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Re: Vomiting Feline Part 2 95-12-02 Ozvet Paul, Shoot..., a tough case with an enormous amount of effort on your part. It can be so discouraging to be trying your heart out and to have these cases continue to decline no matter what you do. It happens to us all. I will try to answer your questions, I'm sure that others will offer their experiences: 1. I think that the timing of the laparotomy was appropriate----conservative therapy had not resolved the problem, and there were US indicators of GI disease. I would have suggested a profile prior to the surgery to investigate metabolic causes of vomiting (renal failure, liver disease). 2. Dx of IBD is well supported in this case. The cat's rapid progression of disease is, however, unusual in my experience with IBD. 3. I can't fault the time at which you commenced pred administration--seeming to do better initially with more conservative tx; had concerns about effects of pred on wound healing and the disastrous consequences of wound dehiscence; hence waited until after the phase of fibroplasia in wound healing to commence pred. Pred is most effective treatment for IBD. No argument from me. The thought of a surgery related infection probably would have crossed my mind at this point and, before starting the pred I might have sounded his abdomen again. Just a thought; not a criticism of your approach. 4. I think that at this point his phosph. was on the decline; I don't know what it was prior to this, but I suspect much higher. 5. There are a variety of suitable protocols for this procedure, Paul. We often use K/V for placing gastrostomy tubes. 6. I have not personally seen ARF that I thought was directly related to K/V. I'm not certain that the cat had ARF. With his vomiting, anorexia, edema and pleural effusion, there is a possibility that he was volume underloaded and so not perfusing his kidneys; thus no urine. A urine SG would have helped you here. Obviously, if prolonged this can lead to ARF due to renal ischemia. In this kitty, hemoglobinuria may have also contributed. Placement of a central venous catheter would have been helpful to help you decide whether or not the cat was volume underloaded or overloaded. In this situation, lasix is most appropriately adminsitered after replacement of fluid volume deficits and the patient is still not producing urine. 7. I think that the volume expansion from hetastarch may have resulted in worsening laboratory values because of a dilutional effect. In addition to anorexia, other factors which may have contributed to hypophosphatemia in this cat included diuretics, and possibly acid base abnormailites (respiratory alkalosis). Usually, this severity of hypophosphatemia in our hands is associated with initial therapy of diabetes mellitus, and sometimes aggressive re-feeding (most often parenterally, sometimes enterally) subsequent to prolonged anorexia. I'm not sure what his feeding status was toward the end. The severe hypophosphatemia is a little puzzling, but I think a large contributor to this cat's unfortunate demise. 8. Commented on in 6, above. 9. Marked hypoalbuminemia is one of our indications to use hetastarch Paul. As far as checking renal function, I think that doing a profile in animals as sick as this makes excellent medicine. Paul, I hope these comments have been of some assistance. I'm sure others will contribute their thoughts. It is easy to sit here and pontificate; it is tough being on the spot and having to make all of the split second decisions. Also, you had the cat in your hands to examine, we did not. My overall impression is that you did a great job in working up and managing a very tough case. Did you, by chance, happen to get a necropsy?

My q's: do we know if there were ketones in his urine?

Are you monitoring blood levels of the keppra and phenobarb?

