists to continue to try to reach them by telephone or by mail, and to be prepared to resume treatment with them once they return (or once they are apprehended). Therapists of patients who reappear following their binges may feel particularly frusttated, disappointed, and angry at the patients over thqir self-defeating and antitherapeutic behaviors. A common auto­ matic thought we have shared in response to this very type of situa­ tion might translate to the following: "After all the work I've done with this patient, he has some nerve leaving therapy to go out on a binge! How dare he rain all the painstaking work we've done together, just for a temporary high. N o w he expects me to pick up all the pieces for him again!" Such automatic thinking needs to be counterbalanced by rational responses that highlight the patient's genuine state of des­ peration, the therapist's opportunity to continue to offer earnest pro­ fessional help even under conditions of adversity (thus, hopefully strengthening the therapeutic relationship), and the realization that the therapist does not have to "pick up all the pieces." It is signifi­ cant just that the therapist demonstrates a willingness to continue to work with the patient. However, much work will need to be done to minimize the risk of a repetition of such an episode. This includes 218 COGNITIVE THERAPY OF SUBSTANCE ABUSE emphasizing the importance of the patient's contacting the therapi on a regular schedule, and whenever cravings for drags are elevated. Loss of Employment Persons who are actively abusing drags rarely make good employees. Often, drag use leads to the patient's arriving late for work, missing days of work, doing inefficient work, and at times losing the job altogether. A patient who loses a job may react with anger, anxiety, frastration, hopelessness, accentuated reductions in self-esteem, and a wide range of other negative emotions. These feel­ ings, along with their concomitant automatic thoughts and beliefs, represent significant threats to the

patient's abstinence. For example, a patient who derived most of his self-worth from his job will prob­ ably react quite adversely to being laid off. He may then believe that he has nothing to lose (including his pride, which has already been damaged) by going out and getting "stoned." In this scenario, the patient might think "1 worked so hard to stay off drags, and look what it got me—nothing but trouble! If that's the way it's going to be, 1 might as well just go out and get messed up!" When a therapist learns that a drug-abusing patient has lost a job, swift and concerted effort is called for to help the patient solve this life-disrupting problem. Obtaining new legal sources of income becomes a high priority agenda item. Such sources include unemploy­ ment insurance, public assistance, or another job. Newly fired patients must not be given tacit permission to give up, to abdicate all finan­ cial responsibilities to their families, to anesthetize themselves with more drags and alcohol, and to seek money through illegal means. Naturally, the substance abuse problem per se will continue to be addressed; otherwise the patient's resultant poor work habits will result in further losses of jobs. If the patient states that he or she no longer can afford to attend therapy, the therapist would do well to show sympathy for this posi­ tion. However, the therapist should impress upon the patient the importance of attending at least one session in order to address this crisis in a productive way. The therapist may then wish to consider making special arrangements for the patient to continue with treat­ ment, such as a reduced fee (when possible) and/or reduced frequency of sessions. In the case of parole-office-referred patients, or research cases, unemployment should have no bearing on the patient's con­ tinuing with therapy, as the expense typically is covered by a third party. The two focal points of the session should involve (1) assess­ ing and modifying the negative feelings, thoughts, and drag urges that Crisis Intervention 219 may have arisen as a result of the loss of the job, and (2) plannin and problem-solving with regard to making ends meet financially, while also beginning the process of looking for new employment. In addition, the therapist needs to engage the patient in an exploration of the possible results of attaining employment. This would involve discussions about such issues as (1) how the patient will "unwind" after work without resorting to drags or alcohol, (2) how the patient will spend and save money, (3) what kinds of thoughts and beliefs are likely to be triggered as a result of adjusting to a new job, and (4) how to respond rationally to drag urges that may crop up or escalate in reaction to the changes associated with the job. Loss of Close Interpersonal Relationships A rift with a significant other represents another cri­ sis that often develops in patients' lives as a result of their substance abuse. W e have seen patients become extremely dysphoric, angry, and hopeless when parents have "disowned" them, mates have broken up with them, contact with their children has been denied them (e.g., by an ex-spouse or the courts), and members of their family or circle of friends die. Needless to say, the therapeutic relationship takes on fremendous significance at these points, as patients may infer that they will lose the support of the therapist as well. Newly broken romantic and marital relationships in particular often put patients at risk for renewed drag use. Patients may seek solace in their drags of choice, hoping to anesthetize themselves from the pain of interpersonal loss. Even if such patients do not attempt to use drags as a form of self-medication, they may deliberately engage in self-destructive behavior out of anger, hopelessness, or a desire to manipulate the other party. In one case, a patient started an alcohol and cocaine binge in order to make his ex-girlfriend feel guilty and responsible for his "fall." He admitted later that he believed that she would take him back if he could convince her that the breakup "drove [him] to drink and drug again." In another case, a patient explained that when her boyfriend threw her out of the house she thought to herself that, "Nothing don't matter no more anyway, so I might as well get wasted." Consequently, she spent the night at a crack house and resumed her heavy use of the drag. A particularly disturbing form of interpersonal crisis related to substance abuse is domestic violence. W h e n the patient is the perpe- frator of physical or sexual abuse of a minor, the therapist will be legally obligated to inform child protection authorities. In order to 220 COGNITIVE THERAPY OF SUBSTANCE ABUSE keep the patient in treatment, and thereby help to control this se ous problem, we strongly advise therapists to encourage their patients to report themselves to the appropriate agencies while in the therapist's presence. The therapist who is willing and able to remain collaborative under these most trying of circumstances stands the best chance of helping abusive patients work toward change. When the patient is the victim of violence in the home, the thera­ pist will need to have ready access to telephone numbers of protec­ tive shelters and support groups. Therapists should pay particular attention to their female patients who are involved with substance- abusing males, as this type of relationship is significantly correlated with domestic violence, and with the victim's retreat into heavier drag and alcohol abuse as a "coping" mechanism (Amaro et al., 1990). When patients experience crises in their most important relation­ ships, it is helpful for therapists to provide support and to encourage their patients to discuss their sense of loss, anger, or guilt. Two criti­ cal points need to be emphasized to the patient: (1) that the therapist will not abandon the patient, even as others may have cut off emo­ tional ties, and (2) that the patient has some measure of control over these interpersonal losses, to wit, the patient is capable of doing things to precipitate loss, and the patient is also capable of changing behav­ iors in order to facilitate reconciliation or new relationships. In cases in which reconciliation is impossible, such as when a loved one dies, the therapist must react with great sensitivity to the patient's grief, yet still be willing to call attention to the patient's increased risk for drag use. As with any crisis, the patient's risk for suicide should be assessed. Medical Emergencies Patients who abuse drugs and alcohol incur substan­ tially greater risk for acute medical crises than does the general popu­ lation. Examples include the alcohol abuser who experiences bleed­ ing gastrointestinal ulcers, the pregnant crack abuser who goes into premature labor, the diabetic who neglects his insulin in favor of shooting heroin and then lapses into a coma, the asthmatic woman who begins to asphyxiate after smoking free-base cocaine, and others. An increasingly prevalent example is provided by "Roland," who discovered that he was seropositive for HIV. He called the therapist in an extreme state of agitation when he received the results of the test, saying over and over again that "I'm going to die, I'm going to die!" The therapist's first response was to offer a great deal of sympa- Crisis Intervention 221 thy and to let the patient vent. Next, the therapist assessed wheth there was any immediate risk for drag use or suicidal behavior. Finally, after spending 30 minutes on the telephone, the patient was suffi­ ciently calmed down to the point where he could be engaged in look­ ing for signs of hope. Specifically, it was noted that although the patient was seropositive, he was asymptomatic and might remain that way for many years to come. Therapist and patient agreed that in order to maximize this incubation period, Roland would have to live as healthy a lifestyle as possible, including abstention from drags. In this manner, Roland would increase his chances of surviving long enough to see the day when effective treatments or a cure could be devel­ oped. Later, when Roland arrived for a face-to-face therapy session, he was in a positive enough state of mind to address issues of sexual responsibility to his partners. In the meantime, the therapist contin­ ued to show empathy for Roland's medical condition, and disproved the patient's hypothesis that even the therapist would now treat him as if he were a social pariah. In many instances, therapists will be unaware of their patients' medical emergencies until after an acute crisis has passed, with treat­ ment already received. Here, the therapist's job is not so much to help solve the crisis as it is to reengage the patient in the work of therapy, with special emphasis on the ways that the patient's drag use and unhealthy lifestyle practices may have contributed to the emergency. The new goal is to take whatever steps are necessary in order to mini­ mize the risk of further medical complications. On those occasions when the patient informs the therapist that a serious medical problem is going untreated, it is imperative for the therapist to encourage the patient to consult a physician, or to go to the emergency room of the nearest (or most appropriate) hospital as soon as possible. W h e n the patient indicates that he or she is inca­ pacitated by the illness, injuty, or disorder, the therapist may be required to take the kinds of life-saving steps described earlier in the section on overdose and suicidal crises. At times, patients will strongly resist the therapist's pleas to seek medical help, either because the patients want to worsen the crisis (e.g., due to hopelessness and passive suicidality), because they resent the implied "weakness" or loss of control over their bodies, or because they fear that hospital tests will reveal their active drug abuse. In such cases, when the therapist's attempt at support and reason fall on deaf ears, the therapist may need to call for medical help without the patient's consent, and hope to repair the therapeutic alliance after the medical crisis remits. The therapist should emphasize that this does 222 COGNITIVE THERAPY OF SUBSTANCE ABUSE not spell the end of the therapeutic relationship, but rather a ne saty break while the patient receives medical treatment. Criminal Involvement When patients slip back into regular drag use they run the risk of getting involved in a wide range of criminal activities, the likes of which will certainly compound a state of crisis. For example, months after Walter precipitously and prematurely dropped out of therapy, it was learned from his parole officer that he had gone into hiding to escape apprehension and beatings at the hands of organized crime figures. It seems that as he resumed his use of cocaine, he began to borrow large sums of money from loan sharks. This was a stark example of his poor judgment and planning skills (especially when under the frequent influence of cocaine), as there was no way that he would ever be able to repay his exorbitant debts. In the end, Walter resorted to committing burglaries in order to attain enough money and goods to pacify the loan sharks. Eventually, he was caught by the police and reincarcerated for a number of months. When he was released, he resumed therapy. When therapists learn that a patient is actively breaking the law, they must first determine whether other parties are at risk of being harmed. If so, there is an obligation to alert the police, as well as the intended victim. Ideally, this can be avoided if the patient is either willing to work with the therapist to cease and desist from the crimi­ nal activity in question or willing to voluntarily come clean to his parole officer or voluntarily commit himself to hospital for inpatient or day hospital psychiatric and drag abuse treatment. If no others are at risk, the therapist and patient must work to find and implement problem-solving behaviors in place of the illegal behaviors. Cognitive techniques can help the patient to generate viable options, and to combat beliefs that "There's nothing I can do about this problem," or "There ain't no way out of this

situation except [to engage in the illegal activities]." Violent Confrontation with the Therapist Another related crisis—that we have been fortunate enough rarely to have encountered at the Center for Cognitive Therapy—is one in which the patient threatens the therapist with bodily harm. If the threat is purely verbal, and the patient has no weapon and does not make physically menacing gestures toward the therapist, the therapist may be able to defuse the situation simply by Crisis Intervention 223 showing a sjmipathetic interest in understanding the reasons for t patient's anger. W h e n the patient has calmed down a bit, the thera­ pist can explain that there is no need for the patient to make threats toward the therapist. For example, the therapist can say, "Mr. Smith, it's okay that you're angty with me. I want to know why, and I want to work things out between us so that we can continue to work together. However, it is extremely unhelpful if you say you're going to hurt me, because then I have to turn m y attention away from your needs and onto m y own need for safety and self-defense. If we are going to continue to work together, I must insist that you never make any threats or take any harmful actions toward m e again. Does this make sense to you?" When the threat is more serious, such as when a patient assaults the therapist or produces a weapon, the therapist has to choose quickly whether to flee from the situation (if possible) or to muster all his or her empathic skills in order to mollify the patient until the acute threat has passed. Under such conditions it is appropriate to enlist the assistance of colleagues and/or the police, and it is also within the therapist's ethical prerogatives to choose to discontinue seeing this patient (principle of self-preservation). If the therapist is out of dan­ ger and the patient is still present, the therapist may also choose to go on with the therapeutic contract after explaining the ground rales as noted previously. Fortunately, we have found the incidence rate of such crises to be especially low in an outpatient setting. SUMMARY: GENERAL PRINCIPLES IN MANAGING CRISES When patients respond to crises by using drags, it is highly advisable that they contact a helper in order to prevent the episode from progressing to a full-blown relapse. Therapists should stress to their patients that a lapse into drag use may serve as grist for the therapeutic mill, and therefore may be used advantageously in treatment. They can explain to their patients that the renewed use of drags does not mean that the patients are "failures" in treatment, and that the therapist still will be willing to help. Therapists can tell the patients that it is not necessaty—indeed, it is often harmful—to isolate themselves from helpful others after using drags. Once the therapist has succeeded in establishing contact with a patient during or following a crisis, there are at least four important principles that the therapist must follow. First, the therapist has to be aware that in such instances the patient will probably want to resort 224 COGNITIVE THERAPY OF SUBSTANCE ABUSE to the abuse of drags as a "coping" technique. Therefore, along wi offering support and accurate empathy, the therapist must assess the patient's intentions to use drags in this manner. A great deal of thera­ peutic work will be required in order to help the patient to remain drag-free under these conditions. Second, it is imperative that the therapist be alert to the patient's hopelessness and fatalism (e.g., "I'm always going to be jinxed. Why should I even tty to get m y life back together again? It won't do any good anyway."). Unless vigorously combatted, such an outlook will put the patient at risk for drag use, flight from treatment, and other self-defeating behaviors. Third, the therapist can help the patient to use the current crisis as an opportunity to practice coping skills without using drags as an escape or cratch. Here, the therapist assists the patient in viewing his or her predicament as a "test" that, if passed, may signal trae progress toward recovety. There is also the added benefit of the patient's gain­ ing a sense of self-efficacy with each such crisis that is handled suc­ cessfully without the use of psychoactive substances. Fourth, in order to prevent treatment from being reduced to focusing on one crisis after another, therapists can look for the com­ m o n dysfunctional beliefs and common problematic behaviors that underlie a seemingly disparate set of crises. For example, a patient's repeated interpersonal rifts (with spouse, family of origin, employer) may aU be linked by a common theme, such as the patient's resis­ tance to being told what to do and what not to do. In such a case, the therapist can help the patient to spell out the dysfunctional beliefs; for example, "If I listen to someone's advice, it means that I'm being controlled," and "If I'm being controlled, I'm not a real man." By focusing on these beliefs and their concomitant problematic behav­ iors, the therapist can maintain better structure and continuity in therapy. As therapists are human, they are not immune to being stymied by crises that patients present to them. At such times, we strongly recommend that therapists consult with other professionals, includ­ ing case workers, parole officers, and fellow clinicians. For example, when legal problems have arisen, we have held therapy sessions that included the patient's parole officer. O n occasion, this has provided an interesting "good cop-bad cop" scenario, with the parole officer reading the patient the riot act while the therapist intervened to reengage the patient in some serious and concerted therapeutic work in order to stay out of further trouble. Finally, we would like to reiterate a rather sobering as well as hopeful point. Substance abuse patients, as a group, will almost cer- Crisis Intervention 225 tainly experience and present with more crises than do most other types of patients. This means that the therapist will rarely be able to rest easily with such cases, no matter how well things may seem to be going in treatment. O n the other hand, therapists who are prepared to handle such crises, and who persevere in teaching patients to deal with them, have the opportunity to make significant positive impacts on their patients' lives. There is a great sense of intrinsic reward in seeing patients through their toughest times, and in witnessing them turn their lives around for the better. C H A P T E R 1 4 T h e r a p y o f D e p r e s s i o n i n A d d i c t e d I n d i v i d u a l s J. T X o o d disorders are a frequent concomitant of substance use disorders. The comorbidity ranges from 13.4% in alco­ holism to 2 6 % among general drag disorders (other than alcoholism) (Regier et al., 1990) to 30.5% specifically for cocaine abusers (Rounsaville et al., 1991). It is important to be aware of the presence of depression: first, because it may be a profound source of suffering for a given patient; second, because it reduces the prognosis for recovery from substance abuse; and third, because it is a clear-cut indication for interaction by a trained professional rather than a coun­ selor (Woody et al., 1983). It should be noted that it may not be possible in some cases to make an absolute diagnosis of depression for several months after a drag- addicted individual has completed a detoxification program since the use of drags may in itself produce a clinical picture similar to a mood disorder or some other syndromal disorder. However, a careful history and clinical evaluation based on an instrament such as the Stractured Clinical Interview for DSM-III-R Disorders (SCID: Spitzer, Williams, & Gibbon, 1987) and the Beck Depression Inventoty (BDI: Beck et al., 1961) may help to tease out a trae depression. In any event, the negative thinking and beliefs typical of depression ("depressotypic") should be addressed as part of the therapeutic regimen. APPLICATION OF THE COGNITIVE M O D E L OF DEPRESSION The approach to depressed drug abusers can be for­ mulated in ways similar to depression in general (Beck et al., 1979; 226 Depression 227 Carroll, 1992). It is helpful to inquire about the negative cogniti triad (Beck, 1967): patients' view of themselves, their immediate life situation, and their future. Much of this negative triad has a particu­ lar coloring relevant to drag use but, in most respects, it is the same for the drag-dependent depressive as for the nonabuser depressive. The depressogenic automatic thoughts and beliefs of each are phrased in similar or identical words and the thinking disorder and pervasive negativity are the same. Individuals who see themselves as trapped in a situation over which they have no control, believe that they are helpless or socially undesirable, and can see only a wall of difficulties and disappoint­ ments ahead are likely to (1) feel sad, (2) express pessimism about the future, (3) consider suicide as the only solution, (4) experience a subjective loss of energy, (5) lose motivation to attempt any construc­ tive activity ("because it is useless and I will only fail"), and (6) lose satisfaction from sex, eating, or other formerly pleasurable activities. In addition, such individuals are likely to become dependent and indecisive. Each of these symptoms can become a target for therapeutic intervention (see Beck et al., 1979). Because of the high risk of sui­ cide in depressed drug abusers and alcoholics (Mirin & Weiss, 1991), special attention must be directed toward suicidal wishes. BELIEFS ASSOCIATED W I T H DEPRESSION Certain negative beliefs are typical of depression but also are observed in some addicted individuals who are not depressed. As described in Chapters 2 and 3 (this volume), these dysfunctional beliefs have a powerful effect on the addicted individual's thinking, feeling, motivation, and behavior. The kinds of beliefs that are typi­ cal of depressed individuals who abuse drags or alcohol are listed below. NEGATIVE SELF-CONCEPT "I am helpless (because I can't control using)." "I am weak (because I can't resist craving)." "I am unlovable." "I am defective." "I am worthless/disgusting (because I have a 'dirty' habit)." "Everything I do is wrong." "I am a failure." "I am frapped." "I don't have the will power to stop using." 228 COGNITIVE THERAPY OF SUBSTANCE ABUSE NEGATIVE VIEW OF PAST "I have never done anything right." "Nothing has worked out for me." "I have always been unhappy." "I have messed up m y whole life." "My whole life is a big failure." NEGATIVE VIEW OF LIFE SITUATION "People despise m e for m y addiction." "My family has given up on me." "There are so many demands on me, I can't handle them." "My family is watching m e all the time." "My neighborhood is impossible." "My job is dull and depressing." NEGATIVE VIEW OF THE FUTURE "If I try something, it won't work out." "I will never get what I want." "My future is hopeless." "Things can only get worse." "I will never be able to stop using." "I don't have anything to look forward to." "I don't deserve anything better in life." These beliefs can be subjected to exploration by the therapist in a series of maneuvers such as (1) looking for evidence to counteract the dysfunctional belief, (2) examining the logical relation of these beliefs to actual experiences, and (3) testing the beliefs in planned experiments. The preceding checklists should be used to help focus on the specific negative beliefs and also to monitor the patient's progress. Therapists should note that it is particularly important to assess and modify patients' beliefs about their "complete inability" to overcome their drug abuse, especially in light of research that sug­ gests that self-efficacy beliefs profoundly affect treahnent outcome and maintenance (Buriing, Reilly, Moltzen, & Ziff, 1989). THERAPEUTIC APPROACH Timing of Intervention By preparing a comprehensive formulation of the patient's depression (see next section), the therapist can make tenta­ tive decisions as to the type and timing of interventions. In deciding

Depression 229 which strategies to use initially, the therapist should consider t following questions: 1. Is the depression so painful that the emphasis should be on symptom relief rather than on an immediate confrontation of the using or drinking problem? 2. Is it likely that relieving some of the symptoms will reduce the pressure to use? 3. Will providing the stracture (inherent in cognitive therapy) for controlling the craving and using itself reduce the depression? 4. Can the therapist use the drag control and antidepression pro­ grams concurrently? 5. Are the suicidal tendencies and hopelessness sufficiently sfrong to warrant robust antisuicidal intervention and precautions? Certainly, if the patient is acutely depressed and suicidal, the therapist's attention should be focused on this serious clinical prob­ lem. By focusing on improving the patient's mood, the therapist not only reduces the patient's risk of suicide, but also may help the patient to feel better equipped to manage the drag problem (Hall et al., 1991). Case Formulation The case formulation is as important in treating depression as it is in treating drag abuse in general. The following symptomatology should be covered: (1) cognitive, (2) affective, (3) physiological (e.g., sleep disturbance), (4) motivational (giving up, avoidance, lack of drive, ambivalence, suicidal wishes), and (5) behavioral ("retardation," inertia, agitation). The cognitive symptoms in particular should be identified—spe­ cifically, the automatic thoughts and the types of distortions. The therapist should also tty to link up the automatic thoughts with the consequent affective or motivational symptoms. For example, the thought "It's useless to do anything, I'll only feel worse" can be linked to the patient's loss of motivation and consequent avoidance or inactivity. The thought "Evetything is hopeless. I can never get what I want" can be linked to patient's suicidal wishes. The thought "I am all alone; nobody cares" can be tied to sadness. The thought "I have messed up m y life" can be tied into the patient's self-criticisms. As the patient's life histoty unfolds, the therapist can constract a diagram such as that shown in Figure 14.1. In this case, the patient attempted to break the rigid pattern of blind obedience to the group's demands, but by becoming isolated he experienced his childhood- based belief in his unlovability and became depressed. 230 COGNTTIVE THERAPY O F SUBSTANCE ABUSE Parents and siblings were hypercritical. Early history IVIother abandoned family at age 8. Nobody helped patient with his problem. i Core belief I am helpless, alone. Nobody cares for me. i Compensatory Join gang: Get acceptance through blind strategy obedience (e.g., using cocaine). Conditional belief If I want acceptance, I have to go along. T Specific stressor Rejected by peer group because won't engage in dealing, etc. I am alone. Sad, lonely Uses cocaine for seif-medication FIGURE 14.1. Relationship of developmental factors to basic beliefs and using. The therapist should prepare a conceptual diagram such as that s h o w n in Figure 14.1. At an appropriate time, the therapist should s h o w it to the patient and explain the sequence of external events and external reactions. SELECTING TARGET SYMPTOMS It is difficult to specify in advance which problems should be selected for intervention during an interview and at what level these problems can be approached most effectively. In general, for the moderately to severely depressed user, the focus of the thera­ peutic intervention is at the level of s y m p t o m s ("target symptom level"). The target s y m p t o m is defined as a c o m p o n e n t of the depres­ sive disorder that involves suffering or ftinctional disability. The spe­ cific target symptoms m a y be divided into five categories (see Beck, 1967, for a more complete description): Depression 231 1. Affective symptoms. Sadness, loss of gratification, apathy, loss feelings and affection toward others, loss of mirth response, anxiety. 2. Motivational. Wish to escape from life (usually via suicide), wish to avoid "problems" or even usual evetyday activities. 3. Cognitive. Cognitive errors such as dichotomous thinking, overgeneralization, selective abstraction, personalization; errors are frequently linked to harsh self-criticisms (e.g., "I am a worthless per­ son" or "I am no good and don't deserve to get any satisfactions"). 4. Behavioral Passivity, (e.g., lying in bed or sitting in a chair for hours on end); withdrawal from other people, retardation, and agitation; total reliance on drags or alcohol to escape or moderate dysphoria. 5. Physiological or vegetative. Sleep disturbance (either increased or diminished sleeping); appetite disturbance (either increased or decreased eating). The therapist (in collaboration with the patient) makes a deter­ mination as to which of the target symptoms should be addressed on the basis of many factors: 1. Which symptoms are the most distressing to the patient? 2. Which symptoms are most accessible to therapeutic interven­ tion? In general, the techniques may be classified as predominantly behavioral—engaging the patient in specific activities or projects, which, in themselves, help to ameliorate some of the suffering; and predominantly cognitive—in which the major focus is on the patient's thinking. When the patient's depression is less severe, the therapeutic focus is often on the kinds of problems that are related to the precipitation or aggravation of the depression. These problems include difficulties at home, school, or work. Many users become depressed after a loss, such as a disraption of a close personal relationship, particularly the death of a close person. Personal losses also occur through legal, financial, and medical problems associated with use. In severe depres­ sion, in which the patient feels totally out of control over drag using, the therapist might want to focus on ways to help the patient to con­ trol his craving and to structure his day in such a way as to distance him from his craving. Some depressed users engage in nondrag activities but derive little pleasure from them. This failure to derive gratification may result from (1) an attempt to engage in activities that were not satisfying even prior to the depressive episode, (2) the dominance of negative cogni- 232 COGNTTIVE THERAPY OF SUBSTANCE ABUSE tions that obscure any potential sense of pleasure, (3) selective tention to actual experiences of pleasure, or (4) a belief that none of these activities can ever replace the high that once was achieved by drug use. Other depressed drag users may not engage in vety many non-drag-related activities, due to lack of skills, inattention to the existence of such activities, a sense of apathy, or the sheer time- consuming nature of finding, using, and responding to drags. There­ fore, simple attention to the cessation of drag use is an incomplete therapeutic strategy. It is imperative that such patients develop sources of nondrug positive reinforcement, such as work, hobbies, and prosocial recreation (Stitzer et al., 1984). Eliciting Automatic Thoughts and Beliefs Some depressed patients find it difficult-or may be unwilling—to bring up topics for discussion in session; which may be the consequence of the depression itself. Among the depressive fac­ tors that may account for patients' lack of productivity are the fol­ lowing: difficulty remembering specific problems since the last ses­ sion, a general passivity and slowing down that interferes with their discussing their problems, avoidance of painful subjects, and inhibi­ tion due to concern of the therapist's possible disapproval. One way to elicit relevant material is to review specific responses to items on the Beck Depression Inventory or the Beck Hopelessness Scale. For example, the therapist's questioning of the patient regard­ ing the reasons for endorsing a particular alternative may start up a fiow of information: PT: I have nothing to talk about today. Nothing important has hap­ pened since last week. TH: {examining the Beck Hopelessness Scale) I see that you have checked the item "My future seems dark to me." When did you have that thought during the past week? PT: Well, last week m y girlfriend said she'd break up with me unless I stopped using. TH: Yes . ? PT: Well, I don't think I can stop. TH: What did you feel when she said that? PT: I felt bad . . . hopeless. TH: What thought went through your mind when she said that? PT: If we break up, I have nothing. Depression 233 TH: And if you have nothing, what then? PT: There's no sense in going on. At this point, the therapist demonstrates the relationship between the sad feeling and the thought "I have nothing." The therapist then explores the basis for his beliefs "I don't think I can stop" and "If we break up, I have nothing." (Both beliefs, of course, contribute to the patient's hopelessness and suicidal tendencies.) The therapist could infer from these ideas that the patient has a set of core beliefs centering around "I am helpless (weak, defective)" and "I am unlovable." Without necessarily explicitly addressing the core beliefs at this time, the therapist could then utilize specific interventions to undercut the dysfunctional beliefs and, thus, to some degree defuse the depressive feelings and suicidal tendencies. The therapist, for example, might initiate a line of inquiry as follows: TH: You have shown a lot of control in the past—and, in fact, you haven't been using for several weeks now. What makes you think that you will not be able to continue [to abstain]? PT: I just feel I don't have any will power any more. TH: I respect your feeling. But remember you felt that way several weeks ago but you were able to apply the techniques and show control. Addressing the sense of loneliness and dependency on the girl­ friend might start with a question: TH: At the moment, your girlfriend seems to be devoted to you. But, if for some reason she did leave you, why does it follow that you are nothing? PT: But I feel like nothing. Depending on the interchange, the therapist might then proceed with a series of questions such as: TH: Did you feel like nothing before you met your girlfriend? PT: I felt O K then. TH: Did you have a girlfriend then? PT: No. TH: So it seems that you don't need to have a girlfriend in order to feel like something. PT: 1 suppose. . But I still feel like nothing. 234 COGNITIVE THERAPY OF SUBSTANCE ABUSE TH: Just because you may feel like nothing, does it follow that you are nothing?" The therapist may then continue with the type of Socratic ques­ tioning described in Chapter 6 (this volume). The therapist should keep in mind that the ultimate goal of questioning patients' inter­ pretations of a particular event is not simply to disqualify an inter­ pretation but also to undermine the basic negative beliefs leading to that interpretation or conclusion. As noted in the above excerpts, many depressed patients are influenced largely by their unpleasant feelings. They "read" these feel­ ings to mean that they are all alone, that they are nothing, and that things are hopeless. The feelings are taken as a source of information to which the patients attach considerable credibility. The therapist needs to reduce the patients' tendency to accept their feelings as a factual representation and to help them turn to objective, verifiable evidence to form their conclusions and interpretations. One of the distressing aspects of the ideation in depressed drag abusers is its saturation with themes of self-deprecation relevant to the meanings attached to the addiction. For example, a patient may apply the following labels to him- or herself: weak character, bad, worthless, immoral, sick. These notions are woven into the patient's belief that he or she is the helpless victim of the addiction, that he or she is defective for having the craving and not exercising will power. The patients consequently may be severely self-critical for their presumed faults ("I'm worthless," "I'm disgusting," etc.). Such think­ ing is apt to perpetuate both depressive symptoms and drug use. It is therefore not surprising that there is an association between depres­ sion and rates of drag relapse (e.g., Hatsukami & Pickens, 1982). The therapist addresses depressotypic beliefs through explanations and reframing. The therapist, however, needs to use judgment to decide whether an explanation is indicated in a given case and how it should be presented to the patient. Table 14.1 illustrates this