Re: Vomiting Feline Part 2 95-12-02 Ozvet Paul, Shoot..., a tough case with an enormous amount of effort on your part. It can be so discouraging to be trying your heart out and to have these cases continue to decline no matter what you do. It happens to us all. I will try to answer your questions, I'm sure that others will offer their experiences: 1. I think that the timing of the laparotomy was appropriate----conservative therapy had not resolved the problem, and there were US indicators of GI disease. I would have suggested a profile prior to the surgery to investigate metabolic causes of vomiting (renal failure, liver disease). 2. Dx of IBD is well supported in this case. The cat's rapid progression of disease is, however, unusual in my experience with IBD. 3. I can't fault the time at which you commenced pred administration--seeming to do better initially with more conservative tx; had concerns about effects of pred on wound healing and the disastrous consequences of wound dehiscence; hence waited until after the phase of fibroplasia in wound healing to commence pred. Pred is most effective treatment for IBD. No argument from me. The thought of a surgery related infection probably would have crossed my mind at this point and, before starting the pred I might have sounded his abdomen again. Just a thought; not a criticism of your approach. 4. I think that at this point his phosph. was on the decline; I don't know what it was prior to this, but I suspect much higher. 5. There are a variety of suitable protocols for this procedure, Paul. We often use K/V for placing gastrostomy tubes. 6. I have not personally seen ARF that I thought was directly related to K/V. I'm not certain that the cat had ARF. With his vomiting, anorexia, edema and pleural effusion, there is a possibility that he was volume underloaded and so not perfusing his kidneys; thus no urine. A urine SG would have helped you here. Obviously, if prolonged this can lead to ARF due to renal ischemia. In this kitty, hemoglobinuria may have also contributed. Placement of a central venous catheter would have been helpful to help you decide whether or not the cat was volume underloaded or overloaded. In this situation, lasix is most appropriately adminsitered after replacement of fluid volume deficits and the patient is still not producing urine. 7. I think that the volume expansion from hetastarch may have resulted in worsening laboratory values because of a dilutional effect. In addition to anorexia, other factors which may have contributed to hypophosphatemia in this cat included diuretics, and possibly acid base abnormailites (respiratory alkalosis). Usually, this severity of hypophosphatemia in our hands is associated with initial therapy of diabetes mellitus, and sometimes aggressive re-feeding (most often parenterally, sometimes enterally) subsequent to prolonged anorexia. I'm not sure what his feeding status was toward the end. The severe hypophosphatemia is a little puzzling, but I think a large contributor to this cat's unfortunate demise. 8. Commented on in 6, above. 9. Marked hypoalbuminemia is one of our indications to use hetastarch Paul. As far as checking renal function, I think that doing a profile in animals as sick as this makes excellent medicine. Paul, I hope these comments have been of some assistance. I'm sure others will contribute their thoughts. It is easy to sit here and pontificate; it is tough being on the spot and having to make all of the split second decisions. Also, you had the cat in your hands to examine, we did not. My overall impression is that you did a great job in working up and managing a very tough case. Did you, by chance, happen to get a necropsy?

Would you not use this drug given the low albumin?

Can i see a couple of the curves on the pzi?

Phenobarb and DM 95-12-11 Myxomatoes I am trying to stabilise a diabetic kitty who may have suffered hypoglycemic cerebral edema. I find that now that he is on phenobarb he has repeatedly low blood glucose readings. On valium the sizures were not controlled and BG was in the high end. I have not given insulin for 3 days and his BG was LOW this morning. Perhaps this is the mechanism that causes most of our patients on phenobarb to eat more. Any thoughts on this?

Is it possible that your kitty was only transiently diabetic?

The owner is only feeding at mealtimes, when the insulin is given, using a measuring cup and the amount is reasonable for a dog this size (sometimes when the weight is falling off of them they panic and start really over-feeding the dog---which means we have to chase after them with an ever-increasing amount of insulin) how many calories/day does he currently get?

Re: Catch-22 Diabetes Mellitus 95-12-11 Hypurr Evan, A frustrating scenario. I would probably use injectable antibiotics for 3 weeks based on a culture ans sensitivity result. We teach our clients (if they are willing) how to give SC injections in this sort of scenario.....but I sure wouldn't choose ABx without a C&S at this point...given the frustration that both you *and* the client must be feeling around abut now! I think that your idea of an ultrasound or a bladder-kidney study (plain and contrast) are a great idea if you don't grow anything on the C&S. (Did you see bacteria &/ wbc in the sed?) Cheers! >M>

(did you see them on the sed?

How many calories/day does he get?

feline cushings 96-01-27 ShortERC I have a 16 yr old male neutered cat with signs very consistent with cushings. He has renal failure and concurrent early diabetes. His cholesterol is 410 and the blood sugar is about 260 at this point in time. I cannot convince the owner to test for this disease since all my reading shows that the best treatment for cushings in cats is bilateral adrenalectomy. Are there any medical solutions out there that will be safe for a cat with renal failure? If not does anyone know of a good way to manage this cats diabetes without treatment since it will be insulin resistant? Any help you can suggest would be greatly appreciated. This owner is really afraid to take any risks Thanks,ERC

Your correct that adrenalectomy cases treated at davis seemed to do slightly better than medical tx. have you ultrasounded the cat?

Are you able to asses serum ketones (specifically beta hydroxybutyrate, bhb)?

IMHA, Pancreatitis, Diabetic 96-01-26 A2JW 6yr. min.schn. w/ IMHA 7mo. duration, stable on Imuran and Pred. Presented today w. Acute pancreatitis and diabetic keotacidosis (DKA). Amylase >4000, Glu 550, lytes OK, slightly dehydrated very depressed. Began IV LRS, insulin, NPO, Glu 281. Patient very depressed still. U/A - glycosuria, ketonuria, WBC and RBC tntc. Finished 6 weeks of Baytril 2 wks ago for probable pylonephritis. Have not given Imuran or Pred today, plan to give injectable pred tommorrow. All help appreciated. I have so many questions I would just like to hear others thoughts. I have discussed referral w/ owner but they have developed a trust in me over the past 7 months. I am posting this on critical care board also. thanks,

What else?

What kind of insulin is she getting?

Lameness in young Lab 95-11-24 MCDVM Pet is 6 mth old female Lab; owner is intelligent & reliable; Pet walks with arched back & a 'tucked' under rear; will walk about 75 yards and must sit down; reluctant to move and prefers sitting;signs have been present for about 3 wks; seems better when housed inside near heat; today: very bad and could hardly walk; Observations at clinic weren't so dramatic, but pup does sit down instantly upon being still; Rads (lat and V/D of pelvic area)=Normal; What is going on here? Can you give me some Rule Outs?

Is proprioception normal in the hindlimbs?

How many calories/meal is he currently getting?

Lameness in young Lab 95-11-24 MCDVM Pet is 6 mth old female Lab; owner is intelligent & reliable; Pet walks with arched back & a 'tucked' under rear; will walk about 75 yards and must sit down; reluctant to move and prefers sitting;signs have been present for about 3 wks; seems better when housed inside near heat; today: very bad and could hardly walk; Observations at clinic weren't so dramatic, but pup does sit down instantly upon being still; Rads (lat and V/D of pelvic area)=Normal; What is going on here? Can you give me some Rule Outs?

Is there any back pain in the tl and lower lumber area (especially when pushing down on the ls juction)?

How was cheeto's diabetes managed?

Lameness in young Lab 95-11-24 MCDVM Pet is 6 mth old female Lab; owner is intelligent & reliable; Pet walks with arched back & a 'tucked' under rear; will walk about 75 yards and must sit down; reluctant to move and prefers sitting;signs have been present for about 3 wks; seems better when housed inside near heat; today: very bad and could hardly walk; Observations at clinic weren't so dramatic, but pup does sit down instantly upon being still; Rads (lat and V/D of pelvic area)=Normal; What is going on here? Can you give me some Rule Outs?

Is there any abdominal pain?

What should he weigh?

Lameness in young Lab 95-11-24 MCDVM Pet is 6 mth old female Lab; owner is intelligent & reliable; Pet walks with arched back & a 'tucked' under rear; will walk about 75 yards and must sit down; reluctant to move and prefers sitting;signs have been present for about 3 wks; seems better when housed inside near heat; today: very bad and could hardly walk; Observations at clinic weren't so dramatic, but pup does sit down instantly upon being still; Rads (lat and V/D of pelvic area)=Normal; What is going on here? Can you give me some Rule Outs?

Is the rectal exam normal?

Finally, how much does dee weigh and what is his bcs?

Lameness in young Lab 95-11-24 MCDVM Pet is 6 mth old female Lab; owner is intelligent & reliable; Pet walks with arched back & a 'tucked' under rear; will walk about 75 yards and must sit down; reluctant to move and prefers sitting;signs have been present for about 3 wks; seems better when housed inside near heat; today: very bad and could hardly walk; Observations at clinic weren't so dramatic, but pup does sit down instantly upon being still; Rads (lat and V/D of pelvic area)=Normal; What is going on here? Can you give me some Rule Outs?