pro­ cedure. Dealing with Suicidal Ideation The therapist needs to be alert to covert suicidal ten­ dencies and to deal with them frankly. A number of interventions are available (see Beck et al., 1979, Chapter 10). As in the preceding illustration, the therapist needs to address the underlying hopeless­ ness and negative self image. Another approach is to list the reasons for living as opposed to Depression 235 TABLE 14.1 Examples of Beliefs and Explanations and Reframing Belief Explanation/reframing Drug abuse is a pattern of behavior that becomes self- I am a bad person. defeating. The effects, thus, are bad but the addicted person is not necessarily bad or immoral. Your problem is a technical one. I am defective You need to understand more about because I can't the working of your addiction and control the habit. then learn special techniques to bring it under control. The painful empty feelings are due in part at least to your personal Life is painful, problems and in part to your empty, without dependence on drugs for relief. using. W e can work together to help solve the problems and develop other ways to get satisfaction. the reasons for dying. This strategy requires considerable skill because it presupposes that the reasons for living will outweigh the reasons for dying. Another strategy is to get the patient intrigued by the thera­ peutic process and the interesting questions that are raised—so that the patient will be motivated to return to the upcoming sessions in order to get some of the answers. Also, the patient can be instructed to call the therapist when the wish to escape via suicide is the stron­ gest. The therapist might say, for example, "You may feel better when you are here but you may feel worse later. That is the time when you can get the most out of therapy. If you call m e then-or at least write down your thoughts-we can help you the most." The therapist should also bear in mind the need to notify the patient's family and con­ sider hospitalization if the suicidal drive is not controllable. Above all, the therapist must appear confident, reasonably upbeat, and in control of the situation. Negative Reactions to Therapy A disruption of the therapeutic collaboration may occur in therapy if the patient lacks objectivity toward his or her negative thoughts. For example, patients often experience new disap­ pointments or frastrations due to traumatic environmental events. 236 COGNITIVE THERAPY OF SUBSTANCE ABUSE When this occurs, they may be fiooded with a stream of negative cognitions that they automatically regard as valid without subjecting them to further considerations. Consequently, they are likely to experience increasing depression and hopelessness. This symptomatic exacerbation may lead them to decide that cognitive therapy is inef­ fective and that their addiction is incurable. This is often a critical point for a relapse. Patients may also feel disillusioned with their therapist. Any of these reactions may lead the patient to stop cooperating, resist carrying out assignments, miss appointments, or drop out of therapy. Their reactions may be compounded if the therapist unques- tioningly accepts the patient's negative construction of his or her progress. If the patient begins to miss appointments, the therapist is advised to contact the patient and clarify the dysfunctional thinking that is disrupting the therapeutic collaboration. Also, the missed appointment may be due to a relapse, which needs to be investigated. Ironically, there is some evidence that patients diagnosed with antisocial personality disorder (ASPD) actually may be more likely to seek out and cooperate with therapists when they are most depressed (Alterman & Cacciola, 1991; Woody, McLellan, & O'Brien, 1990). In such cases, the patients' desire to feel better outweighs their charac­ teristic autonomous need to defy authority figures. By helping these ASPD/depressed drug abusers to improve their mood, therapists may be able to form an interpersonal alliance with patients who otherwise would not form a bond with a helper. Symptomatic recurrences of depression are common during treat­ ment (Rawson, Obert, McCann, Smith, & Ling, 1990; Ziedonis, 1992). The therapist should prepare the patient early in treatment to expect to have negative fluctuations. Such exacerbations provide a valuable opportunity to apply cognitive techniques and skills. Further, they provide "practice" to deal with the problems that inevitably occur after termination of treatment. The therapeutic focus for the depressed addicted person also is directed to external problems that are related to the precipitation or aggravation of the depression (cf. Kosten et al., 1986). These prob­ lems may include stresses or difficulties at home, work, or school. They frequently involve friction in close relationships, difficulties in reference to work, or financial or legal problems. Thus, for example, the therapist and patient may work on helping the patient to make important decisions regarding a problem contributing to or maintain­ ing his or her depression, discuss specific techniques to help to cope better with a difficult life situation, and consider ways of relieving stresses or external demands. Depression 237 This type of approach (concentration on external problems) is also used after the patient's acute or severe symptoms have been relieved. The therapist should bear in mind that situational problems, drag use, and depression may aggravate each other. This multiple reciprocal interaction may be modified to improve both the external stresses and the depressive symptomatology. APPLICATION O F B E H A V I O R A L TECHNIQUES Cognitive Change through Behavioral Change The cognitive therapy of the depressed abuser is based on the cognitive theory of depression (as well as the cognitive theoty of addiction). Working within the framework of the cognitive model, the therapist can vaty his or her therapeutic approach accord­ ing to the specific needs of a given patient at a particular time as long as the treatment is based on a cognitive formulation of the case (cf. Persons, 1989). The therapist is conducting cognitive therapy even though he or she is utilizing behavioral techniques. In the early stages of cognitive therapy with depressed users, it is often necessaty for the therapist to concentrate on restoring the patient's functioning to the predepressed level. Specifically, the thera­ pist attempts to induce the patient to counteract his or her withdrawal and to become involved in more constructive activities. Often the important people in their life have given up on the patient. These significant others may attribute the patient's low mood and impaired performance to drags and conclude that the patient is no longer capable of cartying out his or her expected functions as provider, homemaker, spouse, parent, or student. Furthermore, the patients can see no hope of gaining satisfaction from those activities (other than using) that had previously brought them pleasure. The depressed users are caught in a vicious cycle in which their reduced level of activity leads to labeling themselves as ineffectual or worthless. These negative self-evaluations often reflect the opinions of those around them—as well as society at large. These self-inflicted put-downs lead to further demoralization and ultimately to a drift into a state of immobility. In severe cases, it is difficult to carty out intel­ lectual functions (such as reasoning and planning) as well as perform­ ing complicated acts requiring specialized skill and training. Since these forms of behavior are generally instraments for achieving sat­ isfaction and maintaining one's self-esteem and the esteem of others. 238 COGNTTIVE THERAPY OF SUBSTANCE ABUSE the disruption of these functions as a result of diminished concen tration, fatigability, and low mood produces dissatisfaction and a reduction of self-esteem. The role of the therapist is clear. There is no easy way to "talk patients out" of their beliefs that they are weak, inept, or undesirable. Patients can observe that they simply are not doing those things that once were relatively easy and important to them. By helping patients change certain depressive behaviors (avoidance, passivity), the thera­ pist may demonstiate to them that their negative self-evaluations are biased views and can help to restore their morale. Once a patient begins to get involved in constructive activities, the therapist may show the patient that he or she has not, in fact, irretrievably lost the ability to function at his or her previous level. The therapist points out that the patient's discouragement, pessimism, and giving up make it difficult to mobilize resources to make the necessaty effort. The goal is to get the patient to recognize that one of the prime sources of the problem is a cognitive error: The patient thinks (absolutely) that he or she is weak, helpless, and worthless, and those beliefs seriously impair his or her motivation and behavior. The term "behavioral techniques" may suggest that the immedi­ ate therapeutic focus is exclusively on the patient's overt behavior; that is, the therapist simply prescribes some kind of goal-directed activity. In actual practice, the reporting of the patient's thoughts, feelings, and wishes remains a central factor for the successful appli­ cation of the behavioral techniques. The ultimate aim of these tech­ niques is to produce positive change in the dysfunctional negative attitudes so that the patient's performance will continue to improve. In a sense, the behavioral methods can be regarded as a series of small experiments designed to test the validity of the patients' nega­ tive hypotheses or ideas about themselves. As the negative ideas are contradicted by these "experiments," the patient gradually becomes less certain of their validity and is motivated to attempt more diffi­ cult assignments. Scheduling Activities Many depressed users report an overwhelming num­ ber of self-debasing and pessimistic thoughts when they are withdrawn and inactive. They criticize themselves for being "vegetables," for being addicted, and for having withdrawn from other people. At the same time, they may justify their withdrawal on the basis that activity and social interaction are meaningless or that they are a burden to oth­ ers. Thus, they sink into increasing passivity and social isolation. Depression 239 Depressed patients tend to interpret their inactivity and withdraw as evidence of their inadequacy and helplessness and they are caught up in a vicious cycle. Individuals with a drag problem tend to relapse readily if their life is not stractured. The prescription of special projects is based on the clinical observation that depressed patients find it difficult to undertake or complete jobs that they accomplished with relative ease prior to the depressive episode. W h e n depressed, they are prone to avoid complex tasks, or, if they do attempt such tasks, they are likely to have con­ siderable difficulty achieving their objective. Typically, the depressed patient avoids the project or stops ttying soon after he encounters some difficulty. Negative beliefs and attitudes appear to underlie the tendency to give up. Patients often report, "It's useless to tty," for they are con­ vinced they will fail. W h e n they engage in goal-directed activities, they tend to magnify the difficulties and minimize their ability to over­ come them and carty out the task. The use of activity schedules (see Chapter 9, this volume) serves to counteract the patient's loss of motivation, inactivity, and preoc­ cupation with depressive ideas. Scheduling the patient's time on an hour-by-hour basis is likely to maintain a certain momentum and prevent slipping back into immobility. By focusing on specific goal- oriented tasks the patient and therapist obtain concrete data on which to base realistic evaluations of the patient's functional capacity. As with other cognitive techniques, the therapist should present the patient with a rationale for scheduling activities. Often patients are aware that inactivity is associated with an increase in their pain­ ful feelings. At the vety least, the therapist can induce patients to engage in an "experiment" to determine whether activity diminishes their preoccupations and possibly improves their mood. The thera­ pist and patient determine specific activities and the patient agrees to monitor his or her thoughts and feelings while engaged in each task. If the patient is reluctant, the therapist may seriously question the patient, "What have you got to lose by ttying?" The therapist may choose to provide the patient with a schedule to plan his or her activities in advance and/or to record the actual activities during the day. A "graded task" hierarchy should be incor­ porated into the daily plan. Planning specific activities in collaboration with patients may be an important step in

demonstrating to them that they are capable of utilizing their time constractively. Severely depressed patients may report a sense of "going through the motions" with the notion that there is little purpose in their activities. By planning the day with the 240 COGNITIVE THERAPY OF SUBSTANCE ABUSE therapist, they are often able to set meaningful goals. Later, the patient's record of the actual activities (compared to what was planned for the day) can provide the therapist and patient with objective feed­ back about the patient's achievements. The record also provides a ref­ erence to self-ratings of mastety and satisfaction for successful attain­ ment. It m a y challenge the therapist's ingenuity to get the depressed user sufficiently involved in the idea of cartying out a program of activities or even filling his or her activity schedule retrospectively. Thus, the therapist (1) explains the rationale (e.g., that people gener­ ally function better when they have a schedule), (2) elicits the patient's objections or reservations, and (3) then proposes making a schedule as an interesting experiment. The therapist should emphasize to the patient that the immediate objective is to attempt to follow the sched­ ule rather than to seek symptomatic relief: Improved functioning fre­ quently comes before subjective relief. W h e n patients engage in various activities, it is useful to have them record the degree of mastery and pleasure associated with a prescribed activity. The term "mastery" refers to a sense of accom­ plishment when performing a specific task. "Pleasure" refers to pleas­ ant feelings associated with the activity. Mastery and pleasure can be rated on a 10-point scale with 0 representing no mastery/pleasure and 10 representing m a x i m u m mastery/pleasure. By using a rating scale, the patient can recognize practical successes and small degrees of plea­ sure. This technique tends to counteract the patient's all-or-nothing thinking. S U M M A R Y The approach to the depressed user or alcoholic is similar to the approach to depression in general with the added fea­ ture that the typical depressive negative bias against the self often revolves around the patient's reaction to being on drags or alcohol. Thus, patients m a y be filled with contempt for themselves, may con­ sider themselves lacking in character, and m a y perceive themselves as helpless, defective, and rejected by other people and by society in general. Given the negative bias against the self and the profound hopelessness that often accompanies it, individuals with the combi­ nation of depression and addiction constitute one of the highest-risk groups for suicide (Marzuk et al., 1992; Mirin & Weiss, 1991; Ziedonis, 1992). Consequently, the possibility of suicidal wishes must be Depression 241 addressed early in therapy. Aside from the attention to the suicidal wishes, the therapist can follow the usual guidelines: 1. Conceptualize the case. 2. Apply behavioral strategies if the patient is motorically regressed. 3. Utilize cognitive strategies to undercut the hopelessness and negative self image and suicidal tendencies. 4. Help the patient to acquire greater control over the cravings (see Chapter 10, this volume)-a strategy that in itself m a y help to stem the tide of the depression. The specific techniques include structured activity scheduling, greater task assignment, and improved time management as a way of counteracting patients' regressive tendencies. In addition, Socratic questioning and the use of daily thought records m a y help patients gain more distance from their dysfunctional thinking. As with the stan­ dard freatment of the addict, it is ultimately necessary to come to grips with patients' beliefs that are driving both their drug abuse and their depressive tendencies. C H A P T E R 1 5 A n g e r a n d A n x i e t y ^•nnecessary or exaggerated anger presents a major problem in human relations, whether intimate or casual. The fact is that people tend to overreact to disappointments, hurt, fancied slights, and imperfect behavior of others. This phenomenon is par­ ticularly apparent in substance abusers (Ellis et al., 1988; Walfish et al., 1990). Hostility takes its toll not only in its undesirable effects on other persons but also in terms of its effect on the person who is angered. Substance abusers are prone to act out hostile impulses when they are under the influence of drugs or alcohol. Although they are par­ ticularly prone to use or drink to dampen unpleasant feelings of anger, the substance paradoxically may increase the likelihood of the expres­ sion of anger via disinhibition. The angry reaction is greater if the "noxious action" by another person is perceived as avoidable, unnecessary, intentional, and attrib­ utable to a failing in the other person; the reaction is less (or not all) if the same event is viewed as unavoidable, necessary, unintentional, and not blameworthy. If individuals perceive that they (or somebody they are attached to) have been wronged, they may become angered to a degree that greatly exceeds the degree of damage or discomfort. Much of the anger is the result of the symbolic meaning that is attached to the event, the cognitive mechanism involved in magnify­ ing its impact, and the degree of responsibility attributed to the other person. L O W FRUSTRATION TOLERANCE One of the most common conditions prompting an addiction-prone individual to seek relief through substance use is a feeling of frastration. Patients with low frustration tolerance (LFT) are 242 Anger and Anxiety 243 hypersensitive to any thwarting, nonfulfillment, or interference w their goals, wishes, or actions. The typical patient with LFT goes through life judging situations in terms of the following: "Am I get­ ting what I want?" or "Are people getting in m y way?" Because of the "internal" pressure to attain the objectives of ftilfillment of wishes or completion of a particular task, patients overreact to situations that interfere with satisfying their wishes or reaching a goal. Thus, they tend to be chronically impatient, intolerant, and uneasy. Wish-oriented patients operate under the "now dimension": They experience continuing craving for immediate "reinforcement" (encouragement, praise, recognition) or help. Stuck in the receptive mode, they consider it imperative that their cravings and desires be satisfied without delay. Behind this pressure lurks a fear clothed in dichotomous thinking: "It's now or never." Patients react as follows: "If I can't get what I want right now, I never will." Consequently, any delay in satisfaction is particularly distressing. The fear that they will be prevented from getting what they want arouses anxiety. Any interference with or interraption of an enjoyable activity is perceived as a major deprivation and causes pain. Either pain or anxiety (or both) can lead to anger if the individual holds another person responsible for the deprivation or interference. "Lil," a young woman, told by her landlady to lower the volume of her stereo, felt a sharp pang of disappointment over being deprived of one of her pleasures (high-volume music). She generalized this disappointment to "Nobody ever lets m e do what I want." Conse­ quently, Lil became angry, stomped around the apartment, and started to drink. As Lil's actions demonstrate, rapid, fleeting experiences of disappointment or anxiety trigger and are overshadowed in the patient's awareness by anger toward the thwarting or disappointing individual. It should be noted that a rather subtle mechanism operates between the initial feeling of disappointment (or anxiety) and the experience of anger. This mechanism involves attributing responsi­ bility for the disappointment to the other person in a fashion akin to blame. Attribution of responsibility may be a focus for discussion in therapy. Patient and therapist can explore whether the attribution of responsibility is reasonable. Since these patients have not learned to modulate their wishes and urges, they tend to experience them as "needs" that demand prompt fulfillment. These demands on themselves and others are experienced as dire needs ("1 must") or imperatives ("people should"). Since the needs have a "do or die" quality, their nonfulfillment is experienced as a threat or painful deprivation. The intolerance for 244 COGNTTIVE THERAPY OF SUBSTANCE ABUSE frastration is paralleled by intolerance for the dysphoria produce disappointment. The distress is compounded by thoughts such as "This should not have happened. They have no right to freat me this way." The claims, expectations, and demands on these patients and oth­ ers are not only imperative but also rigid and unrealistic. Karen Homey (1950) refers to these phenomena as the "tyranny of the shoulds"; Albert Ellis (1962) applies the term "musturbation." These individu­ als impose the shoulds on themselves as well as on other people. Individuals driven to achieve success may experience a sense of being dominated by an internal "slave driver." Such individuals often experience stress symptoms (Beck, 1993) and may turn to drugs and/ or alcohol to relieve these symptoms. Action-oriented individuals with LFT operate according to the same rules as the wish- or receptive-oriented individual. They act on the assumption that they must attain a goal promptly. Any delay is per­ ceived as interminable; any interference as unconscionable. The prin­ ciple underlying sensitivity appears to be concerned with "the con­ servation of energy." Impediments to the forward progress of such individuals are experienced as an unacceptable drainage of power or energy, which leads to impatience and restlessness. Wish-oriented and action-oriented people are disposed to ascribe negative motives to other people. They operate on the following premise: "Anyone who does not help me or facilitate m y goals is self­ ish; others' noncompliance with m y wishes is the equivalent of op­ position." The LFT individual interprets lack of support or help as signs of indifference, negligence, or irresponsibility. Ironically, these individuals are not cognizant of the fact that their behavior is con­ trolled by their inner dictates (cravings, demands, imperatives) but perceive themselves as controlled and victimized by other people who are indifferent to their "legitimate needs." Since the patient's pattern of frustration is crade, inflexible, and indiscriminate, the thinking mechanisms are equally crude. Such patients tend to catastrophize and overgeneralize when their wishes are not met: "I will never be able to get the job done." "Others never cooperate with me." "People always get in m y way." In order to ward off the threats and prevent pain, patients with LFT attempt all the more strongly to control their environment and to impose regulations and expectations on other persons. However, the harder they try to compensate for their sense of inner vulnerabil­ ity, the more likely they are to be frustrated. As their demands and claims on others escalate, they are prone to feel let down, disappointed, or blocked. Thus, the strategy of hypercontrol of others is ultimately Anger and Anxiety 245 self-defeating. The social environment simply will not conform to these continual demands and expectations. Sooner or later, other people will fail to respond satisfactorily to their wishes or drives. At a deeper level, patients with LFT perceive themselves as pow­ eriess or helpless. Any obstacle to a goal that the patient encounters primes the sense of powerlessness and produces a transient feeling of weakness. The next step is attributing responsibility to the "frus­ trating" individual and wanting to punish that person for his or her fransgression. This sequence leads, of course, to the most notable char­ acteristic of LFT, namely, explosive rage over relatively trivial inci­ dents. An action-oriented person is enraged by a slow driver in front of him and aggressively and dangerously passes him—with his thumb pressed firmly on the horn. A husband rails over delays in meals or unsatisfactoty food; a wife is incensed at being kept waiting while her husband works late at the office. In each instance, the patient attaches an overgeneralized meaning to the "offense": "She doesn't care about me" or "He treats m e like a servant." These highly personalized mean­ ings attached to the event—not the event itself—lead to the inflamma- toty reaction: the sense of being wronged. This tendency to "person­ alize" situations, to interpret neutral behaviors as a perceived affront, is a hallmark of LFT. The generation and expression of anger and hostility serve sev­ eral related purposes. They constitute a robust attempt to establish control over other persons by "punishing" them for their action or inaction. When the expression of hostility is effective, there is no form of behavior that

exerts as powerful an influence on other people, particularly if the offended individual is in a position of strength. The patient assumes that punishment, whether in the form of a complaint, a reproach, or a tantrum, will help to shape the other person's future behavior properly. The implicit punishment will supposedly be a "leaming experience" for the offender. Further, the punishment con­ tained in the reproach in some vague way undoes or compensates for the damage to the patient's self-esteem: A person is not "a helpless, vulnerable wimp" if he or she can inflict pain on another person. Most important, the expression of anger gives a subjective sense of power (even though fleeting). By acting in a forceful, aggressive way, the patient is able to neutralize the sense of powerlessness activated by the delay in gratification. Since frustration or disappointment accentuates the perception of the self as ineffective, the expression of hostility shifts the self-concept from "I am helpless" to "I do have power." Of course, punishing other people as a consequence of one's own 246 COGNTTIVE THERAPY OF SUBSTANCE ABUSE "neediness" or sense of inadequacy is ultimately self-defeating. O people are pained and often angered when reproached and are prone to retaliate. Further, the frastrated individual is drawn into a power straggle with others over the issue of who will control whom. The individual gets tangled in a vicious cycle of increasingly futile attempts to control others, leading to increasing disappointment and rage. LFT individuals are prime candidates for addiction (Ellis et al., 1988). Using drags and/or drinking can serve several purposes. First, these substances satisfy the desire for instant gratification. Second, they reduce the anxiety and sadness engendered by frustrations. Finally, they can give a transient euphoria and sense of mastety to compensate for the feeling of helplessness and sense of inadequacy. It is important for the therapist to recognize that patients with LFT often are deficient in perceiving important social cues or recog­ nizing the rules that govern human behavior and allow people to interact with a minimum of friction. They are frequently unaware of and overstep the usual boundaries between people. Lil, for example, had no recognition of the fact that the loud noise from her stereo would bother the other boarders. Some patients addicted to drags have Attention Deficit Disorder (Gawin & Kleber, 1986; Glantz & Pickens, 1992; Weiss, 1992) and may rely on cocaine, for example, to sharpen their focus and increase their guarded awareness of other people. CHECKLIST FOR EVALUATING LFT 1. The patients' desires are viewed as imperative needs that requi prompt fulfillment. 2. Delays, interference, and blocks have idiosyncratic meanings such as "1 may not finish this job" or "I can't get what I want." 3. The frastration is overgeneralized to notions such as "I never get what I want" or "People always get in m y way." 4. Patients personalize such frastrations as though the frastrations are deliberately directed against them, and they regard the alleged agent of the frastration as culpable. Patients manifest the usual think­ ing errors associated with emotional distress: all-or-nothing thinking, selective abstraction, overgeneralization, catastrophizing, and person­ alizing. 5. Because of dichotomous thinking ("It's now or never"), patients build up arbitrary rules (shoulds and musts) to enforce their wishes, expressed as rights, entitiements, and claims: "People have no right to withhold what I want," "Others are wrong to get in m y way," and "1 should be able to work without interruption." Anger and Anxiety 247 6. The absolutistic expectations and demands are driven by catastrophizing: The consequences of a delay, obstacle, or difficulty are expected to be disastrous. 7. The patients' rales and demands also represent attempts to control others and prevent problems. W h e n controls break down (a rale is violated, a demand is unfulfilled), patients experience anxiety or hurt resulting from catastrophizing or exaggerated sense of loss. 8. The expression of anger is legitimized: "I have evety right to be angty." 9. Underlying the low threshold for frustration is a core belief such as "I am helpless" or "I am unlovable." Any delay, interference, or problem related to attainment of wishes or goals can evoke the sense of helplessness or unlovability, lead to catastrophizing, then distress, and, finally, to anger. 10. The accumulation of anxiety and anger and the mobilization to punish the offender lead to tension which patients attempt to relieve with drugs. In this context, drug-taking beliefs may take the following forms: "I can't stand the anxiety, sadness, or anger and must relieve it right away." "People want to stop m e from using or drinking because they consider me weak and want to control me." "They are wrong and bad for wanting to control me." "I will regain control by drinking or using when I want to." 11. People may be overly frustrated by their own mistakes, ineptitude, or deficiencies and will manifest extreme self-criticism. This mechanism is especially prominent in the addicted patient with low self-esteem (Tarter, Ott, & Mezzich, 1991). LFT A N D SUBSTANCE ABUSE: A CASE VIGNETTE "Charlotte," a 35-year-old single woman, was in out­ patient cognitive therapy following a 30-day inpatient stay for crack cocaine abuse at a nearby hospital. Charlotte and her cognitive thera­ pist identified many situational and cognitive triggers for her urges to use crack, including family disputes, worries about money, thoughts about deceased relatives, news about old boyfriends, and dissatisfac­ tion with her employment situation. These triggers tapped into a great sense of loss (e.g., "I don't have anything meaningful in m y life any- 248 COGNITIVE THERAPY OF SUBSTANCE ABUSE more, so I might as well drown my sorrows in alcohol and cocaine") and helplessness and hopelessness ("Evetything I do to try to help myself gets messed up in the end anyway, so there's no point in plan­ ning for a future"). Charlotte's dysfunctional beliefs (noted above) underlay her low tolerance for frastration. For example, when she tried to reach her new boyfriend by telephone one evening to talk about some upset­ ting things that happened on her job interview that day, she found that nobody was home. She tried to call numerous times within the following hour, but he still did not answer the telephone. Charlotte became quite agitated and she felt an increasingly strong urge to go out and find a crack dealer. In retrospect, her thoughts included: "I need him now. If I can't talk to him now, I'll go out of my mind." [Imperative: equating wish with need] "I can't stand being alone when I'm hurting. M y only alternative to feel better is to get high." [Myth of intolerability of pain] "Why isn't he home when I need him?" [Excessive demands] "I can't wait any longer!" [Intolerance for frastration] "Maybe he's out with another woman. Maybe he's cheating on me." [Catastrophizing] "If that's trae, then I don't have any reason to stay straight any­ more." [Justification] Charlotte noted that all of these thoughts transpired within only 90 minutes of trying to reach her boyfriend at home. Rather than attempting to solve the problem-calling him back at a later time, calling the therapist, or trying to utilize her own coping skills—she became vety upset that she could not find her boyfriend right at the time she "needed" him. This frustration led her to the premature and maladaptive conclusion that she had no choice but to go out and get high. She believed it was justifiable to do so; after all, if you are alone (as she believed), helpless, and have no future, why shouldn't you find a way to feel better now by any means possible, including drags? This vignette demonstrates how LFT is based on a thinking style that justifies impulsive and self-defeating behavior, and therefore feeds into urges to use drugs. The LFT patient is constantly in danger of exaggerating temporary inconveniences and upsets as indicative of (or equivalent to) unremitting denial of the most important goals in life- forever. Therefore, the LFT patient is likely to conclude that drug use (a short-term "solution") is necessary, given that long-term solutions are unseen or dismissed. Anger and Anxiety 249 DEALING V\^TH SPECIFIC ISSUES Imperativeness of "Needs" Patients require practice in delaying satisfaction of desires—whether in terms of resisting the desire to use or drink or of demands on others for their help, reassurance, and praise. 1. From a practical standpoint, patients should be coached to monitor their wishes: write down the specific desire, note its inten­ sity, and determine how long it takes for the desire to be reduced. This procedure enables patients to distance themselves from the desire and, thus, to control it better. 2. Distraction—for example, getting involved in an absorbing activity such as conversing with another person—often helps to reduce the imperativeness of the need. 3. By delaying their demand for instant gratification, patients can become aware of the exaggerated importance they attach to a particu­ lar desire. Their desires for affection and recognition are similar to the cravings for drugs and alcohol. W h e n an individual is frustrated in his or her yearning for affection (or expects to be frastrated), for example, he or she may channel this yearning into a craving for a drink or a "fix." The kind of pleasure from the chemical agent is perceived as a substitute for the pleasure desired through a loved one's affection. Meaning of the Event: Hidden Fears By delaying the expression of anger or impatience (acting out the frustration), the individual has an opportunity to become aware of (1) the immediate cognitive reaction to an event (e.g., a specific fear of disappointment) and (2) the immediate affective response such as anxiety or sadness. For example, the wife who railed at her husband for not coming home when she expected had an ini­ tial fear, "perhaps something happened to him," and felt consider­ able anxiety. W h e n he did appear, she was angty at him for "caus­ ing" her distress rather than for being late-although she scolded him for being late. In therapy, she recognized that the initial fear was related to her childlike concern of being abandoned. Thus, the therapy was directed toward her confronting her sense of vulnerability, which was aroused by his tardiness. In this case, her hostility served to pun­ ish him for making her feel vulnerable and, at the same time, gave her some sense of power. When an unpleasant event occurs, patients with LFT practically simultaneously assess the consequences and attach responsibility 250 COGNITFVE THERAPY OF SUBSTANCE ABUSE either to themselves or to others (or occasionally simply to bad lu The expectation of negative consequences is not a thought-out, reflective, rational procedure but is molded to a large degree by a ten­ dency to exaggerate. This tendency may take the form of foreseeing the possibility of catastrophic consequences or by exaggerating the current loss. The catastrophizing may be heralded by a "What if. ?" prelude; for example, "What if I hadn't caught the mistake in time. It could have cost m e a large sum of money." The sense of loss places a great premium on the supposed diminution of some resource; for example, "They are costing m e valuable time by their inefficiency" or "I am forced to waste m y energy answering stupid questions." Issue of Responsibility The attribution of responsibility occurs almost at the same time as the estimate of loss or threat. The individual determines that some person is responsible for the loss or threat. The patient's reaction is to fix accountability on the other person as the cause of the frustration. This attribution of responsibility is evidenced in expressions (or thoughts) such as "You should have known better" or "You never pay attention." Words such as should, should not, never, and always are often expressions of attribution of responsibility and simultaneously of reprimand. A more subtle process is also discernible. Noxious events are likely to evoke a sense of helplessness in the LFT-prone patient. If such patients can fix responsibility on another and mobilize reproach, they can regain some of the sense of lost power. By blaming another per­ son, the patient in a sense is saying, "I'm not so weak and helpless. 1 am strong enough to punish you." Of course, if such