Is there any hindlimb atrophy?

Is the same owner giving both the evening and morning injection, is he getting the same amount of food each time, etc.?

Bones cat 96-02-13 CatLover5 Help- we aren't sure what's going on with this cat and would like some input!! 'Gal' born 10/15/93 in TX, fs Siamese cross flame pt. wt 5.75 # (2/9/96)- history of rear limb weakness such that did not jump, but could climb stairs- became worse 10/28/94- diagnosis bilat. Luxating patellae- rads show hip dysplasia bilat (legs, bones 'a mess') with luxation, dysplastic fem. heads, sclerotic bone with no necks present, and proximal coccygeal vertebrea abnormal qwith decreased joint spaces. Sent to orthopedic surgeon and had bilat FHO 11/3/94. After 11/22/94, cat became painful and wiould not walk- surgeon suspected blood clot and cat has been paralysed since then. Owner was taught to express bladder, but cat has complications with UTI's and constipation (on Constilac 2cc BID and propulsis 2.5 mg BID). 12/29/95, cat became diabetic and now getting Humulin U 1 u sid. Rads at that time showed lysis and reactive bone in spinal column, reduced joint spaces in thoracic vertebrea, and malformed ribs. Blood workup- 12/29-Chol- 444 (n82-218), glu 395 (n60-130) ALP-327 (n0-62) ALT-1599 (n28-76) AST 616 (n12-40) TP 8.7 (n5.9-8.5) albu 4.9 (n2.4-4.1) K 5.7 (n3.7-5.2) Calcim 11.8 (n7.2-11.4) Phos 4.8 (n3-7.0) t bili 1.0 (n1-0.4) CBC- rbc- normal, WBC- monocytosis 12.3 % #1045 (n55-780), plates est. adequate. 1/30/96- PTH assay normal values (intact parathormone 1.0, ionizes calcium 1.22 from MSU lab). Cat is FELV neg, not FIV tested (oversight on our part). Can get more info if needed about past history. Any insight would be appreciated. Lori Coughlin, Jennifer Malin

Btw..what diet is this cat on now and what was she eating for most of her life?

Can you tell us the results?

Re: low S.G. 96-01-25 K9DOC Assuming the blood values are real, especially the CA and PO4, (and I would want to recheck them), it looks more like hypoPTH than hypoadrenal to me. I would expect Na to be lower with hypoadrenal. Chloride is low (has dog been vomiting?) but Na should be low too. K is higher than I would like but still, again doesn't jive with the Na value. I've included a reference for you below. Michigan State (Dr. Nachreiner's lab) can do the PTH assay for you. Call them Re: sample handling and sending.

Is it possible that the previous values were switched?

Is it m/d dry or wet or both?

Re: low S.G. 96-01-25 K9DOC Assuming the blood values are real, especially the CA and PO4, (and I would want to recheck them), it looks more like hypoPTH than hypoadrenal to me. I would expect Na to be lower with hypoadrenal. Chloride is low (has dog been vomiting?) but Na should be low too. K is higher than I would like but still, again doesn't jive with the Na value. I've included a reference for you below. Michigan State (Dr. Nachreiner's lab) can do the PTH assay for you. Call them Re: sample handling and sending.

Ie, ca was 20 and po4 was 5?

Was the dog checked on more frequently than every 2 hours?

Re: low S.G. 96-01-25 K9DOC Assuming the blood values are real, especially the CA and PO4, (and I would want to recheck them), it looks more like hypoPTH than hypoadrenal to me. I would expect Na to be lower with hypoadrenal. Chloride is low (has dog been vomiting?) but Na should be low too. K is higher than I would like but still, again doesn't jive with the Na value. I've included a reference for you below. Michigan State (Dr. Nachreiner's lab) can do the PTH assay for you. Call them Re: sample handling and sending.

Will the lab recheck values for you?

Is it the owner that's doing these bg curves?

Re: low S.G. 96-01-25 K9DOC Assuming the blood values are real, especially the CA and PO4, (and I would want to recheck them), it looks more like hypoPTH than hypoadrenal to me. I would expect Na to be lower with hypoadrenal. Chloride is low (has dog been vomiting?) but Na should be low too. K is higher than I would like but still, again doesn't jive with the Na value. I've included a reference for you below. Michigan State (Dr. Nachreiner's lab) can do the PTH assay for you. Call them Re: sample handling and sending.

On a new sample?

How many calories/day does he currently get?

Re: low S.G. 96-01-25 K9DOC Assuming the blood values are real, especially the CA and PO4, (and I would want to recheck them), it looks more like hypoPTH than hypoadrenal to me. I would expect Na to be lower with hypoadrenal. Chloride is low (has dog been vomiting?) but Na should be low too. K is higher than I would like but still, again doesn't jive with the Na value. I've included a reference for you below. Michigan State (Dr. Nachreiner's lab) can do the PTH assay for you. Call them Re: sample handling and sending.

Any possibility that they ran ca on the edta tube?

Has he been on any treatment for this?

Diabetic cat with fat tongue 96-05-13 DrNuke What would be the least disruptive steroid to give a diabetic cat (well controlled for 6 years on 4 to 6 units of insulin)? Gizmo has marked edema of the rostral tongue subsequent to radiotherapy/chemo for a lingual SCC. The tumor may be under control but fibrosis of the tongue may also be causing the edema. I would like to give steroids but which one and at what schedule. He weighs 16 lbs but now has a hard time eating. Any ideas? Thanks.

What's everybody else think?

What does the contralateral adrenal size look like?

Mil. derm. ideas? 96-04-01 MVYVET Formerly feral cat of unknown age, M/N with horrible miliary dermatitis. Flea free, derm caps and chlorpheneramine didn't help. Can't use corticosteroids or Ovaban as cat is probable toxo carrier and had an episode of transient diabetes. Owner's declined allergy testing/desensitization. History supports probable inhal allergy as cat cleared up during a three week visit to daughter's house. Any suggestions for further empirical treatment appreciated.

, how about permanently keeping the cat at the daughter's house?

Maybe pancreatitis?

Mil. derm. ideas? 96-04-01 MVYVET Formerly feral cat of unknown age, M/N with horrible miliary dermatitis. Flea free, derm caps and chlorpheneramine didn't help. Can't use corticosteroids or Ovaban as cat is probable toxo carrier and had an episode of transient diabetes. Owner's declined allergy testing/desensitization. History supports probable inhal allergy as cat cleared up during a three week visit to daughter's house. Any suggestions for further empirical treatment appreciated.

: ) seriously, if owners won't go for allergy testing and can't use steroids, then about only things left are trying an extended course of ibiotics (use a good skin ibiotic) or if can, try a food trial (will have to keep cat inside and remember that if this was a feral cat, probably won't be able to use rabbit and potato for novel diet.) how long did you have the cat on the dermcaps?

Were you able to do a biopsy at the time of the us examination?

Mil. derm. ideas? 96-04-01 MVYVET Formerly feral cat of unknown age, M/N with horrible miliary dermatitis. Flea free, derm caps and chlorpheneramine didn't help. Can't use corticosteroids or Ovaban as cat is probable toxo carrier and had an episode of transient diabetes. Owner's declined allergy testing/desensitization. History supports probable inhal allergy as cat cleared up during a three week visit to daughter's house. Any suggestions for further empirical treatment appreciated.

Biopsy?

Is the owner neither over- or under-shaking the insulin?

Malabsorbtion 96-01-16 Wet Vet 41 Just Dx a 75 lb 7 yr m/n yellow lab that has diabetes with malabsorbtion syndrome. Gave 35 cc corn oil and pulled hematocrit every hour - no fat in serum. then gave same corn oil with viokase - no fat in serum. We have had a very very difficult time regulating this dog. We have watched him go from 110 lbs to his present weight. Tested negative for cushings. Just switched from NPH to Humulin insulin (24 IU bid) with the most success so far with the regulation. Switched to D/D diet with some home cooked meal accordind to Kirk IV. what's the best course of action now. Any ideas on why it's so tough to regulate this guy? Is it related to the malabsorbtion? Thanks

Does the dog have gi signs?

All the stones are out?