patients per­ ceive themselves as the cause of the problem, they criticize themselves and feel even more helpless. Issue of Control The problem of control is particularly pertinent to the treatment of drug abusers since the therapy involves, in essence, the therapist's attempting to control patients' behavior. This problem has been exacerbated in many instances in which patients have been sub­ jected to threats, coercion, and criticism by other well-intentioned persons trying to enforce abstinence or, at least, continence. These attempts by others can produce a chronic resentment in the substance abusers. Most significant from the therapeutic standpoint is the impact Anger and Anxiety 251 of such interventions on the individuals' self-esteem. They are li to respond covertly to the criticism with an increased sense of inad­ equacy, even helplessness, isolation, and unworthiness, although overfly they may devalue the other party. Many of these patients will become infuriated at their "torment- ers" and will attempt to regain a sense of power by counterattacking and thus alleviating the pain. Others will engage in elaborate decep­ tions to disguise their using or drinking and to protect their self-esteem from further blows. Thus, the confrontation by the therapist of the patients' deceptions is a delicate procedure since exposure of a pre­ tense may constitute a significant threat to the patients' self-esteem. Handling Anger Toward the Therapist Situations in which one person is attempting to influence the behavior of another person embody specific sets of prob­ lems. The drug-abusing patient's sensitivity to being controlled is practically a given in the therapeutic situation and is an issue that needs to be addressed by the therapist. As already indicated, the patient's strategy of covering up lapses in order to protect him- or herself from criticism may represent an important defensive maneu­ ver. Consequently, discussions of the patient's drinking and using or of his or her deceptions may arouse the patient's anger and shake the foundations of trast. O n the other hand, if the therapist appears to be "taken in" by the patient's deceptions, the therapist may appear to be a "pushover" and will not maintain the patient's confidence. Patients should be encouraged to discuss their angry feelings toward the therapist. However, while ventilation of the feelings may serve a constructive purpose—up to a point—the therapist must be prepared to set limits to the expression of anger as illustrated below. "I realize that you are very angry at me and I'm glad that you feel safe to express it here. But before we go any further, it is very important to find out all the factors that are fueling your anger. For example, what were you thinking just before you became angry?" Often the exploration of the automatic thoughts preceding the appearance of the angty response serves as a distraction, which allows the patient to gain some objectivity. Further, by eliciting the auto­ matic thoughts, the therapist can get a better grasp of the cognitive aspects of the patient's disposition to anger. The anger is often the consequence of a sequence of automatic thoughts relevant to secret fears or hidden doubts. For example: "He's ttying to control me" therefore "I won't be able to do anything on m y own" (secret fear) 252 COGNITFVE THERAPY OF SUBSTANCE ABUSE therefore "I can't let him get away with this" therefore anger; or must be a weakling to allow him to talk to m e that way" (self-doubt) therefore "He has no right to treat m e that way" therefore anger. However, this therapeutic strategy is not effective all the time, and many times the therapist has to be prepared to absorb verbal expressions of hostility until the patient's anger subsides. Abusive Behavior and Control of Anger Patients with an addictive personality profile are par­ ticularly likely to have difficulties in family relationships and may engage in abusive behavior (Amaro et al., 1990). The various steps for anger control are described in Love Is Never Enough (Beck, 1988). Briefly, these consist first of being able to recognize the earliest sub­ jective signs of anger, which may simply consist of somatic sensa­ tions such as a tightness in the chest or a stiffening of the muscles in the arms. When a patient experiences these premonitory signs, for example, he should then slow down his talking and examine whether he sounds angry. If he is indeed angry, he should stop talking until his anger subsides. If he is still angry, he should leave the room (assuming the hostile interaction is at home). He should then stay away from the targets of his hostility until he has cooled off. At times it may be necessary to leave the house for a while, although it is essential for patients to have a drug-free destination in mind (e.g., the public library). The therapist should explore with the patient various kinds of distraction. While in the heated situation, the patient might try to distract him- or herself by thinking of a pleasant experience. After leaving the room, the patient could get involved in some physical exercise or manual project to "work off" the anger. In order to pre­ pare the patient for using these self-control methods, the therapist should use the therapeutic session to get the patient to practice the techniques. One method is to have the patient recall in vivid detail a recent dysfunctional interaction and then, using imagery, go through the scenario but imagine using techniques of self-control. Induced imagery is also useful for ascertaining the individual's automatic thoughts (see Chapter 10, this volume). The patient is requested to relive a hostile encounter in imagination and then to pinpoint the automatic thoughts associated with the angry feeling. The material can then be dealt with using the standard way of fram­ ing reasonable responses to automatic thoughts. The therapist may also utilize role playing in order to model self- control techniques for the patient. Patient and therapist simulate or Anger and Anxiety 253 recreate a hostile encounter that will provide the patient with an opportunity to recognize his or her anger, detect the automatic thoughts, and rehearse rational responding. It should be kept in mind that an important facet of patients' anger proneness is their deep sense of helplessness and inadequacy in interpersonal conflict. Compounding this defective self-image is the lack of social problem-solving skills (Piatt & Hermalin, 1989) and frequently a lack of assertiveness. In his or her formulation of the patient's difficulty, the therapist needs to diagram the sequence: "I am helpless/inadequate" therefore "I am vulnerable to being insulted, controlled, etc." therefore "He has taken advantage of me" therefore "I have to protect myself" therefore anger and acting out. Patients capable of insight often are willing to accept this formu lation. The therapist's role then is to help the patient to reinforce a self-image of adequacy without having to prove it by expressing anger or abusing another person. Building up a positive core concept in­ cludes not only demonstrating to patients their potential capacity to handle conflicts with other people but also negating their dysfunc­ tional beliefs; for example, "If I don't succeed at something, it shows I'm inadequate" or "If somebody argues m e down, it means I'm infe­ rior." Further, the therapist has to communicate to the patient that "feeling helpless" is not an objective representation of reality; people tend to read their feelings as factual. But one can "feel helpless" and still function adequately. Assertive Training and Problem-Solving Some patients become unnecessarily provoked because they feel inhibited or lack social skills in presenting their own view­ point or expressing their own self-interest. Failure to assert themselves effectively makes them feel put upon and helpless and to view other people as controlling and domineering. These patients often have a particular problem with people in authority. "Steve," who has a histoty of dependence on alcohol and cocaine, worked as a contract mechanic in a automotive garage. W h e n he and the other mechanics were given jobs by the service manager, he noticed that the other mechanics were assigned the more expensive jobs. Although he realized that they were more assertive than he in asking for the good jobs, he concluded that he was being discrimi­ nated against. He was too inhibited, however, to complain to the service manager, w h o m he perceived as authoritarian and callous. One day he felt particularly frastrated because a big job on an 254 COGNITIVE THERAPY OF SUBSTANCE ABUSE expensive foreign car was given to one of the other mechanics. He wanted to say something to the manager but was too inhibited. As he left the garage, he became increasingly angty. He thought of going home but he had an image of his children squabbling with each other and that made him feel more frastrated. Although he had previously resolved not to drink or use, he decided to stop at a bar and have a drink to relieve his anger and frastration. After three or four beers he again thought of going home but this time he had visions of his wife scolding him for being late and drinking so when he left the bar he sought out a friend who gave him a joint of crack cocaine. When he got home eventually, he was filled with remorse for his lapse. The therapist pointed out to him iri their session that his lapse was not a full-blown relapse and that they could do something to overcome his repeated frastration and escalating anger. The therapist then engaged Steve in a series of exercises in assertive training (cf. Alberti & Emmons, 1974; Collner & Ross, 1978). He first modeled for the patient how to approach the manager and state his concern in a reasonable, straightforward manner. The therapist then role-played the manager and Steve rehearsed the approach. During the rehearsal, Steve had a number of automatic thoughts such as "He'll think I'm a troublemaker for complaining" or "He'll make m e look foolish." (These were his "secret fears" that he became aware of only as a result of the role play.) The therapist discussed these dysfunctional thoughts after the role play was concluded and tried to communicate that the important thing was being able to express a legitimate complaint irrespective of whether it was immediately effective. Also, since the other men seemed to be able to make requests or complaints with­ out being "put down," Steve certainly could try. Finally, Steve agreed that he would be no worse off than he was currently without com­ plaining. The result was that the manager denied that he was playing favorites and claimed (probably as an excuse) that he thought Steve preferred working on the American cars. Subsequently, the manager began to give him some jobs on foreign cars. Problem-Solving and Skills Training Addicted patients have difficulty in solving problems, particularly those dealing with interpersonal conflict (Piatt & Hermalin, 1989), for at least two reasons. First, a problematic situa­ tion can arouse such a degree of anger that they are driven to punish (scold, criticize) the other person so that the problem, far from being solved, becomes aggravated. Second, because of poor problem-solv- Anger and Anxiety 255 ing skills, the patient is rapidly frastrated in a difficult situat consequently becomes angry. It is interesting to note that addicted patients are not always de­ ficient in skills. Many know what to say in situations in which they do not have a strong personal involvement. Also, they may know how to advise others to handle difficult situations. However, when they themselves are involved in a difficult situation, they feel they cannot or do not want to tty to resolve the problem other than by berating the other person. Once the patients label others' behavior as an offense against them, they have slipped into the punishment mode. The remedy is for them to detach themselves from the personalized meanings and address the problem in a way leading to solution. "Bob," for example, became infuriated because a mail clerk denied having a package that Bob knew had been delivered to the mail room of his office. Instead of brainstorm­ ing about where the package could be, Bob started to yell at the clerk. The clerk became defensive and retaliated, "You can't speak to me that way." Bob then responded

sarcastically and walked away in a huff. He was so upset that he felt incUned to go to the bar next door and have a few drinks. Much later he learned that one of his colleagues had picked up the package and delivered it to Bob's secretary. In the therapy session, Bob realized that he had "personalized" the problem—as though the circumstances had directed this against him. He also had had a catastrophic thought, "If I don't locate the package, I may lose m y job." Once he took the situation personally, it was played out at a level of interpersonal fighting (conflict) instead of mutual problem-solving (cooperation). Thus, the following steps can be prescribed for situations in which one is angty about a difficulty: 1. Detach self from the personalized meanings (put down, dis­ criminated against, let down). 2. Tty to approach the problem cooperatively despite the pres­ ence of anger: a. Define the problem: the "lost" package and the clerk's dif­ ficulty in recalling where it might be. b. Experiment with explanations: Ask the clerk where it could have been mislaid. Inquire whether one of the other clerks may have seen it. Could somebody else have picked it up? Steve had a problem with his children-when they started to squabble, he became furious and wanted to yell at both of them. Applying the rale of "defining the problem," he discovered that the older child was continuously teasing the younger one. Steve then 256 COGNTTIVE THERAPY OF SUBSTANCE ABUSE could see the solution clearly: Issue a stern reprimand to the old child to stop teasing. This may seem to be a minor example, but it was built up into a major problem because of Steve's inner belief, "I am helpless when there is a conflict." This sense of helplessness made him reluctant to go home at the end of work because of his fear of friction in the fam­ ily. Hence, part of the program of anger management consisted of building up Steve's confidence in his parenting skills. Dealing with Catastrophizing The way that the underlying mechanisms of LFT can be increased is indicated in another interview with Steve. TH: Tell me more about why you decided to use [cocaine] last Thurs­ day. PT: Well, I came home and I asked m y wife whether she had taken the kids to the doctor—like she had promised. She said that they weren't really sick and besides she was too busy today. TH: What did you feel then? PT: 1 felt really mad but I controlled myself and left the room. Then 1 decided to have a line. TH: What went through your mind when she said she hadn't taken them to the doctor? PT: 1 thought, "Suppose they really are sick? Even getting there a day late could be very serious." TH: As you look at it now, do you still believe that it was a serious problem? PT: No, they really weren't sick, but at the time it seemed like they could get much worse. TH: So that's an example of what we know you are in the habit of doing—catastrophizing-a kind of exaggerated worrying. PT: Right. TH: Now, what did you feel in your body when you had that thought? PT: I felt weak all over. TH: Where? PT: Especially in m y muscles. TH: What else? PT: I felt a heavy feeling in m y stomach. Anger and Anxiety 257 TH: Was this weak feeling like a helpless feeling? PT: Well, I did feel helpless at the time. Because I told her some­ thing to do and she didn't do it. TH: So now, it seems that you have a tendency to expect a catastro­ phe when somebody doesn't follow instructions. You start to feel weak and helpless. Then you get mad at the person who you think made you feel that way and you want to punish her. Steve, of course, was more introspective than many patients and was adept at identitying his catastrophic thoughts and his feelings. But many, if not most, patients can be trained the way that Steve was, to recognize and evaluate these automatic thoughts. ANXIETY DISORDERS A N D SUBSTANCE ABUSE Background Anxiety disorders are among the most common of psychiatric disorders. Zung (1986), in a survey of 739 family practice patients, found that 2 0 % had clinically significant anxiety symptoms. In the Epidemiologic Catchment Area study, Regier and his colleagues (Regier et al., 1988; Regier et al., 1990) report that the lifetime preva­ lence of anxiety disorders in the general public is over 14%. In their study, this rate is exceeded only by substance use disorders, with a lifetime prevalence rate of over 16%. DSM-III-R distinguishes between seven Axis I anxiety disorders: Panic Disorder, Agoraphobia, Social Phobia, Simple Phobias, Obsessive- Compulsive Disorder, Post-Traumatic Sttess Disorder, and Generalized Anxiety Disorder. O n Axis II, there are at least two personality disor­ ders characterized by substantial anxiety: Obsessive-Compulsive and Avoidant Personality Disorders. Compared with those who do not have chronic anxiety, people with these disorders may be more vulnerable to abusing certain psychoactive substances (e.g., alcohol, benzodiaz­ epines, and nicotine). They may use drags in an attempt to cope with anxious feelings (i.e., as "compensatoty strategies"). In fact, numer­ ous studies and reviews suggest a significant positive relationship between anxiety disorders and substance abuse (e.g., Beeder & Mill- man, 1992; Helzer & Ptyzbeck, 1988; Hesselbrock, Meyer, & Kenner, 1985; Hudson, 1990; Kranzler & Liebowitz, 1988; Kushner, Sher, & Beitman, 1990; LaBounty et al., 1992; Linnoila, 1989; Mullaney & Trippett, 1979; Quitkin, Riflcin, Kaplan, & Klein, 1972; Regier et al. 258 COGNTnVE THERAPY OF SUBSTANCE ABUSE 1990; Ross et al., 1988; Schuckit, 1985; Walfish et al., 1990; Wilson, 1988). According to Kushner et al. (1990), estimates of alcohol problems in anxious patients have ranged from 1 6 % to 25%. In alcohol treat­ ment programs, estimates of patients with coexisting anxiety prob­ lems have ranged from 22.6% to 68.7%. From a critical analysis of existing literature, these authors conclude that coexistence of alco­ hol problems and clinical anxiety is not a simple, unidirectional, causal relationship. Instead, Kushner et al. (1990) state: It appears more likely that alcohol has the potential to interact with clinical anxiety in a circular fashion, resulting in an upward spiral of both anxiety and problem drinking. For example, increasing alcohol consumption motivated by the short-term relief of anxi­ ety (or the belief that alcohol can relieve anxiety) may lead to increased anxiety related to autonomic nervous system hyper- excitability and anxiety-inducing environmental dismptions which, in turn, may lead to more alcohol consumption to relieve symp­ toms, (p. 692) T h e Cognitive Therapy of Anxiety A text on the cognitive therapy of anxiety disorders (Beck et al., 1985) emphasizes the importance of appraisal processes in anxiety. Anxiety is typically precipitated by a situation in which the individual regards himself as vulnerable to some threatening (i.e., unpleasant, dangerous, or harmful) event or situation. Prior to the onset of anxiety symptoms, a person makes a series of appraisals about a potentially threatening event or situation. The first appraisal, called a "primary appraisal," involves the initial assessment of risk. For example, in response to the social encounter, the socially anxious per­ son might make the primary appraisal "1 a m going to embarrass myself." In response to his rapid heartbeat, a person with a panic disorder might make the primary appraisal "I'm having a heart attack." After the primary appraisal, an individual makes a "secondary appraisal," followed by a series of "reappraisals." Secondaty apprais­ als involve the assessment of a person's resources for dealing with a potentially dangerous event or situation. The following are examples of positive secondary appraisals that enable an individual to cope effectively: "I have been able to handle sihiations like this before." "My heart is strong." "These are m y friends; I don't need to worty about them." Reappraisals involve "reality testing" and the constrac­ tion of risk:resources ratios. Anger and Anxiety 259 The central core of the anxiety process is the individual's chroni sense of vulnerability (i.e., uncertainty and insecurity). Anxious indi­ viduals tend to have core beliefs about their own helplessness that are activated in potentially threatening situations; that is, they char­ acteristically underestimate their ability to cope with the threat. As a natural consequence of this appraisal process, the patient with an anxiety disorder will experience an escalation of symptoms of anxiety: increased heart rate, sweating, shortness of breath (i.e., psychological symptoms); increased fear or terror (i.e., emotional symptoms); and increased ramination or obsessive thinking (i.e., cog­ nitive symptoms). The addicted person may respond to these symp­ toms by using psychoactive substances. For example, a person with a flying phobia may use alcohol as a sedative in order to cope with a necessary flight. A social phobic may use cocaine in order to feel more confident in a social siraation. A person with generalized anxiety dis­ order may smoke cigarettes in order to relax (in spite of the fact that cigarette smoking simultaneously creates autonomic stimulation and sedation). Treatment of the Anxious Substance Abuser Case Conceptualization An essential step in the cognitive therapy of the anx­ ious substance abuser is the case conceptualization. Similar to the freatment of other disorders, the therapist evaluates the patient's typi­ cal cognitive, behavioral, and emotional responses to relevant expe­ riences. The therapist traces these responses to earlier life experiences (e.g., famihal, social, educational) in order to understand their devel­ opment. An accurate case conceptualization ultimately facilitates the selection of appropriate techniques. For example, "Rick" is a 38-year-old unmarried accountant with a history of alcohol dependence and cocaine abuse, who entered treat­ ment as a result of a recent "driving while intoxicated" conviction. He explained that he had been drinking between one and two six- packs of beer per night for several years. He typically drank in the evenings until he would pass out while watching television. Rick admitted to blackouts, absenteeism, hangovers, and severe guilt related to his drinking. In an effort to develop an accurate and useful case conceptual­ ization. Rick's therapist inquired about his current functioning, his problematic situations, his developmental histoty, his basic beliefs and typical automatic thoughts, and his behavioral and emotional 260 COGNITIVE THERAPY OF SUBSTANCE ABUSE responses to these thoughts. The therapist related these to the de opment and maintenance of Rick's alcohol use. Rick described himself as a "loner." He stated: "I wish I had close friends, but I just get so nervous around people. I would like to get married some day, but I'm terribly uptight around women." Rick specifically described the following thoughts: "I have nothing intel­ ligent to say to people," "I will appear stupid," and "People, and especially women, will reject me." Rick occasionally dated women; however, he reported that he had to get intoxicated to tolerate the anxiety triggered by dating. Rick admitted to occasional panic attacks prior to social encoun­ ters. He viewed these panic attacks as supporting his beliefs about his extreme vulnerability. In fact. Rick dreaded all social encounters and he reported that his heavy drinking began when he was required to conduct financial audits for his company (requiring interpersonal contact with numerous business executives). He explained that his fear of criticism and failure, and his resulting anxiety, seemed to be intolerable until he began drinking. Although he was self-medicating with alcohol. Rick's symptoms of anxiety heightened as he developed a tolerance for alcohol. He viewed himself as increasingly fragile and vulnerable, until he was avoiding most social situations. As he reflected on his life, he felt increasingly depressed, typified by such global negative beliefs as "1 am totally worthless," "1 am a loser," and "1 am hopeless." Eventu­ ally, Rick began using cocaine to cope with his boredom, loneliness, and isolation. His cocaine abuse further supported his global nega­ tive beliefs (e.g., "Now I'm reaZ/y worthless!"). Upon inquiring about Rick's developmental history, his therapist learned that Rick's parents were "withdrawn and emotionally unre­ sponsive," only showing appreciation when he received perfect grades in school. Regarding his family history of alcohol use. Rick explained that his parents were "fundamentalists who never drank a drop." Their beliefs about alcohol were global and negative, including "Drinking is evil" and "No booze is good