Malabsorbtion 96-01-16 Wet Vet 41 Just Dx a 75 lb 7 yr m/n yellow lab that has diabetes with malabsorbtion syndrome. Gave 35 cc corn oil and pulled hematocrit every hour - no fat in serum. then gave same corn oil with viokase - no fat in serum. We have had a very very difficult time regulating this dog. We have watched him go from 110 lbs to his present weight. Tested negative for cushings. Just switched from NPH to Humulin insulin (24 IU bid) with the most success so far with the regulation. Switched to D/D diet with some home cooked meal accordind to Kirk IV. what's the best course of action now. Any ideas on why it's so tough to regulate this guy? Is it related to the malabsorbtion? Thanks

How long has dog been diabetic and how well-regulated is the diabetes (do you have a recent glucose curve, or glycosylated hemoglobin or fructosamine to assess degree of regulation)?

It doesn't look like he'd been on the nph until the day you did the curve?

IBD and DM in Feline 96-01-19

Could the cat have lymphoma?

Does he have a normal pitch to his bark?

Feline neuropathy 96-02-26 DrKAT17653 Here is a mystifying case I have also posted on the endocrinology board: Signalment: DSH M(c) estimated age: 7 yrs. History: had some weakness hind legs since adopted as stray 4 years ago. Examined and radiographed 10/94; some discomfort lumbar spine and hips, but no cause of signs found. Presented 9/95 for severe paresis (refused to walk for a few days also) and slight decrease in appetite. CBC and serum chemistries normal. Peripheral neuropathy or myopathy suspected, so trial therapy with prenisolone was initiated at 1mg/kg/day. Still no improvement 2 weeks later, so a series of spinal radiographs were done: no abnormalities. Referred to neurologist at end of November. No cause for problem identified; a repeat of CBC, chemscreen, and T4 tests recommended. This was done, and a blood sugar of 454mg/dl was discovered!. Cool! So, I weaned the cat off pred, rechecked the blood sugar (405 mg/dl) and started this cat on Humulin-U, did serial BG's until dose up to 9 units once daily. Cat seemed well regulated at that time (2/6/96). Returned on 2/20/96. Instead of improving, cat has become progressively weaker, is now down on hocks and carpi (markedly hyperflexed and extended, respectively) and can only move a few steps before sinking to the floor. Is painful when positioned for VD views of spine (this series of radiographs also no help), and BG is 65 mg/dl!! So, we have a generalized weakness. No electrolyte abnormalities, no response to cortisone therapy, no improvement with regulation of diabetes (which may have been initiated or exacerbated by the pred!!) CBC and chemistry done on 2/21 all within normal limits. HELP!!! This cat is really doing badly, owners are contemplating euthanasia, and we are all discouraged (except the neurologist - he's on vacation, so he doesn't know about it). Thanks much for any ssistance you may provide.

As i recall, doesn't pred cause joint and ligament laxity of its own accord as well?

Anything that i am missing?

Atarax Reaction? 96-06-04 MCDocRock I have a 6 month old Eng. Bulldog,F/intact that presented with pruritis(severe) and alopecia etc... This dog has been fairly itchy since 12 weeks old. The first treatment included Cephalexin,paramite dips, and Benadryl. She responded Ok and the Benadryl controlled the pruritis for awhile. (skin scrape and DTM were negative at this time.) There were also a few fleas at the time, so we addressed that as well. The dog relapsed and seemed to be worse and this time a skin scrape produced multiple life stages of demodex. DTM is still negative. We started Iams F&P diet,Primor(owner said vomited Cephalexin) 480mg sid,and Atarax 50mg 1-2 tablets bid/tid. The dog weighs 42 pounds. The dog was also dipped in mitaban. Dog did fine until about the 10th day on medication, the owner noticed the dog seemed sleepy-previously had been fine. On Sat-she presented with the dog who was totally gorked and had not given any medication for 24 hours. On exam, the dog was extremely sedated-could walk but would wobble, slightly dilated pupils,H/R of about 80, and tremors of the head and skin when aroused and while sleeping. CBC was WNL ,SMA was also WNL. Bile Acids= Pre=19.7 and Post 29.6. We put the dog on fluids and supported and she slept until about Tuesday. She improved a little each day but was not able to go home until then. All clinical signs have resolved now, but the pruritis has returned and I am not sure what I should do. It is time for another mitaban dip and she has been off all medication since the sleeping episode. She also is not eating the diet. Suggestions? The only up side of the sleeping episode was the that the skin improved because the pruritis was totally controlled along with most other voluntary functions.LOL. Thanks

Several questions: first, why was the dog treated with paramite dips in the beginning?