booze." Such messages from his par­ ents taught Rick to have dichotomous beliefs about alcohol. For example, he believed, "If 1 am going to drink at all, 1 might as well get totally drunk." As a result of his extreme thoughts about alcohol, Rick had difficulty drinking in moderation. Rick's anxiety, loneliness, and isolation made him vulnerable to heavy alcohol and cocaine use. He responded to his symptoms with thoughts such as "1 need a drink or snort to handle this!" "What the hell!" and "Who cares if 1 use?" These thoughts resulted in urges and cravings to which Rick responded with permissive thoughts such as Anger and Anxiety 261 "I deserve this!" and "Besides, it doesn't really matter!" Following this permission, he focused o n the instrumental strategies necessaty for the acquisition of beer or cocaine. This often led h i m to drink until he passed out or to use cocaine until he had none left. The sequence for Rick's alcohol use is illustrated in Figure 15.1. A similar sequence occurred in his cocaine use. Educating the Patient about Anxiety a n d Substance Abuse Although most anxious individuals are somewhat aware that their fears are exaggerated, they continue to fear that some­ thing unpleasant will actually occur. In cognitive therapy the patient is educated in an alternative, more objective method for understand­ ing his or her problems. Specifically, the therapist teaches the cogni­ tive therapy models of anxiety and substance abuse to the patient as these models relate to the patient. Rick was taught that his anxiety resulted from his perception that he was weak or vulnerable. Further, the therapist taught Rick that his drag-related beliefs, automatic thoughts, and core beliefs fed into his Situation Basic Alcohol- Anxiety, Related Automatic Craving/ loneliness, and Beliefs Thoughts urges isolation Activated •What the "1 need a heil!" drinic to "Who cares?" handle this!" (. because I'm socially inept) Continued Focus on Facilitatiing Use or Instrumental Beliefs Relapse Strategies (permission) Drinl<s until (action) "I deserve he passes Goes to a this!" out store. "Besides it Buys some really doesn't beer. matter!" F I G U R E 15.1. Rick's alcohol use. 262 COGNITIVE THERAPY OF SUBSTANCE ABUSE drag use, more than did the environment or his circumstances. The therapist further taught Rick that there were multiple decision points at which he could control his substance abuse, including modifying the anxiety-arousing beliefs, rationally responding to permission-giving beliefs, and finding non-drag-related ways to cope with the anxiety. Techniques for Managing Anxiety There are numerous techniques used in the treatment of the anxious substance abuser. The particular technique chosen depends on the patient's presenting problem at each session, as well as the therapist's general conceptualization of the case. The efficacy of selected techniques depends on several factors: the quality of the therapeutic relationship, the accuracy of the case conceptualization, the therapist's appropriate use of the Socratic method, and the patient's socialization to the cognitive model. In the Socratic method, the therapist asks questions to guide the patient to more realistic conclusions about himself, his personal world, and his future. For example. Rick initially held the belief "I will be rejected if I allow others to see how anxious I am." At the same time, he held the belief "My mistakes are terrible." Using the Socratic method, the therapist asked questions to lead Rick to more adaptive conclusions: TH: What do you think about when you anticipate an upcoming social encounter? PT: I know that I'll make a fool of myself. TH: What do you mean by "a fool"? PT: I mean that I'll make an idiot of myself. TH: H o w do you picture yourself making "an idiot" of yourself? PT: I see myself having nothing to say. TH: Do you believe that all people who are quiet in public are "fools," and that they make "idiots" of themselves? PT: Well, I guess not. TH What else are other people likely to think about a quiet person? PT They might think that the person is just listening . or that the person is just shy. TH: When you think of yourself as an "idiot" or a "fool," how do you feel? PT: Upset, nervous, uptight, depressed . . . Anger and Anxiety 263 TH: And when you view yourself as "just shy," rather than foolish and idiotic, how do you feel? PT: A little better. Prior to this dialogue, the patient equated "quietness" or "shy­ ness" with "foolishness" or "idiocy." Through the Socratic method, the therapist helped the patient to objectively examine this maladap­ tive assumption. There are five key questions that assist patients in responding rationally to the anxiogenic thoughts that may stimulate cravings and urges for drags (these questions are applicable to all patients across the diagnostic spectram): (1) What other perspectives can I take about this situation? (2) What concrete, factual evidence supports or refutes my automatic thoughts? (3) What is the worst that could happen in this situation and how would it ultimately affect m y life? (4) What constractive action can I take to manage this situation? and (5) What are the pros and cons of m y continuing to have negative automatic thoughts? W e summarize the rationale for each question here. 1. Other perspectives. Here, patients who might otherwise see thing in tunnel vision are asked to broaden their viewpoints in order to ascertain new possibilities. One way to facilitate this process is to ask the following questions: "Could there be a blessing in disguise here?" or "How might this situation not be as bad as it first seems?" This approach helps patients think more divergently and thus opens their minds to more constractive alternatives. 2. Evidence. Patients need to learn that their opinions are not necessarily synonymous with facts. Therefore, therapists teach them the importance of looking for information that can be objectively con­ firmed or disconfirmed. Therapists ask patients for evidence for and against their automatic thoughts because they want patients to be evenhanded in their evaluation—even if that means finding evidence that supports their negative impressions. One useful way to commu­ nicate the nature of "evidence" is to say, "If it wouldn't stand up in court, it's not factual enough to count as evidence." 3. What's the worst that could happen? This is not the rhetorical question that people sometimes ask sarcastically when they are mini­ mizing someone's problems. This is a factual question that asks patients to consider a realistic worst-case scenario and then to evalu­ ate the actual implications for their lives. In general, this question serves to decatasfrophize many patients' extreme worries, as they come to realize that the worst-case scenario is highly unlikely, and that they can cope with the outcome in any event. 264 COGNTTIVE THERAPY OF SUBSTANCE ABUSE 4. What action can I take? Even if patients find that their auto­ matic thoughts are borne out, this question reminds them that they can actively engage in problem solving. By asking this question, patients are more likely to apply higher cognitive processes such as planning and decision making, and less likely to lapse into lower-level catastrophizing. 5. Pros and cons of automatic thoughts. Some patients seem wed­ ded to their negative, dysfunctional ways of thinking. In such instances, it is useful to ask them what benefits (and drawbacks) they derive from such negativistic thinking. This tactic defuses the patients' resistance in that it respects their reasons for maintaining their points of view, however self-defeating they may be. For example, we have encountered the following "reasons" that patients are unwilling to relinquish their automatic thoughts: "I don't deserve to think positively." "Every time I get m y hopes up disaster strikes." "If I think the worst, I won't be disappointed when it actually happens." "Nobody will take me seriously unless I'm really upset." Understanding these beliefs helps therapists to conceptualize patients' core assumptions, helps establish rapport, and may provide a window of opportunity to help these patients find some advantages to improving the adaptive quality of their thinking. An example of Rick's completed Daily Thought Record (DTR) can be seen in Figure 15.2. Any and all of the five questions summarized above can be used effectively within the format of the DTR in order to generate rational responses. Not all of the questions need to be used—note that Rick's DTR seems to address the questions "What other perspectives can I take?" and "What constructive action can 1 take?" Behavioral Techniques Behavioral techniques are particularly useful in the treatment of anxiety disorders. Relaxation and assertiveness training (Alberti & Emmons, 1974; Collner & Ross, 1978), for example, pro­ vide the individual with behavioral skills for coping with potentially threatening situations. Relaxation skills involve the systematic, pro­ gressive relaxation of various muscle groups (Bernstein & Borkovec, 1973) and controlled breathing (Clark, Salkovskis, & Chalkley 1985), which allows the individual to be more physically comfortable dur­ ing times of physiologic distress. Assertiveness training involves learn- Directions: W h e n you notice your mood getting worse, asi< yourself, "What's going through m y mind right now?" and as soon as possible jot down the thought or mental image in the Automatic Thought Column. SITUATION AUTOMATIC THOUGHT(S) EMOTION(S) RATIONAL RESPONSE OUTCOI^E Describe: 1. Wrife automatic thought(s) 1. Specify sad, 1 Write rational response to automatic thought(s). 1. Re-rate belief 1. Actual event leading to that preceded emotion(s). anxious/ 2. Rate belief In rational response 0-100%. in automatic unpleasant emotion, or 2. Rate belief in automatic angry, etc. thought(s) 2. Stream of thoughts, day­ thought(s) 0-100%. 2. Rate degree 0-100%. dreams or recollection. of emotion 2. Specify and leading to unpleasant 0-100%. rate emotion, or subsequent DATE/ 3. Distressing physical emotions TII^E sensations. 0-100%. Friday Alone at home. "I'll mal^e a fool of Nervous "I'm generally quiet when I go out, 1. -Fool" myself." (75%) not foolish." (25%) Coworkers have invited (75%) (100%) 2. "Relieved" me to meet them at a (65%) restaurant. "I don't know how to Anxious "I know how to be polite toward 1. "Don't know act around people." (85%) others." how to act" (85%) (90%) (25%) 2.Relieved (65%) "111 be alone for the Sad "If I take risks, I'll meet someone 1. "Alone for rest of my life." (45%) eventually." life" (50%) (75%) (35%) 2. Hopeful (50%) Questions to help formulate the rational response: (1) What is the evidence that the automatic thougsh tt rue? Not true? (2) Is there an altemative explanation? (3) What's the worst that could happen? Could 1 live through it? What's the best that could happen? What's the mosf reaiistic outcome? (4) What should 1 do about it? (5) What's the effect of my believing the automatic thought? What could be the effect of changing my thinl<ing? (6)f was in this situation and had this thought, what would 1 tell him/ner!" (friend's name) F I G U R E 15.2. Rick's Daily T h o u g h t Record. 266 COGNITIVE THERAPY OF SUBSTANCE ABUSE ing direct, adaptive expressive communication. As a result of incr skills, individuals develop a greater sense of competency. The learn­ ing of behavioral skills is facilitated by the use of covert rehearsal (imagety) and overt practice (role-play, behavioral experiments). Rick's therapist, for example, determined that Rick was particu­ larly vulnerable to feelings of inadequacy and rejection in social situ­ ations. Specifically, social situations tended to activate Rick's core beliefs about his vulnerability, which in turn activated his autonomic nervous system. His anxiety symptoms (perspiration, racing heart, etc.) then escalated into panic attacks, which he self-medicated with alco­ hol. To compensate for his feelings of vulnerability. Rick occasion­ ally used cocaine. Ultimately, Rick found that he had great difficulty controlling his cocaine use, which in turn exacerbated his feelings of vulnerability. In order to treat Rick's anxiety-related substance abuse problems effectively, his therapist began with progressive muscle relaxation and controlled breathing exercises. Such exercises prepared Rick for deal­ ing with the physiological arousal associated with panic attacks. After Rick had mastered relaxation, his therapist asked him to imagine a series of threatening social situations. O n becoming physiologically aroused at the thought of such situations. Rick practiced relaxing to decrease his autonomic arousal. Eventually, Rick began to modify his thinking from "I can't handle m y anxiety" to "I

can at least calm myself to avoid having a panic attack." Rick's therapist also engaged him in assertiveness training in order to provide him with essential communication skills. SUMMARY Unnecessary or exaggerated anger takes its toll not only on other persons but also on the person who is angered. Sub­ stance abusers are prone to act out their hostile impulses when they are under the influence of drugs or alcohol. Although they are par­ ticularly prone to use or drink to dampen the tension associated with anger, their substance use may, paradoxically, increase the likelihood of hostile behavior. Much of the generated anger is the result of the symbolic meaning attached to the provoking event, specifically, the notion "I have been wronged." Addicted individuals with low frustration tolerance (LFT) are hypersensitive to any blocking of their wishes or actions and are consequently prone to experience excessive and inappropriate anger. They fiequently have underlying beliefs such as "If I can't get [or do] Anger and Anxiety 267 what I want right now, I never will" or "Others are wrong to refuse me or get in m y way." Stemming from the other two beliefs is the belief "People are wrong and should be punished for blocking me." When activated, this belief leads to anger. Patients with LFT perceive themselves as powerless or helpless. The generation of anger helps restore a sense of control and power by punishing other people. Whether or not they act out their impulses to punish, however, they are more or less stuck with the anger, which can then lead to using or drinking. Additionally, the physiologic, cognitive, affective, and behavioral correlates of anxiety may place an individual at increased risk for substance abuse. W e presented some methods for conceptualizing LFT and anxious substance abusers, as well as some methods for inter­ vening with people who respond to LFT and/or anxiety with substance use. C H A P T E R 1 6 C o n c o m i t a n t P e r s o n a l i t y D i s o r d e r s T , he term "dual diagnosis" has been used widely to refer to the coJexLisht ence of substance abuse and other psychiatric disorders (Brown et al., 1989; Evans & Sullivan, 1990; O'Connell, 1990). In Chapters 14 and 15 (this volume) we discussed the dual diagnosis of substance abuse and major psychiatric syndromes (e.g., depression and anxiety). In this chapter we discuss the treatment of patients with dual diagnoses involving substance abuse and concomi­ tant personality disorders. Personality disorders (represented by Axis II of the DSM-llI-R clas­ sification system) (American Psychiatric Association, 1987), consist of longstanding affective-behavioral-cognitive patterns that are rigid, maladaptive, and resistant to modification. There have been numerous studies documenting the high preva­ lence of personality disorders among substance abusers. Regier et al. (1990), in their important comorbidity study, reported on data from over 20,000 subjects in the Epidemiologic Catchment Area study spon­ sored by the National Institute of Mental Health. These investigators found that of those with alcohol problems (abuse or dependence), 14% met criteria for antisocial personality disorder (ASPD). They found ASPD among those who abused marijuana (15%), cocaine (43%), opiates (37%), barbiturates (30%), amphetamines (25%), and halluci­ nogens (29%). In accord with these figures, many researchers acknowl­ edge a strong relationship between ASPD and substance abuse (e.g., Grande, Wolf, Schubert, Patterson, & Brocco, 1984; Helzer & Ptyzbek, 1988; Hesselbrock, Hesselbrock, & Stabenau, 1985; Hesselbrock, Meyer, & Kenner, 1985; Lewis, Robins, & Rice, 1985; Penick et al., 1984; Ross 268 Personality Disorders 269 et al., 1988; Schuckit, 1985; Stabenau, 1984; Wolf et al., 1988). Est mates of the lifetime prevalence of ASPD disorder in substance- dependent individuals vaty between 2 0 % and 50%. The high preva­ lence can be explained, to some extent, by the fact that substance abuse is one of the criteria for the diagnosis of ASPD. Several studies conclude that a wide range of personality disorders coexists with substance abuse. For example, Khantzian and Treece (1985) studied 133 opiate addicts and found that 6 5 % met criteria for at least one coexisting personality disorder. These investigators reported that "virtually the entire range of personality disorders [was] represented in [our] sample" (p. 1071). Drake and Vaillant (1985) evaluated 369 middle-age inner-city men, followed in a longitudinal study, for the presence of personality disorders and alcohol problems. Of those who had been alcohol dependent, 3 7 % had a concomitant personality disorder. Borderline personality disorder (BPD) is also commonly associ­ ated with substance abuse (Koenigsberg, Kaplan, Gilmore, & Cooper, 1985; Nace, Saxon, & Shore, 1983; Zanarini, Gunderson, & Franken- burg, 1989). These authors report consistently that among drug and alcohol abusers, BPD is second only to ASPD as a concomitant per­ sonality disorder diagnosis. Beck et al. (1990) have applied cognitive therapy to the treatment of personality disorders. The authors describe these patients as "often the most difficult in a clinician's caseload" (p. 5). Personality-disor­ dered patients typically share some of the following common features that make them especially challenging to treat: 1. Their most chronic symptoms are ego syntonic; that is, the patients do not perceive that there is anything substantially "wrong" with their personality. Although they may come into treatment in order to receive help for depression or anxiety problems, they rarely seek help for problems such as self-centeredness, avoidance of respon­ sibilities, lying, lack of empathy for others, lack of conscience, ten­ dency toward violence, interpersonal manipulativeness, defiance of authority, and other chronic aspects of their character that reflect common Axis II disorders. 2. Their behaviors and attitudes typically are noxious to others. Although these patients may feel that they are in emotional pain, it is common to find that they cause others a great deal of hardship as well. An example is a patient who bemoans the fact that his wife does not give him respect, but conveniently neglects to mention to the therapist that he steals her money, beats her, and cheats on her. 3. These patients are extremely resistant to change. Although they 270 COGNITIVE THERAPY OF SUBSTANCE ABUSE may enter therapy hoping to obtain some relief from their psycho­ logical suffering, they often do not wish to take an objective look at their own shortcomings, nor do they wish to alter their maladaptive behaviors or attitudes. An example is a patient who implicitly expects the therapist to offer him a "magic pill" to make him better, but balks at the idea of dealing directly with his problems at work and at home. 4. Personality-disordered patients have difficulty imagining being any other way. W h e n therapists tty to elicit their cooperation in making important changes in life, the patients often respond by say­ ing, "But this is who I am. I can't change," or "I've always been this way. H o w can I be any different?" or "If you tty to change me, I'll cease to exist." For these patients, their problems often are synony­ mous with their identities. Therefore, they resist change as staunchly as they would fend off personal annihilation. When a personality disorder contributes to drug use the pattern becomes more rigid and compulsive. Once the drug use has begun, the personality-disordered patient may be more likely to continue the pattern of drug use until it becomes a full-blown addiction. For example, the avoidant personality patient who cannot tolerate emo­ tional discomfort may receive temporary respite from his or her upsetting thoughts about their life situations via the use of crack cocaine. As a result, this patient may choose to continue using (and ultimately abusing) drugs as the preferred method to avoid facing up to problems. Furthermore, the patient who suffers from a concomitant person­ ality disorder will be at heightened risk for relapse following a period of successful abstinence. As a case in point, we have seen a border­ line patient relapse on drugs as a deliberate form of self-destructive- ness and interpersonal manipulation in response to arguments with a lover. Another patient, a woman who was diagnosed as having dependent personality disorder, believed that she would not be able to survive unless she had a man in her life. Consequently, she sought out male companionship at all costs, even if the men involved were active substance abusers. Each time she became involved with a new lover, she would subjugate her needs to his and would join him in his drug use. Thus, she knowingly and voluntarily lapsed back into drug use, even after having struggled so hard in therapy to achieve abstinence. Another ramification of patients' personality disorders is their capacity for cooperating and collaborating with the therapist (Carey, 1991). A substance abuser who does not suffer from a personality disorder may be an amiable and earnest patient with w h o m to deal Personality Disorders 271 in session after he or she has been free from drug use for some tim By contrast, we have seen patients who seem to be staying away from dmgs successfully but who have been extremely difficult to manage by virtue of their personality disorders. For example, "Ken" is a parole- office-referred patient who also has been diagnosed as having both paranoid and passive-aggressive personality disorders. In each therapy session, he adamantly insists that he has abstained from drugs in an ongoing fashion, and therefore concludes that his participation in treatment is "an idiotic waste of m y time." W h e n the therapist attempts to engage Ken in productive dialogues about the manage­ ment of general life stressors and maintenance of sobriety, he becomes reticent and projects an air of suspicion. At present, he remains drug- free, but he is not engaged in treatment to an optimal degree. His long-term prognosis, therefore, remains guarded. W e do not mean to imply that the treatment of drug abuse patients with concomitant Axis II disorders is an impossible task, nor do we mean to say that therapy with drug abuse patients without personality disorders is a breeze. The truth, obviously, is less dichoto­ mous and more complex. Nevertheless, it is vital that therapists per­ form a thorough diagnostic assessment of each substance abuse patient, so that the difficulties associated with the treatment of per­ sonality disorders may be anticipated. Treatment plans that address both the patients' drug abuse problems and characterological issues are better equipped to keep patients in treatment, and to prepare them for self-maintenance after regular sessions have been terminated (N.S. Miller, 1991). A S S E S S M E N T Personality disorders have been described in a num­ ber of ways. One simple formula that clinicians have followed over the years states that patients who have personality disorders cause as much or more grief for others in their lives as they suffer themselves (Cummings, 1993). Obvious examples of this are the narcissistic patient, who may be so blindly self-absorbed that he or she completely neglects the physical and emotional well-being of spouse and chil­ dren, and the ASPD patient, who may be having a "grand old time" while he or she lies, connives, and cheats in order to achieve his or her own ends. Another example is the borderline patient, whose affective lability, self-destructive impulsivity, and excessive interper­ sonal demands cause much consternation for significant others and for therapists. 272 COGNTTIVE THERAPY OF SUBSTANCE ABUSE If we use this rule alone, however, most substance-abusing patients will look as if they necessarily have personality disorders as well (Carey, 1991). When patients are in the throes of compulsive, addictive drug abuse, the following maladaptive behaviors are not uncommon: (1) stealing from family members, friends, or strangers in order to fulfill a desperate need to purchase and use drugs (symp­ tom of ASPD); (2) inveterate lying, in order to cover one's drug-abus­ ing tracks (symptom of ASPD); (3) almost delusional suspiciousness, a side effect of heavy usage of cocaine and/or amphetamines (symp­ tom of paranoid personality disorder); (4) angry outbursts and vio­ lence toward self and others due to overdose or withdrawal symptoms (symptoms of borderline, paranoid, and antisocial personality disor­ ders); (5) withdrawal from social activities into solitary drug use (symp­ tom of schizoid personality disorder); and (6) progressive self-absorp­ tion,

such that responsibilities toward others become ignored (symptom of narcissistic personality disorder), as well as numerous other behaviors. As we can see, the particular problems that accom­ pany the Axis I substance abuse disorder often look suspiciously like— and need to be distinguished from—full-blown Axis II disorders (cf. Gawin & Kleber, 1988). In order to clarify the assessment picture, we must look to the criteria of DSM-III-R, and to the diagnostic questionnaires that map onto the DSM-III-R, such as the Structured Clinical Interview for the DSM-IIl-R (SCID: Spitzer et al., 1987). Here, we are instructed to examine the enduring personality traits that exist and persist apart from the primary Axis I diagnoses. In this case the question becomes, "What personality traits were present during those times in the patients' lives when they had not yet begun to abuse drugs?" This question is espe­ cially useful when the substance abuse problem has an adult onset, and therefore there is an extensive premorbid histoty. Another useful source of assessment data comes from previous treatment experiences of patients. It is potentially enlightening to review notes and reports of patients' former therapists, as well as to ask patients themselves about their recollections of therapy contacts (and outcomes) in the past. Such information can shed light on the degree of chronicity of patients' drug problems, "changes" in person­ ality over the course of time as a result of drug use, and clues as to the kinds of interventions that were helpful or unhelpful. Another useful question is, "What personality traits are present during prolonged periods of abstinence, between drug use episodes?" Such an assessment question is salient when abstinence is the norm, punctuated by problematic lapses into drug bingeing. A simple interpretation of DSM-III-R suggests that a serious con- Personality Disorders 273 comitant Axis II disorder is less likely to be present when dysfun tional beliefs and behaviors did not predate the onset of the substance abuse disorder, and when they diminish or disappear during times of prolonged abstinence. The non-Axis-II-disordered patient is iden­ tifiable as one who seems to "change personality" dramatically when under the influence of psychoactive substances or cravings and urges associated with their abuse. This patient may seem quite compliant with the treatment regimen, and may relate in a friendly, coopera­ tive manner with the therapist when he or she is clean and sober. The same patient may break appointments, drop out of sight, and avoid or otherwise disregard the therapist when he or she resumes dmg use, and may engage in activities that seem to be completely "out of character." For example, one of our patients demonstrated herself to be a conscientious, hard-working, likable person when she had been free of dmgs for some time. Unfortunately, when she suffered a relapse, she resorted to thievery in order to obtain money for her habit. The crimes were not malicious but rather a matter of expediency—her values and priorities shifted dramatically when she used drugs (cf. Woody, Urschel, & Alterman, 1992). Family and friends (and the thera­ pist) were shocked when these facts came to light. Based on knowledge of her crimes of theft, and subsequent lies to cover up, this patient could be easily mistaken as having antisocial personality disorder. In actuahty, she did not meet DSM-III-R criteria for any of the Axis II diagnoses. W h e n she was abstinent from drugs, her most salient maladaptive beliefs were depressogenic, but not in­ dicative of longstanding characterological issues. As an example, she believed "I'll never be able to find a job in which I will be trusted to be in a position of responsibility again," and "Something always seems to set me back just when I think I'm getting on m y feet again." On the other hand, while she was actively using, this patient's beliefs became even more problematic (i.e., more similar to those espoused by Axis II patients; see Beck et al., 1990), such as "I have to do what I have to do, no matter what anybody tells me" (similar to beliefs held by ASPD and passive-aggressive patients), and "I have to use drugs because I can't bear to face life in a straight frame of mind" (similar to beliefs put forth by avoidant personality disor­ der patients). After successfully completing an inpatient detoxification program in a local hospital, this patient returned to cognitive therapy. She no longer gave credence to the beliefs that she had maintained during her relapse episode, and she once again became a vety compliant and actively involved outpatient. The depressive beliefs persisted, however. 274 COGNITIVE THERAPY OF SUBSTANCE ABUSE and became ongoing issues, along with a focus on drug relapse pre­ vention. In other cases, it is not necessary for patients to be in a phase of active drug use for them to evince dysfunctional beliefs and behav­ iors that earmark them as personality-disordered patients. For example, when "Lee" was going through his initial intake assessment, he ad­ mitted to abusing amphetamines, and highlighted a myriad of life problems. When asked how the drug use had led to the various life dilemmas, he quickly corrected the intake therapist, saying, "Speed doesn't cause all m y problems. I can get into all kinds of trouble, even if I'm not on the stuff, beheve me!" In this case, the substance abuse coexisted with a number of personality disorders, which would com­ plicate the drug abuse treatment and would need attention in their own right. To identify the presence of a personality disorder in a substance- abusing patient requires a careful evaluation of the patient's drug-free beliefs and behavior patterns, and a comparison of these with beliefs and behaviors that are activated by psychoactive substances. A gen­ eral rule of thumb holds that similarities between drug-free and dmg- using beliefs and actions suggest a high probability of an Axis II com­ ponent, while marked divergences give hope that the most noxious aspects of the patient's functioning will be extinguished if the dmg- taking is brought under control. For example, a patient who main­ tains the belief that he must never follow anyone's rules but his own— and espouses this view whether or not he is drug free—is likely to demonstrate antisocial personality traits that will complicate tteatment even if he is free from drugs. By contrast, a patient who typically believes that it is important to be an honest, responsible, cooperative person—that is, until she submits to her urges to use crack cocaine, whereupon she adopts an "I don't give a damn about anything" atti­ tude—is more likely to make significant therapeutic strides in all aspects of her life if she overcomes her addiction. Unfortunately, this assessment process is fraught with a number of difficulties. First, the optimal method of assessing drug-taking beliefs and actions is not readily apparent. W e have noted earlier in this volume (Chapter 12) that the patient's "hot" cognitions are most salient to assessment and treatment, and that such affect-laden thoughts are highly accessible under conditions that closely simulate the target problems in question. In the case of the patient who suf­ fers from a disorder such as panic, it is relatively safe and straightfor­ ward to contrive therapeutic situations that will elicit panic attacks in session, thus allowing the patient and therapist to have access to the hot cognitions. Personality Disorders 275 In the case of the drug-abuser, however, it is neither wise nor ethical to encourage the patient to engage in substance-taking as a means of gaining access to key cognitions. Instead, we must use more indirect methods. One method involves having patients rely on free recall to remember what they believed and what they did while in the active phase of drug use. This technique is simple and safe, but may be subject to inaccuracies, owing to patients' memoty distortions and deliberate confabulations. Another method involves gaining data from more objective sources, such as the verbal reports of family members and the writ­ ten reports of previous therapists and legal officers. Although these data help the therapist to ascertain the maladaptive actions of the drug- taking patient, they do not facilitate gaining an understanding of the subjective phenomenology of the patient who is under the influence of dmgs. W e have found that the two approaches explained above are most informative when combined with clinical data that are obtained through provocative imagety exercises, such as patients' closing their eyes and imagining the houses where they use crack. These exercises, described earlier in this volume (Chapter 10), provide patients with the kinds of covert stimuli that will likely produce a reasonable experience of their hot cognitions. These techniques, free recall, third- party behavioral reports, and in-session imagery exercises, combine to help therapists to assess patients' drug-using beliefs and behaviors. As these data are obtained, it becomes more likely that therapists will be able to separate those aspects of patients' functioning that are part of a consistent personality characteristic from those aspects that are dmg-related per se. Still, there are further diagnostic problems. For example, when a 35-year-old drug-abusing patient notes that he has used hard-core dmgs such as cocaine since the age of 15, the therapist is hard-pressed to view the patient's drug-related beliefs and actions as anything other than a major part of his personality characteristics. Here, there may not be a single person (the patient himself included) who could guess how the patient would function if he were not on drugs. In such cases, the line of distinction between Axis I and Axis II becomes quite clouded, and therapy may have to involve the teaching and nurtur­ ing of fundamental adaptive ways to view the self, the world, and the future practically from "scratch." Yet another problem in distinguishing personality issues from substance-abuse issues involves the medical complications of long- term drug abuse. Specifically, it is likely that prolonged, heavy use of certain psychoactive substances causes progressive damage to the 276 COGNITIVE THERAPY OF SUBSTANCE ABUSE central nervous system (Karan et al., 1991; Nace & Isbell, 1991; O'Connor et al., 1992). As time goes on, rather permanent changes in personality may result from the abuse of drugs, such that even complete cessation of drug use may still leave behind the residual characterological dysfunction. As an example, one of our patients ended a 20-year habit of daily marijuana use after his wife threatened to leave him. Although he succeeded in stopping cold turkey, the patient then was dismayed that he began to feel perpetually depersonalized, to the point that he was "unable to focus m y atten­ tion on anyone but myself and m y own feelings." In a sense, the after­ effects of the marijuana use seemed to be a narcissistic-schizoid per­ sonality style. This serious problem, along with his chronic anxiety, became the chief foci of therapy over the course of the next six months. Needless to say, there was a concomitant struggle to keep him from returning to regular marijuana use as well. In sum, it is difficult to separate substance abuse symptoms from long-standing personality issues and disorders. Our experience has taught us that the majority of all substance-use cases will necessitate some sort of therapeutic focus on Axis II disorders, either as a con­ tributory cause or as a consequence of the problematic taking of dmgs. The best barometer for the concomitant presence of personality dis­ orders is an assessment of the patient's beliefs—about drugs, and about the self, personal world, and future (the standard cognitive triad; cf. Beck, 1976), when the patient is free of psychoactive substances. BELIEFS THAT FACILITATE DRUG-TAKING ACROSS DIFFERENT PERSONALITY DISORDERS Beck et al. (1990) have outiined common beliefs that are held by patients who suffer from the various personality disorders as described by DSM-III-R. While it is beyond the scope of this text to describe fully each and every one of these disorders, along with their respective lists of beliefs, it is interesting to highlight some of the beliefs that feed into drug-taking. In each of the following examples, the treatment for drug addiction must attend to these con­ comitant maladaptive cognitive sets. Many of our drug-using patients are chronically anxious and fear­ ful, resorting to drugs as a way of feeling a greater degree of "safety" or "confidence." ̂ Ivoidant personality patients, who

experience chronic cross-situational, exaggerated feelings of threat to their physical and psychological well-being, fall into this category. They maintain beliefs that make the use of drugs seem quite enticing, certainly more Personality Disorders 277 attractive than facing up to (and solving) real problems. Such bel include "I cannot tolerate unpleasant feelings" and "If I feel or think something unpleasant, I should try to wipe it out with a drink or a dmg." Another type of anxious and fearful patient is the dependent per­ sonality. These patients do not believe that they can get by without "a little help from their friends" (e.g., drugs, and drug-using cohorts). Their drug-taking is facilitated by implicit assumptions such as "I can't cope as others can" and "I am needy and weak." This mind-set makes a patient easy prey for stimulants such as cocaine, crack, or amphet­ amines, which induce a temporary but powerful sense of confidence and control in the early stages of their abuse. In addition, peer pres­ sure to engage in drug use is magnified greatly when dependent patients think that they must win the approval of their acquaintan­ ces at all costs. Passive-aggressive patients are hesitant to act out their anger directly, instead choosing to ignore the rules set forth by authorities. They believe that it is safer simply to choose not to conform. For these patients, using drugs represents a way to rebel against disapproving members of their families and society, while maintaining erroneously that "It isn't hurting anybody, so what's the problem?" Meanwhile, these patients further neglect the obligations and responsibilities that they resent in the first place. Drug use is also facilitated by obsessive-compulsive beliefs such as "My way of doing things is generally the best way," and "I need to be in complete control." Here, obsessive-compulsive drug-users maladaptively convince themselves that they know what is best; there­ fore the use of drugs "must not be a problem." Additionally, the false sense of omnipotence that cocaine can induce reinforces their mis­ taken notion that they are in complete control of themselves and their life situations. Narcissistic patients believe that they are entitled to special treat­ ment and privileges, and that they do not have to abide by the rules that most others must follow. They believe that they are special and powerful, and that they deserve to have all of their desires fulfilled. Obviously, these implicit points of view contribute to narcissistic patients' feeling free to engage in any behaviors that give them a sense of satisfaction (including the use of illicit drugs) without feeling that they have done anything wrong or unwise. In the case of histrionic patients, drug use is facilitated by their beliefs that "I cannot tolerate boredom" and "If I feel like doing some­ thing, I should go ahead and do it." Furthermore, they want vety much to be the center of attention, something that is more likely to occur 278 COGNITFVE THERAPY OF SUBSTANCE ABUSE if they are acting outrageously as a result of chemical intoxica­ tion. Additionally, the beliefs of patients w h o suffer from paranoid, schizoid, and schizotypal personality disorders potentiate drug use in that these patients are looking for experiences that they can enjoy in solitude, and that help them to feel on their guard against intrusion or attack from others. The Axis II disorders described present significant challenges to the therapist w h e n patients also evidence substance abuse disorders. However, the most difficult and pernicious combinations involve, most notably, the borderline and antisocial personalities, which interact with chemical addictions to form a class of disorders that is substantially resistant to treatment of any kind. Therapy for such noxious composite disorders must involve skilled application of (1) structured sessions, (2) between-session assignments and monitoring, (3) therapeutic relationship-building behaviors, and (4) sophisticated and flexible conceptualizations of patients' problems. In order to approach these objectives, w e alert therapists to the following problems and complications that arise in the course of treatment with such patients. BPD A N D ASPD DRUG-ABUSING PATIENTS: CLINICAL MANIFESTATIONS A N D IMPLICATIONS FOR COURSE OF COGNITIVE THERAPY As separate entities, substance abuse disorders and per­ sonality disorders such as the borderline and antisocial syndromes are difficult to treat. In combination, the clinical picture becomes exfremely challenging indeed. For example, one useful method of eliciting the active cooperation of a dmg-taking patient is to help him or her to realize the long-term personal rewards of abstinence. For most patients, goals that appeal to self-interest are intrinsically atfractive. However, imagine that such a patient has the following schema: "I'm bad, and I deserve to have m y life fall apart." This schema, not u n c o m m o n for a borderiine patient, may motivate the patient to deliberately steer clear of any sfrat­ egy that might bring about personal success or recovery. As a result, the therapist's initial call to look at long-term benefits becomes meaning­ less to this patient. In such a case, the therapist must focus on modify­ ing the extiemely maladaptive beliefs that feed into self-hafred, fear of success, and compulsive self-sabotage. Personality Disorders 279 As another example of the immense difficulties involved in treat­ ing the severely personality-disordered substance-abusing patient, consider the case of a man with antisocial personality disorder. In contrast to the borderline patient described above, self-interest is markedly overdeveloped in the antisocial patient. In turn, the capacity for feeling guilt is profoundly underdeveloped. As a result, the therapist's focusing on the harm that the patient is causing others as a result of the substance abuse loses practically all its motivational leverage. Furthermore, the antisocial patient's thirst for freedom and control, and his or her antipathy for authority (e.g., therapists), often leads such a patient to work extremely hard to fight against the work of therapy altogether. The above examples offer but a glimpse at the dilemmas that face therapists who treat these most problematic of dual-diagnosis patients. W e would like to note that although we present them as separate diagnostic categories, the borderline and antisocial personalities some­ times overlap. In fact, the co-occurrence of multiple Axis II diagnoses in the same patient is a c o m m o n phenomenon (Gunderson & Zanarini, 1987). For the sake of clarity, however, we have chosen to discuss the special therapeutic issues of the borderline substance abuser and the antisocial substance abuser separately. Antisocial Antisocial patients rarely come into therapy of their own accord. They generally do not view themselves as having emo­ tional problems of any sort. Instead, they view others around them as being the source of any problems that they may have ("They're hassling me, ripping m e off, jerking m e around, on m y back all the time, setting m e up," etc.). As a result, their appearance in therapy is likely to have been imposed on them against their will. In the case of substance-abusing antisocial patients, the source of this mandate usually is a legal authority. It is only natural then for such patients initially to view the therapist as part of the "system" that is ttying to oppress them. As a result, patients try to assert control in any manner possible, usually by passive resistance, sometimes by more radical means such as intimidation. It is especially important at times such as these that cognitive therapists remember to be collaborative, rather than acting controlling in their own right. For example, when "Don" told one of us that he resented hav­ ing to see a "shrink," the therapist avoided a response with paternal- 280 COGNITIVE THERAPY OF SUBSTANCE ABUSE sounding imperatives such as "Too bad, but you have to be here, buddy!" Instead, he surprised Don by stating, "I know that if it were up to you, you wouldn't be here in this office. You weren't given much of a choice, and that pisses you off. But you know something? We've got something in common. / didn't ask to see you either. You were assigned to me, and I didn't have much of a choice, just like you. So . since we seem to be stuck with each other, how are we going to make this a tolerable experience for both of us?" This vignette underscores another principle of successfully engaging antisocial patients^eeping them entertained. As they are insatiable stimulus seekers, antisocial patients easily become bored and inattentive in session unless the therapists are willing to be energetic, innovative, and just a little bit confrontational (Doren, 1987). To the extent that therapists can keep their antisocial patients stimulated, the patients will find the sessions engaging enough to want to return for fur­ ther appointments. These patients will be more likely to become actively involved in therapy if they feel that their relationships with their therapists pose interesting interpersonal challenges. As a caveat, thera­ pists need to watch out that they do not fall into the trap of being so entertained themselves by the antisocial patient's tales of daring and horror that they are led completely astray—away from the agenda of drug abuse and other patient maladaptive behaviors. Along these same lines, there is a great temptation on the part of therapists to fight to prevent their antisocial patients from gaining any degree of one-upmanship. These therapists believe that the only way to manage deceptive, manipulative patients is to browbeat them and to "show who's boss." This is a mistake. The therapist's job is not to impress the patient with his or her street smarts, nor to attempt to win evety argument. The goal is to keep the patient interested in a therapeutic process that has the best chance of influencing behavioral change (Cummings, 1993; Doren, 1987). This may mean that the therapist has to allow the patient to "win a few." By being reason­ ably flexible, unpretentious, and willing to own up to mistakes or shortcomings in knowledge, therapists stand a fair chance of disabus­ ing their antisocial patients of their commonly held beliefs that thera­ pists are simply into head games and power trips. To illustrate, one patient claimed that his barroom acquaintan­ ces, members of a local motorcycle gang, were responsible for his dmg relapses. He reasoned that they challenged his manhood by daring him to get high with them. W h e n the therapist suggested a few "middle-class, liberal" assertive comments for the patient to tty out on these hoods, the patient just laughed and said "That intellechial shit might work in your neighborhood, but not in mine!" Rather than Personality Disorders 281 defend his position, the therapist admitted he had goofed on the matter, and said, "Yeh, you're right. I'd probably get m y ass kicked if 1 said that to them." The therapist then proceeded to solicit sugges­ tions for snappy retorts from the patient himself, a strategy that was much better received. Another complicating factor in treating antisocial drug abusers is that their persistence in taking drugs throughout the course of therapy (and after treatment ends) seems to be worse than for the "average" substance abuser (Doren, 1987). While many addicted patients seem to decty their own drug use, and genuinely wish to kick the habit, antisocial patients often seem vety much to want to con­ tinue their drug use. Rather than using therapy as a way to stop, they attempt to use their treatment to learn how to conceal it better. This may account, in part, for the generally poor outcome that has been reported in the literature for the ASPD drug-abusing patient (Alterman & Cacciola, 1991; Woody et al., 1990). Similarly, ASPD patients' self- report data are more likely to be falsified than are the average drug patients'. This would include information on their drug history, present-time drug self-monitoring, attendance at support group meet­ ings, and adverse effects on their employment and relationships. For therapists to be best equipped to catch such patients at baldfaced lying, they must take extensive notes. While this is true in treating all patients, it is especially so in treating these most difficult of patients, who weave elaborate webs of falsehoods around unsus­ pecting, well-meaning therapists. By writing complete notes, not only do therapists protect themselves from unnecessary legal risks, they will also be able to spot the inevitable inconsistencies in patients' reports that

will serve as the basis for necessary therapeutic confron­ tations. For example, a patient who missed an appointment with his thera­ pist gave the alibi that, since his driver's license had been revoked, he was dependent on others to drive him to his sessions. He claimed that his "driver" failed to show up; therefore the missed session was not the patient's fault. The therapist documented this in great detail, including the "fact" that the license would not be restored for almost 6 months. One month later the same patient excused his lateness for a session by saying that he could not find a parking space. After determining that the patient had indeed driven himself to the therapist's office the therapist read aloud from his notes of the ear­ lier session when the patient had bemoaned his lack of a driver's license. The patient, dumbfounded and annoyed at having been caught in a lie, admitted that he was driving on a suspended license. W h e n pressed further, he was forced to admit that his lack of a license had 282 COGNITIVE THERAPY OF SUBSTANCE ABUSE been scarcely a deterrent to his driving, and that his absence fro the previous session was due to something else—taking a "detour" to a bar, where he got drunk. The remainder of the session was spent discussing the patient's drinking, his illegal driving, and his avoidance of therapy sessions. Without the detailed therapy notes, this patient's important area of deceit might have gone unnoticed at the time. When therapists challenge patients on the veracity of their state­ ments, they may do so in a respectful, supportive way, but they must not shy away from expressing disbelief where it is called for. The following dialogue serves as an example: TH: This is only the second time you've attended a therapy session in about two months, "Jackie." I'm wondering why it took so long for you to return m y phone calls. Have you been in some sort of trouble? PT: Oh, no! I've just been busy, you know. I'm working double shifts, you know, and I just didn't have time to get back to you, you know. [Therapist noticed that Jackie was overly animated, and won­ dered if she was anxiously withholding important information. Her overuse of "you know" statements was a giveaway that Jackie was pretty wound up.] TH: Jackie, I know that you work very hard at your job. You have always done so. But that never stopped you in the past from returning m y calls, except for those times when you were actively using drugs. PT: Oh, no, no, no! I haven't been using drugs. TH: OK. I want to believe that. But I'm puzzled that you didn't call me for four weeks, even though I left numerous messages. PT: 1 told you. I just didn't have time! TH: Jackie, it's hard for m e to accept what you're saying right now, because there have been many times in the past when you were very, very busy with your job, and with your family's problems, and you still managed to come to therapy sessions every week. You proved to me that you were capable of keeping your life organized and of not letting anything stand in the way of what you had to do. It's something I've always admired about you. PT: (starts to cry) TH: [Therapist wondered what Jackie was thinking as she started to cry, but did not want to get sidetracked just yet. He thought that the patient's tears might be real, but they might also be a Personality Disorders 283 manipulative ploy. Therefore, he decided to continue to press for the truth, albeit in a vety supportive manner.] I'm on your side Jackie. I'm totally on your side, and I want to help you. What kind of frouble have you been in lately with drugs? I really want to help, but you have to be honest with me. PT: {Crying) Everything's all messed up. [Jackie went on to say that she lost her job, and that she felt vety ashamed. She and the therapist spent the rest of the session assessing her degree of drug abuse, hopelessness, and suicidality, and they arranged to have daily phone contacts for the next three days until the next face-to-face session. None of this would have come out had the therapist accepted everything that Jackie had said at face value.] In this example, the therapist was very careful not to communi­ cate an air of self-satisfaction because he had successfully caught the patient in a deception. The goal was to elicit information that could lead to the appropriate assessment and intervention, not to demon­ strate that the therapist had superior savvy or to shame the patient. This underscores an important tenet of working with the antisocial dmg abuser, namely, always treat the patient with respect, even as you are "winning" the struggle for control of the therapeutic agenda. By leaving the patient with a sense of dignity, collaboration is main­ tained and facilitated. Antisocial patients are not altruists. They are not responsive to entreaties to "do the right thing"; they are turned off by the percep­ tion that others are moralizing, and they generally focus only on their own immediate wants and needs (e.g., a drug-based high). Therefore, the therapist can make headway in treatment only to the extent that the patient becomes convinced that it is in his or her best interest to change. Simply put, this involves helping patients to understand the relative costs and benefits of moditying the various aspects of their current functioning. Unfortunately, antisocial patients are notoriously inept assessors of the consequences of their actions. Likewise, they are deficient in ascertaining the consequences of their thoughts, beliefs, and emotions as well. Walter is an excellent case in point. Each time he got a new job, he went out and "celebrated" by getting drunk and then using cocaine. This invariably led to tardiness, absenteeism, and the loss of the job. Walter once again would become depressed, and adopt the attitude "I don't give a shit anymore. Fuck it!" This would in turn lead to more drug use, and the downward cycle would continue. A great deal of work (over a long time in therapy) was required in order for Walter to comprehend the amazingly simple fact that his 284 COGNITIVE THERAPY OF SUBSTANCE ABUSE own behaviors and thoughts were responsible for his downfall. A breakthrough of sorts was achieved when he was able to articulate the idea that his "celebrations" were at the root of his repeated fir­ ings. It took him considerably longer before he realized that the thoughts "I don't give a shit," and "Fuck it!" were also responsible for his continuing self-defeating behaviors. One of the most effective methods of teaching patients to moni­ tor the consequences of their responses is the advantages-disadvan­ tages analysis (Chapter 9, this volume). For example, when a patient experiences a strong craving for drugs, he or she is instructed to examine the advantages and disadvantages for using, as well as the advantages and disadvantages of not using. Similarly, this same tech­ nique may be used for other maladaptive aspects of functioning, such as the pros and cons of (1) acting on an urge to seek revenge, (2) quitting a job, (3) engaging in high-risk sexual behavior, (4) dwell­ ing on anger-producing thoughts, (5) discontinuing therapy, (6) con­ tacting drug-using associates, and (7) adopting an "I don't give a damn" attitude, as well as many other "popular" modes of operation of the drug-taking antisocial patient. As the patient begins to learn to use this technique with some degree of proficiency, he or she can be taught the next level on the hierarchy of difficulty, namely, distinguishing short-term pros and cons from long-term pros and cons. Typically, antisocial patients are driven by short-term rewards, and therefore often act out impulsively in a manner that is decidedly destructive in the long run. They seem to have a block in even thinking about or imagining long-term conse­ quences. It is a difficult task to help these patients to learn to envision the future and to delay gratification. One method is guided imagery exercises, where the therapist describes various outcomes for patients to picture in their mind's eye. Typically, the images depict aversive consequences for patients if they continue to use drugs, consequences such as loss of money, job, family, health, and freedom. It is impor­ tant to make these images as graphic as possible, such as waking up in one's own urine in a roach-infested house, facing an accusatory tirade from the spouse or children, or having handcuffs slapped on in front of the neighbors. As this exercise is repeated, patients are asked to provide more and more of the description themselves. Along with the negatives mentioned above, positive images of the outcomes asso­ ciated with abstinence from drugs should be generated in a detailed fashion as well. Therapists can teach their patients to practice these images every day, to help provide regular incentive to stay away from drugs. Personality Disorders 285 Another technique encourages patients to "test their ability" (an appealing challenge to antisocial patients) to withstand urges to engage in impulsive behavior, such as drug use, violence, unsafe sex, and so on. When they get one such urge, they are instructed to monitor how long they can "bravely" fight off the temptation. While they are doing this, the second part of the skill involves thinking (and writing) of ways that it might be advantageous to "lay low, size up the situation real carefully, stay cool, and bide your time." An important goal here is to appeal to patients' intelligence by suggesting that they exercise their ability to think before they act (out). As a warning, therapists should emphasize to their patients that this technique works best when it is applied to cravings that arise spontaneously. It is inappro­ priate to use this technique by contriving high-risk and craving situ­ ations under the guise of "testing" oneself. The methods described above are most effective when they are incorporated into regular therapeutic homework assignments. W e cannot overemphasize the importance of between-session practice of the techniques and principles that are reviewed in the therapist's office (Newman, 1993; Newman & Haaga, in press). Without such regular application of therapy techniques, much of what goes on in session will go "in one ear and out the other." W e advocate the taking of notes (by both the patient and the therapist) during the session. Fur­ ther, we suggest that patients keep a spiral notepad or folder where they can compile important therapeutic notes and homework assignments as they progress through treatment. In addition, we encourage patients to allow us to audiotape the goings-on in therapy, and for patients to take the tapes home to review the contents of the session again and again. Sometimes, we have increased compliance by asking patients to listen to the tapes in order to remind us where we as therapists "goofed up," and where the patients made their most astute observations in the previous ses­ sion. In addition to their benefits as teaching devices and general interventions, homework assignments serve a useful assessment func­ tion as well. Patients with the higher levels of motivation will be the ones who are most likely to make earnest efforts to complete the assignments. The antisocial patients who are simply "playing the game" of therapy will find dozens of elaborate excuses for fail­ ing to do the homework as assigned (Doren, 1987). In this sense, a patient's willingness to collaborate in the therapeutic process can be gauged via his or her responses to homework assignments. In any event, it is potentially useful to elicit the thoughts and beliefs that inhibited the patient from following through with the assignment. In the case of benign procrastination or lack of under- 286 COGNITIVE THERAPY OF SUBSTANCE ABUSE Standing, this is a rather straightforward task. On the other hand antisocial patient who is clandestinely ttying to subvert the therapy process will be more difficult to pin down. Here, it may be more useful to ask the patient to express his or her complaints about the home­ work as an entty point into the assessment of

thoughts that discour­ aged the patient from doing the assignment. Sometimes the responses are quite surprising, such as one patient who resisted reading a book that we had recommended, even to the point of purchasing it and then throwing it out when he got home. After much careful probing by the therapist, the patient was finally able to explain that he noticed that the author of the book had been employed by the Center for Cognitive Therapy. He then reasoned, "You all just want to make more money by asking people like me to buy your books. You don't really care about helping me\" The fact that he was receiving free treatment in the first place did not seem to fac­ tor into his thinking, nor did the fact that the book was a very inex­ pensive paperback. He was simply primed to assume that "everyone will always tty to get one over on me, if they get the chance." In his way of thinking, he certainly was not going to cooperate with any­ one who was trying to take advantage of him, even if it meant wast­ ing his money in the self-defeating act of throwing away a brand new book. This maladaptive mode of operation then became a focal point in therapy, along with his problematic substance abuse. Although not commonly associated with the treatment of sub­ stance abuse or antisocial personality disorder, assertiveness training (Alberti & Emmons, 1974; Collner & Ross, 1978) is a useful part of treatment with this population. Most of these patients engage in dichotomous, all-or-none social behavior, acting either passively or aggressively. Assertiveness is not typically part of their repertoire. This leads to many obvious problems, such as an inability to say no to peers who want them to use drugs, and inappropriate ways of deal­ ing with conflict situations with employers, significant others, parole officers, and therapists, among other people. Although one may argue that teaching antisocial patients the skills of assertiveness is tantamount to instructing them in ways to be better manipulators of others, we have found that this is generally not the case. These patients wreak far more havoc by being pas­ sive aggressive (e.g., "forgetting" to pay child support) and aggres­ sive (e.g, deliberate high-speed tailgating on the highway), rather than assertive (cf. Doren, 1987). Furthermore, the vicious cycles that are perpetiiated by dysftinctional thoughts that lead to dysftmctional interpersonal behaviors that then lead to interpersonal consequences that further refuel maladaptive thoughts are slowed down when Personality Disorders 287 assertive behaviors prevail. An additional potential benefit of assertive ness training is that it m a y help patients to identify and articulate thoughts and feelings that previously were ignored or deliberately suppressed by the patients. For example, a patient w h o believes that a therapist is trying to control and manipulate her m a y react in a hostile manner that results in greater attempts from the therapist to gain control over the patient's maladaptive behaviors, thus "confirming" the patient's suspicions. O n the other hand, if a patient assertively and directiy tells a therapist that she does not appreciate his heavy-handed therapeutic tactics and wishes that he would be a bit more lenient and understanding, the therapist is more likely to understand the patient's actions in a con- stmctive light. Thus, a potentially destructive power struggle m a y be averted. Borderline Similar to the antisocial drug abuser, the borderline patient tends to act out impulsively, to experience extremely low frus- ttation tolerance, to be deficient in learning from past mistakes, to use drugs in lieu of attempting to cope with stress, and to have diffi­ culty in establishing stable, trusting relationships with caregivers. In contrast to antisocial patients, borderline patients m a y use drugs more out of a sense of hopelessness than as thrill-seeking behavior. In addition, their behaviors are m u c h more deliberately self- destructive than are the behaviors of antisocial patients or other per­ sonality-disordered patients. Owing to the borderline patients' ten­ dency to maintain powerful negative beliefs about themselves, their hopelessness, and poor impulse control, the threat of suicide is far more prominent in the case of the borderline substance abuser. In contrast to antisocial patients, w h o often feel that they do not need to see a therapist, borderline patients more frequently are desperate for help. Nevertheless, they are apt to act in ways that sabotage the process of therapy, owing to their erratic emotionality, their difficulty in using thoughts (rather than raw emotions) to modulate their o w n behavior, and the extreme, conflicting demands that they make on their therapists. Borderline patients pose a peculiar challenge to therapists in that they so readily avoid acting in their o w n best interests. It is one thing to motivate a patient to give up the use of drugs by appealing to an improved quality of life in the future. It is quite another thing to attempt this with a patient w h o states "I don't give a d a m n about what happens to me, n o w or ever, so I might as well do whatever it takes 288 COGNITIVE THERAPY OF SUBSTANCE ABUSE to kill the pain," or who maintains the belief "I hate myself and 1 deserve to have a messed up life." O n the other hand, borderline patients may be more likely than antisocial patients to profess concern and love for others in their lives, in spite of their lack of caring about themselves. For example. Dee experienced a life filled with sexual, physical, and emotional abuse, leading her to conclude that she was a "bad" person who was "dirty and used up." At the start of treatment, she professed not to care for herself, and she took a cavalier attitude about the possibility that she might wind up killing herself with a drug overdose. It was clear that she was not intent on doing the work of therapy in order to obtain the benefits for herself. Instead, Dee and her therapist focused on her baby daughter, w h o m she loved dearly. Therapeutic goals were set on the basis of the premise that the baby would become the ultimate beneficiary. This served as the "hook" that got Dee involved in the active process of trying to curtail her drug taking. She knew that she would take proper care of her beloved baby if she practiced abstinence from drugs. O n the other hand, if she used drugs. Dee knew from experience that she would disregard everything in her life, even her own daughter. The prospect of this happening again frightened her and therefore served as an initial motivator for treatment. Dee's case typifies the difficulties involved in treating this popu­ lation. When she experienced a drug lapse, she would tend not to bring herself back into line by thinking about what was best for her daughter. Instead, she would look at her drug-using experience as "proof" that she was an evil person and a bad mother who deserved to die. She would think to herself that her baby would be better off if she had a different mother, and Dee would proceed to escalate her drug use into a full-blown relapse. As a result. Dee would get her "wish," in that her aunt would take custody of the baby. As she began the next cycle of recovery. Dee once again would yearn for her daugh­ ter, thus leading to more depressed affect, frustration, and rifts in the family. Such stressors precipitated significant drug-taking cravings and urges, which again would feed into Dee's extremely low self-esteem. In dealing with cases such as Dee's, the therapist must be on the lookout for a number of emotional and cognitive dysfunctions typi­ cal of the borderline patient that exacerbate the patient's drug-taking habits. First, as mentioned above, borderline patients are prone to self- sabotage, believing that they are undeserving and unable to change things for the better (Layden, Newman, Freeman, & Byers-Morse, 1993). Such a mindset is wholly unconducive to acting in one's own best inter­ est, in planning for the future, in collaborating with the therapist, and Personality Disorders 289 in resisting the temptation to abuse drugs. Therefore, the borderline patient's pathologically low self-image (i.e., beliefs about the self) must be assessed and addressed as part of the treatment for substance abuse. Another factor is the borderline patient's propensity for feeling profoundly lonely and empty. M a n y of our patients have reported that the use of cocaine, crack, or heroin temporarily alleviates these feel­ ings, causing them to feel no need for other people during the euphoric surge. It is therefore not surprising that borderline patients turn to drugs in response to interpersonal difficulties and the result­ ant dysphoria. Complicating matters is the fact that some of these patients view their drug-taking cohorts as their only source of "friends." The thought of losing these associates as a result of becom­ ing abstinent is simply too threatening to entertain, and the drug use continues. In order to deal with the problems associated with extreme lone­ liness, therapists must help their drug-using borderline patients to work at building new, drug-free relationships. In addition, it is often beneficial to assist these patients in trying to repair old relationships (e.g., with immediate family members) that were strained or severed due to their substance abuse. These are difficult tasks for the border­ line patient, but they are necessary in order to provide an attractive alternative to the "loneliness-killing" qualities of drugs. Yet another problem borderline patients pose is their hair-trig­ ger hopelessness. As w e discussed earlier in this volume (Chapter 12), patients are more likely to resort to the quick fix that drugs produce if they believe that the future holds no promise. The implication for therapy is that the patients' degree of hopelessness is a critical vari­ able with which to contend if w e are going to succeed in helping them become and remain drug-free. Borderline patients, w h o are notorious for their extreme black- and-white thinking (cf. Beck et al., 1990; Layden et al., 1993), can change their outlook on life from optimistic to completely hopeless with relatively little provocation. W e have seen such patients leave a productive therapy session in very high spirits, only to call the thera­ pist the same evening in a state of deep dysphoria due to an objec­ tively mild stressor. W h e n drug abuse is part of the clinical picture, these patients are more likely to resort to getting high than they are to call their therapists for assistance. The upshot is that the border­ line patient can flip vety quickly from hopeful and abstinent to hope­ less and using. Therefore, therapists need to remain vigilant in help­ ing these patients to learn, practice, and, it is hoped, master the skills of decatastrophizing and problem-solving in the face of setbacks. 290 COGNTnVE THERAPY OF SUBSTANCE ABUSE An offshoot of the borderline patient's problems with hopeless­ ness is a pronounced risk for suicide (Linehan, 1987). Ideally, the patient's wish to live or die should be assessed at every session, and a verbal antisuicide contract should be made and renewed frequently. For example. Dee was periodically suicidal, and the therapist repeat­ edly stressed that she was to call him at work or at home in the event that she wanted to harm herself. She agreed to do so, but she was agonizingly inept in keeping ready access to the therapist's telephone numbers. Therefore, as a matter of ritual, the therapist assigned Dee the task of memorizing his telephone numbers, and quizzed her sud­ denly at various points during every therapy session. As a population, substance-abusing borderline patients are more frequently in need of hospitalization than many other clinical patient groups. Even in an inpatient setting, such patients pose considerable management problems. If the patient is suicidal, the first order of business is to provide constant professional supervision. Although the acute risk for suicide may pass, this type of patient rarely is able to stay in the hospital long enough to deal adequately with the border­ line disorder. When these patients reenter outpatient treatment, the therapist's tasks are daunting. As with

the antisocial drug-abusing patient, it is vitally impor­ tant to carefully nurture and make clinical use of the therapeutic relationship (see Beck et al., 1990; Layden et al., 1993; Young, 1990; Chapter 4, this volume, for more detailed explications). The all-or- none thinking style of the borderline patient often shows itself in the way that the patient views the therapist, who may be seen as a savior one week (e.g., "Nobody else understands m e the way you do. You're cool and I can trust you.") and a villain the next week ("You're just like all the rest! You don't care about me! You don't know what you're talking about! You're not helping m e at all!"). Under such adverse interpersonal conditions, therapists must not allow themselves to buy into patients' extreme positive or negative feedback. Instead, they would do well simply to maintain their composure, to express an ongoing willingness to help, and to focus on the thoughts and beliefs that are behind the patients' polarized reactions. Likewise, therapists must make every effort to teach these patients to think carefully before acting. This involves painstaking training in problem-solving (D'Zurilla & Goldfried, 1971; Nezu et al., 1989) and rational responding (Beck et al., 1979; Newman & Beck, 1990), skills that are most difficult (yet most necessary) to employ at times of extreme distress. Also similar to the treatment of the antisocial patient is the focus on helping the borderiine patient acquire assertiveness skills, so as to reduce conflict in interpersonal situations. Personality Disorders 291 All these interventions require numerous repetitions with both antisocial and borderline patients, as their psychological learning skills and levels of motivation to change are notoriously deficient. SUMMARY The existence of severe Axis II disorders in substance- abusing patients significantly complicates the treatment picture with these patients. In particular, antisocial and borderline patients pose tremendous challenges to therapists w h o are working diligently to help them to overcome addictions to drugs. W e have suggested ways that therapists m a y detect concomitant personality disorders in substance abusers, taking into account the fact that patients w h o are actively on drugs often seem to "change personality," thus confusing the diagnostic picture. Nevertheless, w e posit that it is important to assess the presence or absence of person­ ality disorders in substance-abusing patients, as the more extreme personality disorders will require awareness of special issues in clini­ cal management, the likes of which w e have reviewed. Furthermore, assessing and understanding the substance abuser's characterological issues provides a window into the patient's beliefs or schemas about the self, world, and future, thus assisting the thera­ pist in reaching a sound conceptualization of the case (Beck et al., 1990; Persons, 1989). Finally, w e would like to add that there is no tried-and-true start­ ing point in the treatment of Axis II dual-diagnosis patients. The question whether to focus first on the substance abuse or on the personality disorder is a "chicken and egg" issue. Therapists must be prepared to attack these problems simultaneously, using their under­ standing of the patient's idiosyncratic dysfunctional beliefs to sym­ pathetically earn increments of trust and cooperation in cartying out the treatment for drug abuse. C H A P T E R 1 7 R e l a p s e P r e v e n t i o n i n t h e C o g n i t i v e T h e r a p y o f S u b s t a n c e A b u s e A f̂ter the patient has quit using drugs, an even more formidable challenge begins. It is relatively easy for many people to change undesired behaviors temporarily; however, maintaining behavioral changes is much more difficult. In fact, it was Mark Twain who said, "To cease smoking is the easiest thing 1 ever did. 1 ought to know because I've done it a thousand times" (Prochnow, 1969). Most people who quit using drugs have a lapse or a relapse (Saunders & Allsop, 1987; Vaillant, 1983), with the most hkely time being within 90 days of the initiation of abstinence (Mackay, Donovan, & Mariatt, 1991). A lapse, or a "slip," is defined as the ini­ tial use of a substance after an individual has made a commitment to abstain from that substance. A relapse, on the other hand, is a full return to the maladaptive behaviors originally associated with use of the substance. In the cognitive therapy of substance abuse, a major goal is to have patients learn from whatever setbacks in long-term abstinence goals they may have (Moorey, 1989). It is hoped that the lessons learned from such experiences will ultimately improve an addict's planning skills, resolve, and self-confidence. In this chapter we present cognitive therapy techniques for relapse prevention. Some of these techniques are an extension of methods used to help patients discontinue drug use in the first place (e.g., the development of a collaborative relationship, conceptualizing the patient's problems, guided discovery, structured sessions, advantages- 292 Relapse Prevention 2 9 3 disadvantages analysis, and homework assignments.) Other techniques (e.g., identification of high-risk stimuli) are uniquely designed to assist patients in the relapse prevention process. Prior to presenting these techniques, the cognitive model of drug use and relapse is reviewed. This model provides a framework within which these techniques may be understood and applied. THE COGNITIVE MODEL OF RELAPSE The cognitive model of relapse (nearly identical to the model of ongoing use) is presented in Figure 17-1. The cocaine addict is vulnerable to high-risk stimuli (HRS) (Marlatt & Gordon, 1985). These are internal and external "triggers" that stimulate the addict's appetite for drugs. Internal stimuli include emotional and physical factors such as depression, loneliness, bore­ dom, anger, frustration, and physical pain (Mackay et al., 1991). External stimuli include people, places, and things that are related in some way to drug use (Shulman, 1989). HRS vary greatly from per­ son to person. For example, possessing money may trigger some patients to use, while other patients may be more tempted to use when they feel upset about not having money. The difference lies in the personal meaning that the patient attaches to the stimulus. The importance of HRS is that they may activate basic drug-related beliefs that have been overlearned by the patient. Examples of these beliefs are the following: "Drugs are problems for some people, but they won't be for me." "Drugs enhance m y life by making it more fun." "People who are against drugs don't really understand them." High-risi< Basic stin'iuli drug-related Automatic Craving/ (internal or beliefs Thoughts urges external) activated Focus on Facilitating Lapse instrumental beliefs strategies (permission) (action) F I G U R E 17.1. Cognitive m o d e l of relapse. 294 COGNTnVE THERAPY OF SUBSTANCE ABUSE "As long as I am careful, drugs won't hurt me." "Without drugs, life would be boring." "When I have problems, drugs relieve the pain." From these basic beliefs, automatic thoughts may be stimulated (e.g., "I need a hit!" "Time to party!" or "I've got to get high!"). Automatic thoughts are associated with craving and urges, and like other feelings, craving and urges themselves become internal HRS. In response to craving and urges, the patient may engage in some facilitating beliefs. Facilitating beliefs are a subset of basic drug-related beliefs that give patients "permission" to use. Examples include the following: "I can use just one more time." "Nobody will find out." "It will be O K to use again. I'll keep it limited." Facilitating beliefs increase the likelihood that the addict will and eventually use drugs. Instrumental strategies are the actual behaviors and activities involved in seeking, acquiring, and using drugs. These sfrategies, like basic drug-related beliefs, may vary from person to person and from time to time. For some, the craving for cocaine is so intense that the addict becomes obsessed with drug seeking, to the exclusion of all other considerations. Like a heat-seeking missile, the craving addict may focus on a target and let nothing get in the way of drug acqui­ sition. As a result of this "drive" some addicts engage in violent or criminal behaviors to acquire cocaine. If a patient has proceeded through the steps above, he or she is likely to have a slip. This slip, or lapse, then becomes a high-risk stimu­ lus for the cycle to begin again. That is, on taking a hit, the addict may focus on his or her basic belief that "one hit means I'm out of control." This belief might be followed by a cascade of self-derogat­ ing automatic thoughts and negative feelings. The resulting urges may become stronger, and the use of drugs may escalate until the patient has a full-blown relapse. To illustrate this process, we review the case of Mike, a 35-year- old salesman who had been abstinent from cocaine for six months. After two years of heavy use Mike chose to quit while hospitalized for cardiac problems (tachycardia and arrhythmias) associated with his cocaine use. Mike agreed to inpatient addiction treatment and, on completing a 28-day program, he entered outpatient psychotherapy and Narcotics Anonymous to deal further with his addiction. Prior to Relapse Prevention 295 quitting, Mike had been having serious marital problems, as his wi "Judy" had recently given birth to their first child and had become increasingly frustrated with Mike's cocaine-related problems. In spite of Mike's extended inpatient and outpatient drug treat­ ment, he continued to crave cocaine. His internal (emotional) HRS included feelings of boredom, frustration, irritability, and anxiety. External high-risk stimuli included friends who used, parties, and arguments with Judy. After initial treatment Mike often "found him­ self" in high-risk situations. For example, he continued to spend time with his cocaine-using friends. Such behaviors made Judy quite angry and she eventually separated from him. In response to his separation, Mike felt depressed, anxious, bored, frustrated, and irritable; thus, he was at extremely high risk for relapse. Mike's cocaine-using friend "Ryan," seeing Mike in "such bad shape," offered him a line of coke to "boost his spirits" (introducing another high-risk situation as well as a facilitating belief). Mike chose to accept Ryan's offer and in doing so he perceived himself as being "out of control." His automatic thoughts included "I can't resist" and "I can't handle life without drugs." He began to imagine and antici­ pate the extreme positive feelings he had previously associated with getting high: "I'll feel great!" and "It will relieve all of m y pain." After vety brief deliberation he took his first "hit," which led to a second, a third, and so forth (this episode became his initial lapse). As the effects of the drugs wore off, Mike began to feel dysphoric, agitated, and confused. He perceived this experience as proof that his substance abuse was an irreversible condition and he thought "once an addict, always an addict!" and "Now that I've started again I can't possibly stop using." As a result of this dichotomous thinking, Mike set the stage for a full relapse. Relapses pose important challenges to both patient and therapist. They may trigger counterproductive thoughts in the therapist, such as "This patient's condition is hopeless!" and "I am wasting m y time." Counterproductive thoughts in the patient might include, "I have failed and I always will fail," "I can't ever tell m y therapist about m y using," and "My therapist would surely reject me, or even hate me, if he knew I've been using!" The disadvantage of such all-or-none think­ ing processes is that they may result in a sense of hopelessness or apathy in the patient or therapist. Ideally, the therapist helps the patient to construe lapses and relapses as opportunities to practice more adaptive ways of combat­ ting drug use. For example, Mike's therapist could help him to understand that there were more adaptive ways to deal with his dysphoria over his marital separation than to use drugs. Rather than 296 COGNITIVE THERAPY OF SUBSTANCE ABUSE believing that his situation was hopeless, and that his only relie be to accept his friend's offer of cocaine, he could focus on produc­ tive activities that would boost his mood and self-esteem. Further, even if he did begin to use cocaine, Mike did not

have to believe that he was in an irreversible free fall. Instead, he could practice reciting some control beliefs that might help him to "pull out of the nose dive" (Shiffman, 1992) if confronted with similar situations in the future. Such control beliefs might be "If I stop now, I can show myself that I am stronger than the dmg." "Walking away from drugs is the same as moving toward saving m y marriage." "I must seek drug-free friends when I feel this badly." When the patient has maintained abstinence for an extended period of time and the therapist and patient are confident in the patient's ability to maintain abstinence, formal therapy may be ter­ minated. At this time, "booster sessions" are arranged, which may include telephone calls, written correspondence, and face-to-face con­ tacts. These sessions serve several purposes. First, they focus the patient's attention on the need for vigilance in combatting the relapse process. Second, the therapist's continued interest in the patient pro­ vides social support that motivates further abstinence. Third, the thera­ pist can continue to provide expert guidance to a patient who may be at renewed risk for relapse. Substantial gains may result from extended contact with the patient. Each booster visit or telephone call might decrease the like­ lihood that the patient will relapse, or at least will remind the addict that the therapist is a potential resource for coping with HRS. If the addict does relapse after therapy has been terminated, it is recom­ mended that he or she be invited to return to therapy as soon as pos­ sible to work on improving coping skills. Again, careful analysis of each lapse and relapse provides the patient with an increased under­ standing and ultimately greater control over the relapse process. At the same time, we must note the following two caveats. First, although we as therapists endeavor to pro'vlde ongoing help to patients who continue to be in need, we agree with Gawin and Kleber (1992) that, "The goal of relapse prevention is gradually to decrease the external controls placed on the abuser, by family and therapist, dur­ ing initiation of abstinence, and gradually to facilitate development of the abuser's internal controls" (p. 47). Second, although it certainly is preferable for patients to learn from their lapses and relapses than merely to succumb to them, we must be careful not to convey the Relapse Prevention 297 wrong message that we encourage lapses and relapses as growth-enha ing experiences. Therapists must make it clear to patients that the best learning occurs via ongoing drug-free coping with life's evetyday and long-term demands. TECHNIQUES FOR THE PREDICTION A N D C O N T R O L OF RELAPSE Identification of High-Risk Stimuli People who suffer from drug and alcohol addictions inevitably encounter HRS. This is especially apparent when one con­ siders the fact that all human beings experience some sadness, anxi­ ety, nervousness, anger, or frustration (all internal HRS) at times. The identification of internal and external HRS is an extremely important component of the relapse prevention process, as it is not uncommon for the addict to lack an awareness of HRS. By increasing awareness of HRS, the addict may reduce the like­ lihood of exposure and/or reflexive reaction to them. In sessions, patients are encouraged to carefully review recent and remote memo­ ries of relapses in order to discover the full range of HRS that might lead to future relapse. Here, a therapist^atient dialogue is presented to illustrate this "trouble-shooting" process: TH: Mike, what types of situations are most likely to cause you to crave cocaine? PT: I don't know. TH: Well, let's tty to think of some, so that you might learn to pre­ pare and cope more effectively with them PT: Yeah, I guess that makes sense. N o w that you ask, when I am with certain friends I want to get high . but 1 can't think of anything else. TH: OK, let's review your last binge. H o w did it begin? PT: I had been clean for almost a month when I suddenly got the urge one night. The next thing I knew, I was with Bob and Ryan, smoking crack. TH: Now think careftilly, what actually happened that night? I would like to hear the details. PT: Well, I was at home and m y wife was in one of those moods where nothing I did was right. TH: What happened next? 298 COGNTTIVE THERAPY OF SUBSTANCE ABUSE PT: I got pissed off at her and really let her have it. What I mea 1 really started to fight back. TH: What happened next? PT: She let me have it, even worse. She started screaming about how I'm a lazy, good for nothing so and so. TH: And then? PT: I stormed out of the house and went for a walk around the neighborhood. Sure enough, I saw Bob and Ryan sitting in front of the convenience store. TH: What happened next? PT: I walked over to them, and the next thing I knew we were all at Bob's house. The rest is history. TH: So, there were actually several high-risk stimuli involved, weren't there? They included your wife's criticisms, your anger and fms­ tration in response to her comments, your leaving home with the problem unresolved, walking around late at night, the con­ venience store where you guys typically meet. Bob and Ryan, and finally, being at Bob's house. PT: Yeah, now that you mention it, I guess the situation was kind of complicated. TH: H o w could you make this kind of situation "simpler" in the fu­ ture? PT: I don't know. TH: Well, this is something we have to work on. For starters, you could make things simpler if you know how to recognize when you're upset and looking for an escape. Does that ring tme for you? PT: Yeah. In this dialogue it became apparent that Mike had exposed him­ self to multiple HRS, thus dramatically increasing his likelihood of a lapse. Interestingly, Mike had difficulty seeing how he made decisions that led to a chain of events that led up to an ultimate lapse. Marlatt (1985) talks about such "accidental" exposures to HRS as resulting from "apparently irrelevant decisions." Carroll, Rounsaville, and Keller (1991) explain that such exposures may reflect underlying ambiva­ lence about changing addictive behaviors. Thus, it is important that the therapist, under these circumstances, evaluate the status of the patient's decision to become abstinent from drugs and alcohol. For example, Gorski and Miller (1982) highlight a number of telltale signs that signal a patient's starting along the road to relapse- Relapse Prevention 299 that is, being prone to exposure to high-risk situations, and ill- equipped to manage the thoughts, feelings, cravings, and actions that result. Such signs include, for example, (1) an increasingly noncha­ lant attitude about remaining actively involved in ongoing self-help activities (e.g., attending therapy or support-group meetings, con­ tinuing with homework derived from therapy), (2) regression into affective lability and hypersensitivity, (3) reduced willingness to talk about problems and concerns, (4) social withdrawal, (5) breakdown of healthy daily routines and structure, and (6) impulsive decision­ making. A concrete example is a patient who begins to cancel therapy sessions for spurious reasons, and who denies any symptoms on the Beck inventories (BDL BAI, BHS, etc.) in spite of obvious signs of stress. These early-warning indicators set the stage for the relapse process as depicted by the cognitive model flowchart, and must be given attention in their own right. It is apparent that HRS are highly idiosyncratic for individual drug abusers (Carroll, Rounsaville, & Keller, 1991). It is recommended that the cognitive therapist carefully evaluate HRS for each individual patient. A useful method for doing so is self-monitoring homework. Specifically, the patient keeps a journal of hourly changes in cocaine (use and) craving in relation to internal and external events. This journal is reviewed in session to assess "previously unseen patterns in cocaine use" (Carroll, Rounsaville, & Keller, 1991). At the end of each session, the patient is asked to anticipate specific HRS that might occur between the present and the next session. Furthermore, the patient is asked to plan strategies for coping with such HRS. Cognitive Strategies for Coping with HRS The significance of HRS is that they trigger basic drug- related beliefs that increase vulnerability to lapses and relapses. Thus, a fundamental cognitive strategy for relapse prevention is the devel­ opment of "control" beliefs that reduce vulnerability to lapses and relapses. The following are examples of control beliefs that reduce vulnerability to lapses and relapses: "I don't need drugs to have fun." "My life will improve without drugs." "I can cope with unpleasant emotions without using drugs." "I have control over m y own behaviors, including m y drug use." "Even if I slip I don't have to continue using drugs." "A lapse is not equivalent to failure." 300 COGNITIVE THERAPY OF SUBSTANCE ABUSE The following patient-therapist encounter illustrates the process of guided discovery, used here to modity drug-related beliefs and to build control beliefs. TH: I wonder how you make sense of your continued use of cocaine in spite of the destructive results? PT: Well, for one thing, I feel like I have no control over m y dmg use when I am emotionally upset. TH: What do you mean when you say "I have no control"? PT: I just don't feel like I have any control. TH: So you believe that you have "zero percent" control? PT: I guess. TH: Are you saying that each and every time you've ever had a crav­ ing for coke you've used? PT: Well, no. TH: H o w many times have you succeeded in not using in spite of having cravings and urges? PT: Well, lots of times, actually. I guess most of the time now that I think of it. TH: Does this mean that you've been able to demonstrate control? PT: It never seems that way to me, but I guess I do have some con­ trol. TH: And so you have just changed your belief from "I have no con­ trol" to "I have some control." As we have discussed, the first belief is an example of dichotomous, or "all-or-nothing" think­ ing, while the second thought is probably more objective, because it takes into account the "shades of grey." PT: Yes, I know. So when I think that I have no control I am more likely to give in to the urges and use cocaine. But when I look carefully and 1 see that 1 have greater control, I'm likely to tty to stay with m y program. TH: Yes, that's right. In this example the patient is helped to see the advantages of changing his drug-related belief "1 have no control" to "I have some control." Another cognitive strategy useful for dealing with HRS is distraction (Carroll, Rounsaville, & Keller, 1991). Specifically, the patient is encouraged to compile a list of distracting activities that might be used when HRS are encountered. Distracting activities may include any non-drug-related activity (e.g., exercise, singing, playing with children, and writing a letter). Although distraction techniques Relapse Prevention 301 are only a short-term coping device, they serve the all-important tion of providing a delay between the onset of cravings and the act of seeking and using drugs. Such a delay may provide patients with time to think of the full negative ramifications of using, as well as an opportunity to witness the diminishing of cravings if no drugs are taken (Carroll, Rounsaville, & Keller, 1991; Horvath, 1988). Behavioral Strategies for Coping with HRS After patients identify HRS and examine drug-related beliefs, they are helped to practice (i.e., rehearse) strategies for cop­ ing with certain HRS. For example, Mike might be assisted in devel­ oping and practicing methods for resolving conflicts with his wife. He might be encouraged to think about ways to give her and to ask her for more emotional support. He also might be encouraged to think about alternatives to going out alone, especially to areas where drug- using friends are located. Additionally, he would be helped to imag­ ine ways of saying "no thanks" to his friends when they invite him to use drugs,

in spite of his cravings and urges. As Mike's case illus- frates, relapse prevention necessitates that patients learn to cope with both general life stressors (e.g., marital discord) and discomfort that specifically is related to temptation to use drugs (Wills & Shiffman, 1985). A long-term goal for Mike, essential to most drug users' contin­ ued abstinence after termination from therapy, would be to establish and maintain meaningful relationships with people who are drug-free (Frances & Miller, 1991; Havassy et al., 1991). The phrase in 12-step groups that reflects this philosophy is "hugs, not drugs." Ultimately, the patient must learn to seek human contact, rather than drugs, in order to obtain gratification of dependency needs. As an important part of this process, Mike would be taught to examine the beliefs that led to his high-risk behaviors. For example, the therapist might ask, "What were you thinking when you yelled at your wife?" The patient's automatic thoughts might have included: "I'll put a stop to this!" or "She can't talk to m e that way." Underly­ ing these thoughts are Mike's beliefs about his personal inadequacy and powerlessness, beliefs that trigger both drug urges and the accompanying belief that giving in to the urges is the only way to feel powerful. Another behavioral relapse prevention strategy involves planned, gradual exposure to HRS (Mackay et al., 1991). Specifically, the patient and therapist construct a hierarchy of increasingly salient high-risk triggers and the patient is actually exposed to these in sessions {in 302 COGNITFVE THERAPY OF SUBSTANCE ABUSE vitro) and through homework {in vivo). The efficacy of this techniq may be attributable to the cognitive changes in patients as they per­ ceive themselves effectively dealing with these situations. In other words, patients gain an increased sense of self-efficacy as they suc­ cessfully cope with increasingly high-risk situations. Again, a word of caution is due. While we believe that exposure to high-risk situations is inevitable in life, and therefore gradually "inoculating" patients to these situations makes excellent clinical sense, this technique must be handled with care. Therapists must make sure that their patients have the requisite skills and motivation to man­ age their induced cravings in session before being asked to cope with cravings outside the office (Childress et al., 1990). Patients must be told that this type of assignment requires a detailed plan, as well as a safety valve contingency (e.g., calling the therapist) in case the cravings become hard to manage. Otherwise, patients may misuse this assignment by cavalierly "testing" themselves before they are ready to handle the resultant cravings (Carroll, Rounsaville, & Keller, 1991; Washton, 1988). An example is the patient who drives through the neighborhood where he used to buy heroin, "just to see if I can do it," without preparing a plan of action in advance, thus taking a huge gamble with his abstinence. By contrast, therapist-instructed graded- exposure assignments must be small, calculated risks that have excel­ lent chances for success and backup plans in case things go wrong. Keeping a Lapse from Becoming a Relapse As mentioned earlier, lapses provide the addict with opportunities to apply cognitive skills and promote further under­ standing of the mechanisms involved in relapse. Thus, a lapse is not necessarily perceived as "bad"; instead it is "grist for the mill." An important theme of relapse prevention is helping the patient keep lapses from becoming relapses (Mackay & Marlatt, 1991). There are many reasons why lapses occur. For example, addicts may choose to "slip" in order to test their ability to control their substance use. They might think, "I'll try' it just this once. It will prove that I am in control of m y addiction." As we've mentioned above, addicts may also "accidentally" or intentionally expose themselves to a high-risk stimulus without being prepared to respond cognitively or behaviorally to this stimulus. Another reason for a lapse may be that the addict once again believes that the advantages of using dmgs outweigh the disadvantages. Given the many reasons for lapses, an important component of relapse prevention involves the identification of decision points along Relapse Prevention 303 the cognitive model of relapse. For example, did the lapse occur because the addict failed to avoid an external HRS? Or, did the lapse occur because the addict lacked appropriate control beliefs for resist­ ing an inevitable HRS? Or, did the patient automatically engage in instrumental strategies for acquiring drugs in response to cravings, without waiting? A lapse usually becomes a relapse as a result of underlying all- or-none beliefs; for example, "A lapse means I don't have any con­ frol," "Since I could not stay abstinent, the therapy isn't working," and "A lapse is a failure." Marlatt and Gordon (1985) call this think­ ing process and the resulting relapse the "abstinence violation effect." An important strategy for relapse prevention, then, is to challenge such dichotomous thoughts about lapses so that they do not become relapses. When an addict has a lapse, imagety techniques are useful to reconstruct the sequence of stimuli, basic beliefs, automatic thoughts, and behaviors leading to the lapse. Additionally, it is important to use post-hoc rehearsal of techniques at each decision point to pre­ pare the addict for similar future circumstances. This sfrategy is illustrated in the following dialogue between Mike and his therapist. Prior to this interaction, the therapist learned that Mike had been walking near the areas where his drug-using friends, Ryan and Bob, get high together. In fact, Mike almost avoided his friends but he suddenly felt "obligated" to stop to talk to them. Bob asked Mike why he hadn't been around for awhile and he offered to drive Mike home. Mike accepted the offer and got into Bob's car. Once on the road, Bob explained that he had to make a quick stop at his house. While Bob was inside, Mike began to think that maybe he should join him in the house in order to be "sociable." Inside the house, Bob offered Mike "a quick hit." Although Mike felt that he did not really want any, he accepted the offer and took the hit. There were several choices and decision points leading to this lapse. First, Mike decided to walk through a "high-risk zone" instead of choosing a "safe" route. Upon seeing his friends, he had the option of choosing to keep walking. When he was in the car outside of Bob's house he had the option of staying outside, rather than entering the house. And finally, when Bob offered him the hit, he had the oppor­ tunity to accept or refuse. The following dialogue is the therapist's and patient's "postmortem" evaluation of the sequence of events lead­ ing to the lapse. Mike had his eyes closed and was imagining the scene as if it were happening now. TH: You were walking along and you happened to wander past the old hangout. What was the risk involved in taking that route? 304 COGNITIVE THERAPY OF SUBSTANCE ABUSE PT: I guess that I might have seen Bob and Ryan. I knew it could have been a problem in the long run, but I like spending time with them. W e really enjoy each other. TH: What happened when you saw Bob? PT: He called out to me and I thought "I ought to stop." TH: Is there any problem with that thought? PT: I couldn't turn m y back on m y friend. TH: What do you risk by following the dictates of that thought? Do you give up your freedom of choice? PT: I guess I could get into trouble that way. TH: What happened next? PT: I stopped and he offered to take m e home. TH: Did you have a choice? PT: I felt that 1 should take him up on the offer. TH: You often act instinctively but perhaps following those instincts may work against you . . . {pause) . . . Now, you're waiting in the car. What's going through your mind? PT: I'm thinking that maybe I should go up there and be sociable. TH: Are you feeling the urge to get high? PT: Maybe in the back of m y mind 1 may be thinking that it would feel good to take a hit. TH: What are you thinking when Bob offers you some? PT: I'm thinking that maybe I don't want to. But Bob offered it as a gesture of his friendship . I felt I should accept. TH: Could you have asked yourself, "Am I being 'nice,' or am I just giving myself permission to use?" PT Yeh, 1 guess so. TH And what would the consequence have been of that thought? PT Maybe 1 would have realized how impulsive I was being. Maybe 1 wouldn't have taken the hit. TH: After you took the hit, what were the thoughts that ran through your mind? PT: 1 was thinking, "might as well finish the job I've started." TH And what was the meaning of that thought? PT; It meant "one hit and I'm over the edge." TH That sounds like "all-or-nothing thinking." PT: Yeh, you're right. Relapse Prevention 305 TH: And you proceeded to smoke crack at Bob's house all afternoon. PT: Yes. In this example, Mike was "guided" through the thoughts and images of his recent experiences so that he might review the deci­ sion points leading to his lapse. Upon arriving at his lapse, his thera­ pist helped him to see that his dichotomous thinking led him to con­ tinue using after his initial hit. In the section that follows, Mike's therapist encouraged Mike to rehearse alternative methods for cop­ ing at each decision point. TH: What could you have done instead of walking along the old route, past the old hangout? PT: I guess there were lots of walks I could have taken which would have avoided those guys. TH: And if you had still passed them, what could you have thought when they called out to you? PT: I could have thought "Those guys put m e at risk for relapse. Better keep walking." TH: And what would your resulting behaviors have been? PT: I would have waved in a friendly way and said "Hi guys! I'm in a hurry. Gotta run." TH: And what if Bob had pulled up in his car and offered you a ride anyway? PT: I could have continued to think "bad news. ." TH: And the resulting behavior would have been what? PT: I would have turned down the ride. TH: And what if they convinced you to get in the car and you ended at Bob's house anyway? PT: 1 still could have thought "Don't get out of the car. The house is a danger zone." TH: And then what would have happened? PT: Bob probably would have come back to the car and taken m e home without using. TH: And if that would have happened, how would you have felt? PT: Probably relieved and proud of myself for exercising control over m y life. At this point, the therapist realized that Mike had other types of beliefs (relating to "loyalty" and "responsibility") that made him vul- 306 COGNTnVE THERAPY OF SUBSTANCE ABUSE nerable to lapses and relapse. In the next segment, the therapist explored these beliefs. TH: What were you thinking when you walked over to Bob's car? PT: I thought, "I have really neglected m y friends." TH: What do you mean by that? PT: I mean that I have to be friendly to these guys. After all, they are m y friends. TH: What do you mean when you use the phrase "have to"? PT: I like to think of myself as a loyal friend. TH: And what does "loyal" mean? PT: It means that I should go along with what they want. TH: Shoulds and musts. PT: Yes. TH: What do you know about shoulds and musts? PT: I know that they aren't the best. TH: And what are the results of shoulds and musts? PT: Well, they can get m e into trouble. Like in this case, they got me back into using. Advantages -Disadvantages Analysis Marlatt and Gordon (1985) explain that positive out­ come expectancies contribute to relapse. Specifically, individuals who have been addicted to a substance perceive substantial

positive advantages from using that substance. In fact, such people typically minimize or ignore the disadvantages of their drug use, especially when in high-risk situations. The advantages-disadvantages analysis is a technique commonly used in cognitive therapy (see Chapter 9, this volume). This technique is particularly useful in relapse prevention, where addicts selectively perceive the advantages of drug use. In the advantages-disadvantages analysis, the therapist constracts a four-cell matrix, with advantages-disadvantages on one axis, and use- nonuse on the other axis. Patients are asked to discuss the advantages and disadvantages of using and abstaining. The role of the therapist is to elicit objective data from patients, regarding such advantages and disadvantages. Additionally, patients are encouraged to understand that their exaggerated views about the advantages, along with their mini­ mized views of disadvantages, contribute to their addiction. Relapse Prevention 307 The following dialogue is a continuation of the session with Mike. It illustrates the advantages-disadvantages analysis: TH: Mike, when you were in the high-risk situation with your frien Bob and Ryan, what was going through your mind? PT: I guess I thought, "Soon I'll get some relief from this bullshit." TH: So you believed that an advantage of smoking crack was relief from your bad situation. PT: I'd forget about m y old lady for a few hours. TH: What other advantages could you see? PT: {pauses) Well, I can't think of any others. TH: What were the disadvantages of using? PT: Oh, the relief is only for a short time. I know that I am really making m y marriage and m y life worse. TH: What other disadvantages are there to using? PT: Well, I could lose m y kid if m y wife decides to split. TH: What else? PT: I can tell that m y life is changing for the worse from this stuff. When I am really honest with myself I know that m y health and self-confidence are going down the tubes. TH: OK, What are the advantages of abstaining? PT: Well, as I just said, I'm kinda wasting m y life. Maybe m y life would start to improve if I abstained. TH: Can you think of any other advantages of abstaining? PT: {pause, tears in his eyes) I guess I could start to be more of a father to m y son; I never really had a father myself. TH: Sounds like a vety big advantage! PT: Yeah, if I could only remember later how I feel right now! In fact, Carroll, Rounsaville, & Keller (1991) suggest a method that facilitates remembering the advantages-disadvantages analysis. They suggest that the addict list the advantages of using cocaine on one side of an index card. The therapist then helps the patient to see the ultimate negative consequences of all advantages. For example, the "terrific high" is following by the "dreaded crash." O n the flip side of the index card the patient lists the disadvantages of continued cocaine use. The card is then placed in the addict's wallet, near the money, so it will be accessible during periods of high vulnerability. 308 COGNITIVE THERAPY OF SUBSTANCE ABUSE Development of Social Support Netvkrorks Interpersonal conflict is a common high-risk stimu­ lus for many addicts (Mackay et al., 1991). In fact, Cummings, Gor­ don, and Marlatt (1980) found that 4 4 % of relapse experiences were linked to interpersonal conflicts. Loneliness is also a high-risk trig­ ger, for two reasons. First, loneliness is an uncomfortable emotion (i.e., internal trigger) that may be anesthetized temporarily by cocaine. Second, heroin and cocaine use often take place in a social environ­ ment, which temporarily provides the addict with a sense of having "company" to relieve the loneliness. From these assumptions, we assume that relapse prevention efforts will be enhanced by the patient's acquisition of a drug-free social support network (cf. Frances & Miller, 1991). It is important to understand that patients have numerous basic beliefs and automatic thoughts about relationships that influence their behaviors in relationships. For example, some addicts may believe "Only other users can understand me," "1 will never be accepted by those who have never used drugs," "Nonusers are boring," and so forth. Obviously, such beliefs result in social discomfort, or anxiety, and a certain degree of social avoidance. Patients can be helped by the therapist's understanding of this process, as well as by modifica­ tion of such beliefs. Friends and family who do not use drugs may be excellent sources of support to the patient. Many addicts have avoided their nonusing family members and friends for fear of criticism and rejection. Twelve- step programs (e.g. Alcoholics Anonymous and Narcotics Anonymous) may also be sources of support for the addict. Therefore, patients should be encouraged to make use of these programs. By doing so they may experience multiple benefits, including social support, col­ laboration, an environment that is supportive of abstinence, and a way to spend time when suffering from boredom. Of course, cogni­ tive therapists strive to be part of the patients' support network as well, but it is vital that drug-abusing patients have drug-free friends in their everyday lives "for the long haul." SUMMARY In this chapter, relapse prevention was presented as part of the cognitive therapy framework. This model emphasizes the role of beliefs as well as high-risk situations in the relapse process. Techniques were presented for predicting and controlling relapse, Relapse Prevention 309 including identification of HRS, cognitive and behavioral strategi for coping with HRS, keeping a lapse from becoming a relapse, advantages-disadvantages analysis, and social support networks for relapse prevention. W e also alluded to the fact that long-term abstinence from drugs and alcohol entails broad-sweeping changes in attitudes and lifestyle. When therapists note that their patients are reverting back to former ways of viewing themselves, their world, and their future, it signals a need for the patients to reassess their self-efficacy and commitment to positive change. In sum, the conceptual and technical skills that patients learn during the actual course of cognitive therapy must be practiced and "lived" in the months and years after formal treatment has terminated. Toward that end, we emphasize to our patients that they must learn to become their own cognitive therapists, and that the work of therapy needs to become a way of life. POSTSCRIPT The following is our version of the "Serenity Prayer," adapted for cognitive therapy substance abuse patients: Cognitive Therapy Serenity Pledge I pledge that I will strive to gain the strength to stay away from those drug triggers that I can avoid, the serenity and know-how to cope with those drug trig­ gers that can't be avoided, and the wisdom to know the difference. APPENDIX 1 BELIEFS ABOUT SUBSTANCE USE* Name: Date: Listed below are some c o m m o n beliefs about d m g use. Please read each state­ ment and rate how much you agree or disagree with each one. Totally Disagree Disagree Neutral Agree Agree Totally Disagree Very Much Slightly Slightly Very Much Agree 1. life without using is boring. 2. Using is the only way to increase m y creativity and produc­ tivity. 3. I can't function without it. 4. This is the only way to cope with pain in m y life. 5. I'm not ready to stop using. 6. The cravings/urges make m e use. 7. M y life won't get any better, even if I stop using. 8. The only way to deal with m y anger is by using. 9. Life would be depressing if I stopped. 10. I don't deserve to recover from d m g use. 11. I'm not a strong enough person to stop. 12. I could not be social without using. 13. Substance use is not a problem for me. 14. The cravings/urges won't go away unless I use dmgs. 15. M y substance use is caused by someone else (e.g., spouse, boy­ friend/girlfriend, family member). 16. If someone has a problem with dmgs, it's all genetic. 17. I can't relax without dmgs. 18. Having this drug problem means I am fundamentally a bad person. 19. I can't control m y anxiety without using dmgs. 20. I can't make m y life fun unless I use. *This form was developed by Fred D. Wright, Ed.D. 311 312 Appendix 1 CRAVING BELIEFS QUESTIONNAIRE (CBQ)- Name: Date: Please read the statements below and rate how much you agree or disagree with each one. Totally Disagree Disagree Neutral Agree Agree Totally Disagree Very Much Slightly Slightly Very Much Agree 1. The craving is a physical reaction, therefore, I can't do anything about it. 2. If I don't stop the cravings they will get worse. 3. Craving can drive you crazy. 4. The craving makes m e use drugs. 5. I'll always have cravings for dmgs. 6. I don't have any control over the craving. 7. Once the craving starts I have no control over m y behavior. 8. I'll have cravings for dmgs the rest of m y life. 9. I can't stand the physical symptoms I have while craving dmgs. 10. The craving is m y punishment for using dmgs. 11. If you have never used dmgs then you have no idea what the craving is like (and you can't expect m e to resist). 12. The images/thoughts I have while craving dmgs are out of my control. 13. The craving makes m e so nervous 1 can't stand it. 14. I'll never be prepared to handle the craving. 15. Since I'll have the craving the rest of m y life I might as well go ahead and use drugs. 16. W h e n I'm really craving drugs I can't function. 17. Either I'm craving drugs or I'm not; there is nothing in between. 18. If the craving gets too intense, using drugs is the only way to cope with the feeling. 19. W h e n craving dmgs it's O K to use alcohol to cope. 20. The craving is stronger than m y will power. *This form was developed by Fred D. Wright, Ed.D. Appendix 1 313 RELAPSE PREDICTION SCALE* Name: Date: As you know, there are many situations that can trigger an urge to use cocaine or crack. This scale has two parts: (1) to determine how strong you think the urges will be in certain situations and (2) to determine the likelihood that you will use in these situations. Listed below are several situations that might trigger strong urges to use cocaine or crack. Read each item and imagine yourself in that situation. In the first column, "Strength of Urges," indicate h o w strong you think the urge will be. In the second column indicate the "Likelihood of Your Using" in these situations. 0 1 2 3 4_ None Weak Moderate Strong Very Strong PREDICTION Strength Likelihood of of Urges Using 1. I am in a place where I used cocaine or crack before. 2. I a m around people with w h o m I have previously used cocaine or crack. 3. I just got paid. 4. I see coworkers using. 5. I a m leaving work. 6. It's Friday night. 7. I a m at a party. 8. I a m thinking of the last time I used. 9. I start talking with someone about using. 10. I feel bored. 11. I feel great! 12. I see a lover/ex-lover. 13. I a m having a drink. 14. M y friend is offering m e some cocaine or crack. 15. I feel sad. (OVER) *This form was developed by Fred D. Wright, Ed.D. 314 Appendix 1 PREDICTION Strength Likelihood of of Urges Using 16. I see a prostitute. 17. I a m out looking for sex. 18. I feel sexy. 19. I remember how good the high feels. 20. I feel angry. 21. I feel stressed out. 22. I feel guilty. 23. I just used dmgs. 24. I just broke m y abstinence. 25. I a m getting ready for work. 26. I a m tired. 27. I a m fmstrated. 28. I see an anti-drug use poster. 29. I see a pipe. 30. I am out gambling. 31. I just had a "coke dream." 32. I a m watching sports. 33. I a m getting dressed up. 34. I a m

under pressure at work. 35. I a m thinking about having sex. 36. I a m angry at m y spouse/partner. 37. M y spouse/partner is bugging m e about m y using. 38. M y family is bugging m e about m y using. 39. I was just told I have a positive urine. 40. I didn't use, yet m y urine was positive. 41. I a m watching a dmg-related movie. 42. 1 feel anxious. 43. Someone just criticized me. 44. I haven't used for a long time. 45. I feel tense. 46. Someone I care for is terminally ill. 47. I am in pain. 48. I feel a burden on m y shoulders. 49. I am at a bar having a good time. 50. I had a fight with m y family. APPENDIX 2 CHECKLIST FOR DEALING WITH AMBIVALENCE AND LAPSES* 1. Set goals related to abstinence. "I want to keep job." "I'd like to get along better with family/girl friend/boyfriend." "I'd like to have more money to spend on things I want. 2. Assess cocaine practices: a. Look for specific stimuli: money, cocaine paraphernalia (pipe, syringes, materials used in the preparation of freebase cocaine, etc.), exposure to cocaine itself or any white crystalline substance resembling cocaine, such as salt, sugar, snow, and even plaster dust; individuals and settings previously associated v«th cocaine use and cocaine paraphernalia. (Some intravenous users have reported intense subjective craving w h e n their blood is drawn for determi­ nation of blood levels each week.) b. Determine whether other individuals in the patient's home, neigh­ borhood, or workplace use cocaine; whether the patient is involved with selling cocaine and the nature of the patient's cocaine re­ sources. c. Determine availability of money, use of other psychoactive sub­ stances, contact with cocaine using associates, and unstmctured time spent without monitoring of the patient's activities. 3. Begin therapy sessions with a review of all high-risk stimulus situa­ tions that were encountered by the patient during the past week and the coping sttategies used by the patient, and whether or not they were successful. 4. At end of interview, ask patient to anticipate any high-risk situations that m a y be encountered during the week ahead: Plan in advance h o w these might be avoided or successfully coped with. 5. Address distress from abstinence. • Acknowledge patient's stmggle • Acknowledge sense of deprivation 6. Acknowledge patient's justifications for using. "There's nothing like a cocaine high." "Sex and coke go together." "I feel less anxious with people." "I get most of m y money from dealing." •Many of the items for this checklist were based on the text of Relapse Prevention Strate­ gies for the Treatment of Cocaine Abuse by K. M. Carroll, B. J. Rounsaville, and D. S. Keller, 1991, American loumal of D m g and Alcohol Abuse, 17, pp. 249-265. Adapted by permission of Marcel Dekker Inc. 315 316 Appendix 2 7. Identify patient's "compromise" with abstinence. • Spacing out use of cocaine (but not giving it up). • Continuing on high levels of alcohol or other psychoactive drugs • Staying in treatment only until "spouse or lover gets off m y back" 8. Remind patient of the crash and dysphoria. 9. Assess whether patient has taken steps toward reducing cocaine avail­ ability. Has the patient informed cocaine using associates of his/ her intention to stop using? 10. Question: Has the individual resisted telling family and friends of his or her decision to stop using or reluctance to break ties with dealers? 11. If the patient has made no independent steps toward limiting cocaine availability, consider whether patient expects that mere exposure to treatment will "magically" produce abstinence with little or no participation or stmggle on the part of the patient. 12. Determine whether the abusers, after an initial brief period of abstinence, expose themselves to a situation in which cocaine is available as a "test" of their ability to withstand temptation. 13. Encourage patient, at least at the beginning, to minimize deliber­ ate exposure to cocaine-related cues and situations. Be ready to iden­ tify unforeseeable "accidental" subintentional exposures ("appar­ ently irrelevant decisions"). Example: A patient decided that since ills problem was with cocaine, he would have a beer. After two beers, however, he ran into a friend w h o happened to have a gram of cocaine and a relapse occurred. 14. Teach the patient h o w to recognize and interpret such a decision chain leading to a lapse before it actually occurs. 15. Teach the patient h o w to detect the decisions that commonly occur during the beginning of the "accidental exposure" chain where risk, craving, and the availability of cocaine are relatively low. The patient should be able to regard certain feelings, such as boredom, as a "red flag." Part of the subintentional exposures (accidents) are manifested in the patient's "having" to do certain things that lead to high-risk activities or locations. 16. Elicit patient's relapse interpretation: "I blew it this time. 1 guess I'll never stop using cocaine, so I might as well keep using." 17. Check on psychological background to lapse: For example, some­ times defiance or rebellion becomes a factor, as in the case of a person w h o had an argument with his wife and then had the thought that her efforts to monitor his actions made him her "pris­ oner." Appendix 2 317 18. Look for "entitiement." For example, cocaine's initial euphorogenic properties m a y be sought to enhance positive feeling and then will be later used when the person feels "I a m entitled to a reward." 19. Self-monitoring: Patient is asked to keep a log of hourly changes in cocaine craving and/or uses in relation to various external and internal events. 20. Increase abuser's ability to anticipate problems, prepare for them in advance, or avoid them entirely. 21. Maintain a balance between encouraging patient to avoid high-risk situations (at least initially) and utilizing behavioral and cognitive coping strategies when exposure/craving occurs. 22. Early in treatment, inquire about the intensity of craving. Patients often deny any craving at all. In later sessions, the patient might mention any of the following: "Seeing myself doing cocaine" or having a dream about cocaine or other experiences which may be indicative of some form of craving. Some descriptions are somatic ("a knot in m y stomach . . . m y blood racing . . . sweating . . . heart pounding," nervousness, excitement, smell or taste of cocaine). 23. Look for episodes of intense subjective craving for cocaine that are reported weeks or even months before the violation of abstinence. 24. Demystify the experience of craving by offering an explanation of conditioning experiments. Help the patient identify and tolerate conditioned craving when it occurs. 25. Explain the time-limited nature of cocaine craving. Craving usu­ ally peaks and dissipates in less than an hour if not followed by cocaine use. Distraction may be an effective strategy. 26. Lifestyle modification involves developing rewarding behavioral alternatives. 27. If the abuser is still working, the job in many cases has become only a means of acquiring money to buy cocaine and the fulfilling or challenging aspects of work have faded. 28. Anhedonic cocaine abusers may have difficulty seeing any activity or experience other than cocaine use as enjoyable. All other expe­ riences are perceived as inferior to cocaine. 29. Encourage patient to look at slips as isolated incidents that can be conceived of as opportunities for learning. APPENDIX 3 TYPICAL EXAMPLES OF DRUG USE ADVANTAGES A N D DISADVANTAGES ADVANTAGES OF USING 1. Feel like superman. 2. Took away shyness and insecurities. 3. Feel like king of the mountain. 4. Confident. 5. More sex. 6. It makes m e feel good. 7. Fit in with the crowd. 8. I have more friends (until your money mns out). 9. Made m e more social. 10. Reduces social anxiety. 11. Relaxes me. 12. It's fan. 13. A glass of wine is sometimes nice with dinner. 14. There are times when a single drink with a friend is a good thing—a little relaxation, sometimes mildly euphoric (nothing wrong with one drink, a lot of nice things about). 15. Reduced guilt (when leaving m y daughter). 16. Ran away from loneliness. 17. Take mind off things. 18. Nothing bothered m e when high. 318 Appendix 3 319 DISADVANTAGES OF USING 1. Mental/physical beating your body is taking. 2. Relationships suffer. 3. Work suffers (don't show up for work because you are hurting so bad). 4. Big debt. 5. I lead a life that is a lie. 6. I'm in danger of legal consequences. 7. After using cocaine, feel bad about myself for picking up. 8. Hangover. 9. Sleep most of the day. 10. Stopped eating. 11. N o motivation. 12. Didn't talk about anything meaningfal. 13. Feel guilty in front of children. 14. Impotence. 15. Sterility. 16. Paranoia. 17. Laziness. 18. Loss of short-term memory. 19. Tensions in family. 20. Could get fired. 21. Injury to myself or others. 22. Less respect from others. 23. Self-esteem drops. 24. Not as comfortable meeting new people. 25. You don't achieve as much, you can't do constmctive things after you've been drinking. 26. Interacts with medication. 27. Don't know if I'm helping myself when I go out and do in vivo expo­ sures—whether it's m e or the Xanax getting m e through. 28. Hangovers. 29. Loss of control (e.g., saying something indiscreet during blackouts). 30. D m n k driving. 31. Discouragement for not being in control of a senseless urge. 320 Appendix 3 32. I do and say things that I regret. 33. Have sex when I wouldn't normally. 34. Become too aggressive. 35. Impairing m y reasoning. 36. Lack of control. 37. May lose house. 38. I could die. 39. Endanger self in bad areas of town. 40. Become isolated. Appendix 3 321 A D V A N T A G E S OF N O T USING 1. Keep your sanity. 2. Feel less paranoid. 3. Better relationship with spouse. 4. Feel great physically. 5. Save money. 6. Would not have to look over m y shoulder. 7. Feel better about myself. 8. I can think clearly. 9. I feel like going to work. 10. Can pay m y bills. 11. Not lazy. 12. Not flying off the handle. 13. Don't have to lie to family. 14. More time to practice hobbies. 15. It's a depressant and since I'm having problems in that area it's good to avoid. 16. Good for m y weight (less calories). 17. You can accomplish more in the evening if you don't drink. 18. All around easier on m y body not to drink. 19. Don't have-to worry about making a fool of yourself at parties. 20. Don't wake up wondering what I did the night before (skinned hands, etc.). 21. No hangovers. 22. Self-confidence at having overcome a self-destructive urge. 23. Moral reward for overcoming unnecessary desire. 24. Wouldn't have bad reputation. 25. Wouldn't regret things—punching doors, being aggressive. 26. Health reasons. 27. Improved communication-not so snappy, talk better in some groups. 28. Sleep better. 29. Not so worried about others knowing. 30. Able to plan fature. 31. Better relationship—better sex. 32. Less jealous. 33. More time (for self and family). 322 Appendix 3 DISADVANTAGES OF N O T USING 1. I'm bashfal around other people and it's hard to get over that. 2. Can't m n away from the problems. 3. I'll be lonely. 4. I have to deal with urges. 5. Can't fall asleep at night. 6. Agitated. 7. Withdrawn—wouldn't talk to other people. 8. Feel hyper. 9. Social tension (being tempted). 10. Losing friends. 11. I wouldn't have the feelings that I get when I drink (the relaxed buzz). 12. It makes bars not quite as much fan. 13. It's awkward at cocktail parties or dinner having one drink or no drink and everyone else is having more. 14. I sometimes miss it (glass of good red wine with certain dinners). 15. Fear of intimacy while fally sober. 16. Uncomfortable in social sitaations. 17. Life wouldn't be as fan. 18. I'll have to deal with things. 19. Troubled by thoughts of fafare craving and relapse. APPENDIX 4

DAILY RECORD OF CRAVINGS (DTR ADAPTED FOR USE SPECIFICALLY WITH CRAVINGS) Degree Thoughts of or craving Rational response Date Situation Feelings (0-100) and/or coping 6-12 Boss came down Felt stupid. Thought: 50 1 can try to work it hard on me. 1 need a smoke. out—waited it out for half an hour and craving went away. 6-25 Guys were going It's O K to be with 50 Went to bar and to the bar. them—1 can handle thought, "This is a craving now. mistake, and so 1 left." 7-4 I had to make a Felt anxious, "I need 40 "1 don't need a drink. presentation. a drink to do it." 1 can do it without it." 7-16 Had a fight with Felt depressed and 30 Decided to take a walk. m y wife. angry. Thought of taking a hit. 7-28 Got paid today. Thought I should 20 "I'll only feel worse celebrate. later" so 1 went home. M y wife will raise hell when she finds out. 323 APPENDIX 5 PATIENT'S REPORT OF THERAPY SESSION Patient's Name: Date of Session: Time Session Began: a.m. p.m. Therapist's Name: .^_^ PART I. Please circle your response to each of the following: 1. Before you came in today, how much progress did you expect to m dealing with your problems in today's session? M U C H PROGRESS SOME PROGRESS N O PROGRESS 2. In today's session, how much progress do you feel you acfaally made? MUCH SOME N O THINGS GOT PROGRESS PROGRESS PROGRESS WORSE 3. In future sessions, how much progress do you think you will be able to make in dealing with your problems MUCH PROGRESS SOME PROGRESS N O PROGRESS 4. How satisfied are you with today's session? VERY SATISFIED SATISFIED INDIFFERENT DISSATISFIED 5. In today's session, how well do you think your therapist understood your problems? VERY WELL FAIRLY WELL POORLY 6. How well were you able to convey your concerns or problems in this ses­ sion? VERY WELL FAIRLY WELL POORLY 7. In today's session, how much did you think you could trust (have confi­ dence in) your therapist? VERY MUCH SOME NOT AT ALL PART II. Please answer the following questions about homework. 1. Was homework assigned last session? YES NO 2. Did you discuss last week's homework in today's session? YES NO 3. How helpfal was the homework and the discussion of it? VERY SOMEWHAT NOT AT ALL NOT HELPFUL HELPFUL HELPFUL APPLICABLE 324 Appendix 5 325 4. How pleased are you with the homework that was assigned for this com­ ing week? VERY SOMEWHAT NOT AT ALL NOT PLEASED PLEASED PLEASED APPLICABLE PART III. Rate the extent to which you believe you gained the following skills in this therapy session. Please refer only to this session, realizing that not all of these skills can be gained in any one session. VERY M U C H SOME NONE 1. Better insight into and understanding of my psychological problems. 0 2. Methods or techniques for better ways of deal­ ing with people (e.g., asserting myself). 3. Techniques in defining and solving m y everyday problems (home, work, school). 4. Confidence in undertaking an activity to help myself. 0 5. Greater ability to cope with m y moods. 0 6. Better control over m y actions. 0 7. Greater ability to recognize m y unreasonable thoughts. 8. Greater ability to correct m y unreasonable thoughts. 2 0 9. Greater ability to recognize m y self-defeating or erroneous beliefs. 2 0 10. Greater ability to evaluate m y self-defeating or erroneous beliefs. PART IV. Rate the extent to which your therapist was the following in this session. VERY NOT MUCH SOME AT ALL 1. Sympathetic and caring 2 0 2. Competent (knew what he/she was doing.) 2 0 3. W a r m and friendly 2 0 4. Supportive and encouraging 2 0 5. Involved and interested 2 0 326 Appendix 5 PART V. Please circle the response that applies to the way you perceived your therapist (or therapy) in this session. 1. M y therapist talked down to me. YES NO 2. He/she was too quiet and passive. YES NO 3. He/she talked too much. YES NO 4. He/she was too bossy. YES NO 5. He/she seemed to miss the point. YES NO 6. This therapy (cognitive therapy) does not seem to be suited to me. YES N O PART VI. In the remaining space, describe the most outstanding aspect of today's session and elaborate on any of the difficulties you experienced. APPENDIX 6 POSSIBLE REASONS FOR N O T DOING SELF-HELP ASSIGNMENTS* (to be completed by patient) The following is a list of reasons that various clients have given for not doi their self-help assignments during the course of therapy. Because the speed of improvement depends primarily on the amount of self-help assignments that you are willing to do, it is of crucial importance to pinpoint any rea­ sons that you may have for not doing this work. It is important to look for these reasons at the time that you feel a reluctance to do your assignment or a desire to put off doing it. Hence, it is best to fill out this questionnaire at that time. If you have difficulty filling out this form and returning it to the therapist, it might be best to do it together during a therapy session. [Rate each statement with a "T" (Tme) or "F" (False). "T" indicates that you agree with it; "F" means the statement does not apply at this time.] 1. It seems that nothing could help me so there is no point in trying. 2. I really can't see the point of what the therapist has asked m e to do. 3. I feel that the particular method the therapist has suggested will not be helpfal. It doesn't really make good sound sense to me. 4. "1 a m a procrastinator, therefore I can't do this." Then I end up not doing it. 5. I a m willing to do some self-help assignments, but I keep forgetting. 6. I do not have enough time. I am too busy. 7. If I do something the therapist suggests it's not as good as if I come up with m y o w n ideas. 8. I feel helpless, and I don't really believe that I can do anything that I choose to do. 9. I have the feeling that the therapist is trying to boss m e around or con­ trol me. 10. I don't feel like cooperating with the therapist. 11. I fear the therapist's disapproval or criticism of m y work. I believe that what I do just won't be good enough for him/her. 12. I have no desire or motivation to do self-help assignments or anything else. Since I don't feel like doing these assignments, it follows that I can't do them and I don't have to do them. This form was developed by David Burns, M.D., and Aaron T. Beck, M.D. From Bec (1979). Copyright 1979 by The Guilford Press. Reprinted by permission. 327 328 Appendix 6 13. I feel too bad, sad, nervous, upset (underline appropriate word(s)) to do it now. 14. I am feeling good now and I don't want to spoil it by working on the assignment. 15. Other reasons (Please write them in) APPENDIX 7 COGNITIVE THERAPY INTERVENTION W I T H HIV-POSITIVE D R U G ABUSERS* Many chronic dmg abusers engage in behavior that puts them at high risk for becoming HIV infected. The following is a brief outiine for working with the HIV-positive population with regard to the emotional distress they will most likely experience w h e n they become aware of, and try to cope with, their condition. 1. Educate patients about the physiological symptoms associated with psychological stress. Anxiety and depressive symptoms, such as hyperventi­ lation and lightheadedness, or fatigue, anhedonia, lack of libido, irritability, and distractibility, are often misinterpreted as signs of a physical illness by distressed patients w h o have been informed that they are HIV positive. This c o m m o n misinterpretation increases the sense of threat and loss, and inten­ sifies the anxiety/depressive symptoms, which then reinforce the belief of a developing crisis ("I'm losing m y mind," "I'm getting AIDS," etc.). 2. The therapist should encourage the dmg abuser to remain free of drugs and alcohol in order to improve overall health in an effort to stay well long enough to see the day when more effective treatments are available for the disorder. 3. Review with patients cognitive coping techniques such as thought stopping, distraction, coping statements or flashcards, rational responding. 4. Help patients identify and modify dysfanctional thoughts and atti- fades associated with being HIV positive. A typical thought might be, "This disease is m y punishment for being a bad person." This dysfanctional thought is generated from unarticulated fandamental beliefs such as "I a m bad" or "1 a m defective." 5. In addition to teaching patients to recognize distortions and the dys­ fanctional nature of specific automatic thoughts, therapists should train patients to label these distortions. Listed below are some c o m m o n distor­ tions associated with HIV-related emotional distress: • Catastrophizing. "This is the end for me." • All-or-nothing thinking. "If I'm not perfectiy healthy, I can't enjoy any­ thing." • Overgeneralization. "This coughing means that m y whole body is fall- *From Stress Prevention Training after HIV Antibody Testing: A Trainer's Manual man, 1992, unpublished manuscript, Cornell University Medical College, New York. Copyright 1992 B. Fishman. Adapted by permission of the author. 329 330 Appendix 7 ing apart." • Jumping to conclusions. "My friend didn't want to go out this week­ end; she must know I'm contagious and doesn't want to be around me." • Personalization. "The grocer did not treat m e well because he wants m e to stay away from his store." 6. Teach patients to identify and modify dysfanctional behavioral hab­ its. Throughout the treatment emphasize controlling high-risk sexual and IV d m g use behaviors. Not only are unsafe IV d m g use and sex dangerous in spreading HIV to uninfected individuals, but these behaviors also expose the HIV-infected patient to reinfection, which may increase chances of the full AIDS syndrome. Furthermore, the practice of high-risk behaviors is often experi­ enced by patients themselves as impulsive and self-harming. Patients experi­ ence guilt, shame, loss of esteem, and an increased sense of vulnerability or "being out of control." Therefore, achieving effective control over these behaviors is extremely important. Controlling high-risk behaviors requires three components: a. Reliable information and practical understanding about how HIV is transmitted, and how transmission can be avoided or prevented. b. Impulse control—habifaal and automatic effort to perform the pro­ cedures necessary to avoid HIV transmission (using condoms, "bleach­ ing" needles, etc.). c. Assertiveness—the ability to assert one's position under external social pressure without submission or aggression. Oftentimes difficulties in asserting wishes are based on distorted cognitions and dysfanctional assumptions such as "If I insist on using a condom, she will make fan of me," or "If I bleach m y 'works,' they will think I'm not a real •brother.'" Summary This outiine has examined ways that therapists can help HIV-positive dmg abusing patients cope with their disorder: (1) by educating them about the physiological symptoms associated with psychological stress and how these symptoms can be misinterpreted as signs of their illness, (2) by encouraging them to remain free of drugs and alcohol in order to improve overall health, (3) by reviewing with them the basic cognitive therapy techniques for cop­ ing with stress such as thought stopping, distraction, coping statements or flashcards, and rational responding, (4) by helping them identify and modify dysfanctional thoughts and attitudes associated with being HIV positive, (5) by teaching them to recognize and label distortions associated with HIV- related emotional distress (e.g., catastrophizing and all-or-nothing thinking), and (6) by teaching them to identify and modify dysfanctional behavioral habits such as not using condoms and not bleaching needles. R e f e r e n c e s Abrams, D.B., & Niaura, R.S. (1987). Social learning theory. In H.T. Blane & K.E. Leonard (Eds.), Psychological theories of drinking and alcoholism (pp.

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Author Index Abrams, D.B., 13 Brown, G., 94 Adlaf, E.M., 7 Brown, S.A., 33 Alberti, R.E., 254, 264, 286 Brown, V.B., 10, 268 Allsop, S., 292 Brownell, K.D., 11 Alterman, A.I., 7, 51, 236, 273, 281 Bunt, G., 10 Amaro, H., 196, 220, 252 Buriing, T.A., 228 Ananth, J., 10 Burns, D.D., 109, 117, 136, 143, 185, 327 Anderson, L.R., 33 Annis, H.M., 157 Cabral, H., 196 Arif, A., 3 Cacciola, J.S., 236, 281 Arnold, M., 4 Cameron, D.C, 3 Auerbach, A.H., 109, 136, 185 Carey, K.B., 187, 270, 272 Carroll, K.M., 30, 32, 57, 124, 152, 154, Babor, T.F., 3 157, 298, 299, 300, 301, 302, 307, Baker, CD., 7 315 Baker, T.B., 12 Castaneda, R., 10, 27, 59, 152, 158 Bandura, A., 13, 33 Chalkley, A.J., 264 Barnett, L.W., 10, U Chang, G., 206 Baumeister, R.F., 38 Chiasson, R.E., 209 Beck, A.T., 10, 14, 27, 35, 42, 48, 49, 50, Chiauzzi, E.J., 11 51, 52, 69, 82, 93, 94, 95, 100, 135, Childress, A.R., 50, 51, 52, 157, 159, 302 140, 143, 169, 173, 226, 227, 230, Clark, D.M., 264 234, 244, 252, 258, 269, 273, 276, Clayton, R.R., 5, 9 289, 290, 291, 327 Closser, M.H., 197, 208 Beck, J.S., 86 Cohen, S., 7 Beeder, A.B., 257 Collner, D., 254, 264, 286 Beitman, B.D., 257 Cooper, A.M., 269 Bentler, P.M., 13 Covi, L, 7, 55, 124, 157 Bernstein, D.A., 168, 264 Crowther, J.H., 38 Blackburn, I.M., 108 Cummings, C, 308 Blane, H.T., 12 Cummings, N.A., 216, 271, 280 Bogardis, J., 16 D'Aulaire, E., 7 Borkovec, T.D., 168, 264 Davidson, K.M., 108 Bowser, B.F., 209 Davis, C.W., 27 Branch, L.G., 10, 11 Davis, D.H., 24 Brecher, E.M., 3, 5, 6 Davis, D.I., 10 Brocco, K.J., 268 DePhilippis, D., 50 Brodsky, A., 4 346 Author Index 347 DiClemente, C.C, 15 Gross, S.A., 209 DiGiuseppe, R., 28 Grossman, J., 203, 208 Dilts, S.L., 8 Gunderson, J.G., 269, 279 Donovan, D.M., 292 Doren, D.M., 280, 281, 285, 286 Drake, R.E., 269 Haaga, D.A.F., 13, 285 D'Zurilla, T.J., 290 Hall, S.M., 28, 167, 229 Haller, D.L., 3 Hansen, K.V.,

5 EUinwood, E.H., 6, 7, 25, 31, 37, 51, 197 Harrison, R., 95 Ellis, A., 28, 242, 244, 246 Harstone, E., 5 Emery, G., 27, 42, 327 Hatsukami, D., 27, 234 Emmons, L., 254, 264, 286 Havassy, B.E., 28, 57, 124, 167, 301 Epstein, N., 94, 95 Heath, A.W., 5 Erbaugh, J., 93 Heatherton, T.F., 38 Estroff, T.W., 7 Helzer, J.E., 257, 268 Evans, K., 59, 268 Henningfield, J.E., 8, 9, 126 Hermalin, J., 150, 194, 253, 254 Fingarette, H., 4 Hess, J.M., 7 Fiore, M.C, 9 Hesselbrock, M.N., 10, 257, 268 Fishman, B., 209, 329 Hesselbrock, V.M., 268 Fox, S., 57, 76 Hester, R.K., 14, 17, 18, 19 Frances, R.J., 5, 23, 55, 77, 209, 301, 308 Hole, A., 50 Franco, H., 27 HoUon, S.D., 10 Frankenburg, F.R., 269 Horney, K., 244 Freeman, A., 49, 288 Horvath, A.T., 25, 31, 32, 37, 152, 157, Fried, L.E., 196 163, 166, 301 FuUilove, M.T., 209 Hudson, C.J., 257 Fullilove, R.E., 209 HInunn,t ,A .W,. A3.3, 10, 11 Galanter, M., 10, 27 Isbell, P.G., 276 Garrison, B., 94 Gaspari, J.P., 27 Jellinek, E.M., 3 Gawin, F.H., 6, 7, 25, 30, 37, 51, 57, 197, Jennings, P.S., 25,13 0 207, 246, 272, 296 Jones, R.T., 6 Germanson, T., 10 Gibbon, M., 226 Kaplan, J., 257 Gilmore, M.M., 269 Kaplan, R.D., 269 Glantz, M., 246 Karan, L.D., 3, 6, 7, 34, 276 Glaser, F.B., 10 Keller, D.S., 30, 32, 57, 124, 152, 154, Goldfried, M.R., 290 157, 298, 299, 300, 301, 302, 307, Goldman, M.S., 33 315 Goldsmith, M.F., 209 Kenner, J.J., 10, 257, 268 Gomberg, E.S.L., 192 Khantzian, E.J., 27, 152, 158, 269 Good, S.P., 3 Kleber, H.D., 23, 25, 27, 59, 207, 246, Goodwin, D.W., 3, 24 272, 296 Gordon, J.R., 11, 12, 31, 33, 37, 47, 49, Klein, D.F., 257 293, 303, 306, 308 Koenigsberg, H.W., 269 Gorski, T.T., 12, 298 Korner, P., 3 Gottheil, E., 7 Kosten, T.R., 23, 59, 212, 236 Grabowski, J., 8, 126 Kovacs, M., 94 Grande, T.P., 268 Kranzler, H.R., 10, 27, 257 Grant, M., 3 Krone, A., 27 Greenberg, J., 194 Kushner, M.G., 257, 258 Greenberg, R.L., 42 348 Author Index LaBounty, LP., 27, 257 Newman, C.F., 65, 70, 77, 82, 109, 211, Ung, A.R., 192 214, 285, 288, 290 Layden, M.A., 288, 289, 290 Nezu, CM., 153 Leo, G.I., 16 Nezu, A.M., 153, 290 Leonard, K.E., 12 Niaura, R.S., 13 Lester, D., 94 Nirenberg, T.D., 59 Levin, J.D., 4 Nolen-Hoeksema, S., 109 Levine, I.S., 10 Norcross, J.C, 15 Lewis, C.E., 268 Novotny, T.E., 9 Lichtenstein, E., 11 O'Brien, C.P., 7, 48, 51, 167, 197, 236 Liebowitz, N.R., 10, 27, 257 O'Connell, D.F., 268 Lifshutz, H., 10 O'Connor, P.G., 206, 276 Linehan, M.M., 290 Obert, J.L., 236 Ling, W., 236 Ola, P., 7 Lingswiler, V.M., 38 Ott, P.J., 247 Linnoila, M.L, 257 Overholser, J.C, 103, 136 Lyon, D., 194 Mackay, P.W., 66, 292, 293, 301, 302, 308 Patterson, M.B., 268 Marlatt, G.A., 11, 12, 13, 14, 16, 31, 33, Peele, S., 4, 23, 24 37, 47, 49, 66, 292, 293, 303, 306, Penick, E.C, 10, 268 308 Pepper, B., 10 Marzuk, P.M., 216, 240 Perez, J.F., 57 Massey, R., 27 Perioff, J.M., 109 McCann, M.J., 236 Perri, M.G., 153 McCord, J., 5 Persons, J.B., 10, 80, 109, 136, 185, 237, McDermut, W., 13 291 Mclnerney, J.F., 28 Pickens, R.W., 27, 234, 246 McLellan, A.T., 7, 18, 51, 124, 209, 236 Pierce, J.P., 9 Mendelson, M., 93 Piatt, J.J., 150, 194, 253, 254 Metzger, D., 209 Pollin, W., 9 Meyer, R.E., 10, 257, 268 Prochaska, J.O., 15, 26 Mezzich, A.C, 247 Prochnow, H.Z., 292 Miller, M., 12, 298 Pryzbeck, T.R., 257, 268 Miller, N.S., 9, 22, 271 Quitkin, F.M., 257 Miller, R.L., 4 Miller, S.L, 5, 23, 55, 77, 209, 301, 308 Rawson, R.A., 236 Miller, W.R., 4, 14, 17, 18, 19, 124 Regier, D.A., 10, 22, 27, 29, 226, 257, 268 Millman, R.B., 5, 6, 257 Reilly, P.M., 228 Mirin, S.M., 27, 29, 227, 240 Rice, J., 268 Mock, J., 93 Ridgely, M.S., 10 Moltzen, J.O., 228 Rifkin, A., 257 Moorey, S., 47, SO, 64, 151, 292 Robins, L., 268 Morgan, S.F., 27 Robins, L.N., 24 Morse, S.B., 288 Rollnick, S., 14, 124 MuUaney, J.A., 257 Ross, H.E., 10, 258, 268 Munoz, R.F., 4 Ross, S., 254, 264, 286 M RounsaviUe, B.J., 27, 30, 32, 57, 59, 124, Naucrer,a yE,.P G.,F .1,0 ,3 2 7, 59, 269, 276 Musto, D.R., 3 152, 157, 226, 298, 299, 300, 301, Nathan, P.E., 10 302, 307, 315 Nelson, L., 27 Rush, A.J., 27, 327 Newcomb, M.D., 13 Rush, B., 3 Ryglewicz, H., 10 Author Index 349 Salkovskis, P.M., 264 Trippett, C.J., 257 Saunders, B., 292 Tucker, J.A., IS Saxon, J.J., 10, 269 Schneier, F.R., 10 SchnoU, S.H., 3 Urschel, H.C, 273 Schottenfeld, R., 208 Schubert, D.S.P., 268 Vaillant, G.E., 269, 292 Schuckit, M.A., 258, 269 Velten, E., 31, 51 Schwartz, J.L., 19, 20 Shaw, B.F., 27, 327 Shayne, V.T., 13 Walfish, S., 27, 242, 258 Sher, K.J., 257 Ward, C.H., 93 Shi, J., 206 Washton, A.M., 37, 157, 163, 302 Shifftnan, S., 296, 301 Wasserman, D.A., 28, 167 Shore, N., 10, 269 Weiner, H., 57, 76 Shulman, G.D., 51, 157, 293 Weinstein, S.P., 7 Siris, S.G., 10 Weiss, C.J., 5, 6 Skinner, W., 16 Weiss, R.D., 27, 29, 227, 240, 246 Smart, R.G., 3, 7, 197, 208 Weissman, A.N., 94, 173 Smith, D.P., 236 Westermeyer, J., 2, 3 Sobell, L.C., 15, 16, 59, 81 Wilber, C, 3 Sobell, M.B., 16, 59 WiUiams, J.B.W., 226 Spitzer, R.L, 226, 272 Wills, T.A., 301 Stabenau, J.R., 268, 269 Wilson, G.T., 11, 13, 258 Stacy, A.W., 13 Wolf, A.W., 268, 269 Stanton, M.D., 5 Woody, G.E., 45, 209, 226, 236, 273, 281 Steer, R.A., 94, 100 Wright, F.D., 82, 211, 214, 311, 312, 313 Stephens, M.A.P., 38 Yeager, R.J., 28 Steriing, R.C, 7 Young, J.E., 290 Stimmel, B., 22, 208, 209 Stine, S.M., 7 Stitzer, M.L, 8, 126, 168, 232 Zanarini, M.C, 269, 279 TSaurltleirv,an ,R. EJ.,M .2,4 759 , 268 Ziedonis, D.M., 25, 34, 236, 240 Thomason, H.H., 8 Ziff, D.C, 228 Tiffany, S.T., 13, 30, 37, 157, 166 Zotter, D.L, 38 Treece, C, 269 Zuckerman, B., 196 Trexler, L., 94 Zung, W.W.K., 257 Subject Index Abstinence, 2, 124-125; see also Relapse Assertive training, 253, 264 prevention Attention deficit disorder, 246 Abstinence Violation Effect (AVE), 12, 13, Attribution, 250 303 Automatic Thoughts about Substance Action stage; see Stages of change Abuse; see Psychometric inventories Active listening, 150-151 Automatic thoughts, 44, 48, 55, 75, 82, Addictive beliefs; see Beliefs 114, 159, 229, 251, 264, 294 Advantages-disadvantages analysis; see examples of, 165 Techniques five basic questions, 164 Agenda; see Structure Autonomous craving, 32, 40 Alcohol(ism) Autonomy, 88-89, 93 Alcoholics Anonymous; see Models of addiction Beck Anxiety Inventoty; see Psychometric crimes associated with, 5 inventories history, 3 Beck Depression Inventoty; see Psycho­ medical problems associated with, 4, 5 metric inventories morbidity and mortality, 4, 226 Beck Hopelessness Scale; see Psychomet­ negative social consequences, 5 ric inventories prevalence, 1, 4, 226 Behavioral experiments; see Techniques role in illicit drug-abusing patients' Behavioral rehearsal; see Techniques therapy, 66 Belief(s), 42-53, 169-186; see also treatment interventions, 17-19 Schemas Alcoholics Anonymous (12-step program); addictive, 38, 43-46, 52, 116, 169-189 see Models of addiction anticipatoty, 45^6, 48, 53, 169 All-or-none thinking; see Cognitive conditional, 82 distortions conflicting, 46, 170-171 Anger, 242-267 control, 170, 178-185, 299, 300 and abusive behavior, 252-253 core (basic), 28-31, 37, 40, 43-14, 51, low frustration tolerance, 242-248 140, 149, 201 toward therapist, 251-252 drug-related, 30, 43, 48, 51, 82, 116, Anticipatoty beliefs; see Beliefs 149, 154, 293, 300 Antisocial; see Personality disorders dysfunctional, 25-26, 32-33, 38, 40, Anxiety (disorders), 169, 242-267; see also 227 Anger facilitating, 48, 294 case conceptualization, 259 levels of, 43 cognitive therapy of, 258 permissive (permission-giving), 31, 35- management of, 259, 262-264 350 36, 38, 46, 48, 53, 169 and substance abuse, 23, 24, 257-267 Subject Index 351 relief-oriented, 45, 48, S3, 169 Collusion; see Therapeutic relationship romanticized beliefs, 45 Conditional beliefs; see Beliefs substance-using, 42 Confidentiality; see Therapeutic relation­ system(s), 51-115, 171 ship Beliefs about Substance Use inventoty; Confrontation, 77-78; see also Power see Psychometric inventories struggles Black and white thinking; see Cognitive Contemplation stage; see Stages of distortions, all-or-none thinking Change Borderline; see Personality disorders Control beliefs; see Beliefs Bridge from last session; see Structure of Coping techniques, 11, 51, 80, 126, 130 therapy session Core beliefs; see Beliefs Cost-benefits analysis (advantages- Capsule summaries, 107-108, 172; see disadvantages analysis); see Tech­ also Structure of therapy session niques Case conceptualization; see Case Cravings, 23, 31-32, 48, 157-168; see also formulation Urges Case formulation, 80-96, 135-136 automatic thoughts associated with, anxiety, 259 159 case study of, 83-85 Daily Record of Cravings, 323 components, 80-85 scenario, 119 definition, 10, 27 spontaneous, 49 depression, 229-230 techniques for coping with, 160-168 diagram of, 86 types of, 43, 157-159 Ulusttation of, 90-93 Craving Beliefs Questionnaire; see questions and scales for, 93-95 Psychometric inventories Case formulation profiles; see also Case Crisis, 211-225 formulation definition, 211 cognitive, 85, 87-88, 136 related to substance abuse, 214-223 developmental, 85, 87, 136 typical crises, 211-212 integration and conceptualization of, warning signs, 212-214 85, 88, 92 Daily Activity Schedule; see Techniques Catastrophizing; see Cognitive distortions Daily Record of Cravings; see Cravings Checklist for Dealing with Ambivalence Daily Record of Dysfunctional Thinking; and Lapses, 298, 315-317 see Daily Thought Record (DTR) Cigarette smoking; see Nicotine Daily stressors; see Life problems Cocaine, 5-7, 208 Daily Thought Record (DTR); see prevalence, 7, 197, 208 Techniques medical problems associated with, 7 Depression, 10, 45, 226-241 Co-dependency, 194 automatic thoughts and beliefs, 169, Cognitive blockade, 51-52 232-234 Cognitive conceptualization worksheet, behavioral techniques for, 237-240 89 beliefs associated with, 227-228 Cognitive dissonance, 153 case formulation, 229-230 Cognitive distortions, 58, 123, 231, 246 characteristics of, 227 all-or-none thinking, 14, 243, 246, 303 co-morbidity, 226 catastrophizing, 141, 244, 246-247, dysphoria, 34 250, 256-257 suicide, 234-235 overgeneralization, 77, 115, 244, 246 target symptoms of, 230-231 personalizing, 246 therapeutic approach to, 228-230 selective abstiaction, 246 Developmental profile; see Case formula­ Cognitive profile; see Profiles tion profiles Cognitive therapy model of addiction Diagnostic and Statistical Manual of (diagrams), 22-53, 174-175, 261, 293 Mental Disorders, (3rd ed., rev.) Cognitive tiiad, 140, 227 (DSM-III-R), 257 Collaboration, 68-70; see also Therapeutic psychoactive substance classes, 2 relationship 3 5 2 Subject Index Diagnostic and Statistical Manual of opioids, 5, 8, 24 Mental Disorders (continued) treatment, 19 Structured Clinical Interview for DSM- Imagety, 144-147, 159, 183, 208, 252, III-R Disorders (SCID), 226 275; see also Techniques substance abuse definition, 2 image mastety, 161 substance dependence definition, 2 image refocusing, 161 Dichotomous thinking; see Cognitive image rehearsal, 161 distortions, all-or-none thinking negative image replacement, 161 Disease model of addiction; see Models of positive image replacement, 161 addiction Inductive questioning, 117 Distraction, 160-161, 249, 252, 300; see Internal reality, 112 also Cravings, techniques for coping with; Anger; Anxiety; Relapse Lapse, 13-14, 294, 302-306 Downward arrow technique; see Tech­ Life problems, 83, 187-210 niques daily stressors, 200-203 Drug-related beliefs; see Beliefs legal, 203-206 DSM-III-R; see Diagnostic and Statistical marital and family, 192-197 Manual of Mental Disorders (3rd ed., medical, 206-209 rev.) socioeconomic, 88, 197-200 Dual diagnosis, 10, 29, 59, 268 Limit-setting; see Therapeutic relationship Dysfunctional Attitude Scale; see Low Frustration Tolerance (LFT), 24, 28, Psychometric inventories 39^0, 242-248; see also Anger; D Anxiety Eymsppahtohryi,a ;7 4se,e 7 6D-e7p7r,es 1s3i5o,n 151 Enabling, 70 Maintenance stage; see Stages of change Exercise; see Techniques Models of addiction, 12-16 Alcoholics Anonymous, 12, 16, 34 cognitive-behavioral model, 12 Feedback; see Structure cognitive models, 13-14 Flashcards; see Techniques disease model, 3, 4, 12 M o o d check; see Structure Goal setting, 121-134 Negative image replacement; see Imagety Graded task assignments; see Techniques Nicotine, 9 Guided discovety (Socratic method), 29, DSM-lIl-R, 9 48, 103-107, 136, 142, 156, 177, 185, histoty, 8 300 interventions, 19 morbidity and mortality, 8 Helplessness, 40, 83, 201 prevalence, 1, 8-9 High-risk situations (HRS), 11, 13, 47, 50, as a psychoactive substance, 2, 9 293-294, 297-299, 302, 308; see also relation to illicit drug abuse, 9 Stimulus situations HIV patients, cognitive therapy with, 329 Open-ended questions, 104, 144, 155, Homework; see Structure of therapy 171 session Overgeneralization; see Cognitive Hopelessness, 83, 100, 201, 234, 236 distortions Hot cognitions, 76, 159, 202, 274 Patient's Report of Therapy Session Illicit drugs, 5-8 (questionnaire);

see Structure prevalence, 5 Permissive (permission-giving) beliefs; see crimes, 5 Beliefs deaths, 5 Personality disorders, 10, 27, 29, 268-291 marijuana, 5-6 antisocial, 236, 268-269, 278-287 Subject Index 3 5 3 assessment, 271-276 Relapse Prediction Scale, 93, 95, 313- avoidant, 254, 270, 276 314 borderiine, 269-270, 287-291 Sociotropy-Autonomy Scale, 93, 95 common features of, 269-270 dependent, 270, 277 histrionic, 277 Rapport; see Therapeutic relationship narcissistic, 277 Rational response(s), 36, 76, 144, 155, obsessive-compulsive, 254, 277 163, 180 passive-aggressive, 277 Rationalizations; see Beliefs, permissive prevalence, 268-269 Reality principle, 35 schizoid, 278 Reattribution of responsibility; see schizotypal, 278 Techniques Personalizing; see Cognitive distortions Reframing, 130, 132, 157, 234-235 Physiological addiction, 2 Reinforcement, 62, 126, 168 Pleasure principle, 35 Relapse/relapse prevention, 10-12, 14, Polysubstance abuse, 6, 9 30-31, 236, 292-309 Positive image replacement; see Imagety behavioral strategies, 301-302 Positive outcome expectancies, 12-13, 33, cognitive sttategies, 299-301 306 depression, 234-235 Possible Reasons for Not Doing Self-Help goals of, 296 Assignment Checklist, 109-110, 327- models of relapse prevention, 293-297 328 prediction and control of, 297-308 Precontemplation stage; see Stages of prevalence, 10 change social support network, 308 Preparation stage; see Stages of change Relapse Prediction Scale; see Psychometiic Problem solving; see Techniques inventories Profiles; see also Case formulation Relaxation training; see Techniques cognitive, 85, 87-88 Relief-oriented beliefs; see Beliefs developmental, 85, 87 Research on the tteatment of substance integration and conceptualization of, abuse 10, 85, 88, 92 alcoholism, 17-19 Programmed practice (covert rehearsal), illicit drug treatment, 19 183 smoking cessation interventions, 19-20 Psychoactive substances Scthreemaatsm,e n5t0 ,o u81t-c8o2m e goals, 16 addictive potential, 2 Selective abstraction; see Cognitive attitudes regarding, 3 distortions definition, 2 Self-efficacy, 13, 228 DSM-III-R classes, 2 Self-medicating, 27, 151, 158, 206 histoty of use, 2-4 Social network, 194 most commonly used 4-9 Socioeconomic; see Life problems multiple substances (polysubstance Sociottopy, 88-89, 93 abuse), 9 Sociotropy-Autonomy Scale; see Psycho­ Psychometric inventories metric inventories Automatic Thoughts about Substance Socratic method; see Guided discovety Abuse, 173 Stages of change, 15-16, 26-27 Beck Anxiety Inventoty, 87, 93, 94, Stimulus circumstance; see Stimulus 101, 299 situations Beck Depression Inventoty, 87, 93-94, Stimulus control; see Techniques 101, 173-174, 212, 226, 232, Stimulus generalization, 33-34 299 Stimulus sihiations, 47, 50, 52-53, 81-82, Beck Hopelessness Scale, 87, 93, 94, 191, 293, 297-302 101, 232, 299 Structure (of therapy session), 97-111 Beliefs about Substance Use, 93, 94, bridge from last session, 101 117, 311 capsule summaries, 107-108 Craving Beliefs Questionnaire, 93, 95, 173, 312 Dysftinctional Attitude Scale, 93, 94, 173 3 5 4 Subject Index Structure (of therapy session) (continued) downward arrow technique, 118, 140- discussion of agenda items, 101-103 142, 178 feedback, 62, 110-111 flashcards, 160-168, 183 homework, 108-110, 136, 144, 155, 185 identitying and modifying drug-related mood check, 100-101 beliefs, 139-140 Patient's Report Of Therapy Session imagety, 144-147, 159, 161-163, 166, (questionnaire), 101, 324-326 252, 266, 303 setting the agenda, 98-100 reattribution of responsibility, 142- Structured Clinical Interview for DSM-III-R 143 Disorders (SCID), 226 Theories of addiction; see Models of Substance using beliefs; see Beliefs addiction Suicide, 4, 100-101, 214, 227, 234, 240 Therapeutic relationship, 54-79, 135 Symptom exacerbation, 236 building trust, 62-64 Target symptoms; see Depression collaboration, 57, 68-70, 235 Techniques (of cognitive therapy), collusion, 70-72 behavioral, 147-154 confidentiality, 55, 67 behavioral experiments, 149-150, 266 credibility, 68 behavioral rehearsal, 150-151 power struggles, 74-78 Daily Activity Schedule, 147-149, 167- rapport, 57-62 168, 238-240 setting limits, 64-66 exercise, 153-154 Therapy drift, 97, 122-123 graded task assignment, 152, 239 Trust-building; see Therapeutic relation­ problem solving, 152-153, 201 Urgess,h i3p1 -32, 157-168; see also Cravings relaxation ttaining, 151-152, 168, 264 stimulus conttol, 154 Techniques (of cognitive therapy), Vulnerable situations; see Stimulus cognitive, 137-147 situations advantages-disadvantages analysis, 28, 37, 126-130, 137-139, 180-182, Will power, 36-37 284, 306-307, 318-322 Worid Health Organization ( W H O ) , 3 Daily Thought Record, 109, 143-145, 164, 180, 203-204, 265 PSYCHOLOGY COGNITIVE THERAPY OF SUBSTANCE ABUSE Aaron T. Beck, Fred D. Wright, Cory F. Newman, and Bruce S. Liese "I will refer to and recommend this book as a bountiful clinical guide.Bolst by outcome data, this wise and hopeful book will greatly advance integration of cognitive therapy into addiction treatment programs." —Contemporary Psychology "One important aspect of this cognitive format is that its techniques can be combined with other therapeutic approaches to addiction, such as the use of AA, family supports, and social network supports.Practitioners of these modalities would do well to adapt the cognitive approach in their work." —^Amencon Journal of Psychiatry "[This] textbook explicates and expands on Aaron Beck's applications of cogniti therapy to the addictions with lucid, useful integration and a wide explanation of theory and practice." —General Hospital Psychiatry "The strength of the authors' approach is exemplified by the clarity and concisi of their writing, and by the operationalization of their constructs.Constitutes a 'gold standard' for the field." —Journal of Cognitive Psychotherapy Cognitive therapy offers a well-documented and cost-effective psychosocial treatment model for working with substance abuse disorders. Comprehensive and accessible, this volume clearly details the cognitive model of substance abuse, the specifics of case formulation, management of the therapeutic rela­ tionship, and the structure of the therapy sessions. It discusses how to educate patients in the treatment model and procedures and manage their cravings and urges for drugs and alcohol. Specific cognitive and behavioral strategies and techniques are described, as are methods for understanding and working with patients who present concomitant problems of depression, anxiety, low frustration tolerance, anger, and personality disorders. Also addressed are such significant issues as crisis management and relapse prevention. Also available in hardcover: ISBN 0-89862-1 15-1, Cot. #2/15 Cover des/gn by James Ty Cumbie I S B N l - S 7 2 3 D - b S T - T The Guilford Press 72 Spring Street New York, N Y 10012 www.guilford.com

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. The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. The publisher, the authors and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the editors give a warranty, expressed or implied, with respect to the material contained herein or for any errors or omissions that may have been made. The publisher remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. 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