Are these digestive enzymes, as in the ones you would use for exocrine pancreatic insufficiency?

Atarax Reaction? 96-06-04 MCDocRock I have a 6 month old Eng. Bulldog,F/intact that presented with pruritis(severe) and alopecia etc... This dog has been fairly itchy since 12 weeks old. The first treatment included Cephalexin,paramite dips, and Benadryl. She responded Ok and the Benadryl controlled the pruritis for awhile. (skin scrape and DTM were negative at this time.) There were also a few fleas at the time, so we addressed that as well. The dog relapsed and seemed to be worse and this time a skin scrape produced multiple life stages of demodex. DTM is still negative. We started Iams F&P diet,Primor(owner said vomited Cephalexin) 480mg sid,and Atarax 50mg 1-2 tablets bid/tid. The dog weighs 42 pounds. The dog was also dipped in mitaban. Dog did fine until about the 10th day on medication, the owner noticed the dog seemed sleepy-previously had been fine. On Sat-she presented with the dog who was totally gorked and had not given any medication for 24 hours. On exam, the dog was extremely sedated-could walk but would wobble, slightly dilated pupils,H/R of about 80, and tremors of the head and skin when aroused and while sleeping. CBC was WNL ,SMA was also WNL. Bile Acids= Pre=19.7 and Post 29.6. We put the dog on fluids and supported and she slept until about Tuesday. She improved a little each day but was not able to go home until then. All clinical signs have resolved now, but the pruritis has returned and I am not sure what I should do. It is time for another mitaban dip and she has been off all medication since the sleeping episode. She also is not eating the diet. Suggestions? The only up side of the sleeping episode was the that the skin improved because the pruritis was totally controlled along with most other voluntary functions.LOL. Thanks

Did you see sarcoptes.or was this for fleas?

How are you giving the cobalamin?

Atarax Reaction? 96-06-04 MCDocRock I have a 6 month old Eng. Bulldog,F/intact that presented with pruritis(severe) and alopecia etc... This dog has been fairly itchy since 12 weeks old. The first treatment included Cephalexin,paramite dips, and Benadryl. She responded Ok and the Benadryl controlled the pruritis for awhile. (skin scrape and DTM were negative at this time.) There were also a few fleas at the time, so we addressed that as well. The dog relapsed and seemed to be worse and this time a skin scrape produced multiple life stages of demodex. DTM is still negative. We started Iams F&P diet,Primor(owner said vomited Cephalexin) 480mg sid,and Atarax 50mg 1-2 tablets bid/tid. The dog weighs 42 pounds. The dog was also dipped in mitaban. Dog did fine until about the 10th day on medication, the owner noticed the dog seemed sleepy-previously had been fine. On Sat-she presented with the dog who was totally gorked and had not given any medication for 24 hours. On exam, the dog was extremely sedated-could walk but would wobble, slightly dilated pupils,H/R of about 80, and tremors of the head and skin when aroused and while sleeping. CBC was WNL ,SMA was also WNL. Bile Acids= Pre=19.7 and Post 29.6. We put the dog on fluids and supported and she slept until about Tuesday. She improved a little each day but was not able to go home until then. All clinical signs have resolved now, but the pruritis has returned and I am not sure what I should do. It is time for another mitaban dip and she has been off all medication since the sleeping episode. She also is not eating the diet. Suggestions? The only up side of the sleeping episode was the that the skin improved because the pruritis was totally controlled along with most other voluntary functions.LOL. Thanks

Second,why was the dog on cephalexin?

Any elevation in cholesterol, lowish pcv?

Atarax Reaction? 96-06-04 MCDocRock I have a 6 month old Eng. Bulldog,F/intact that presented with pruritis(severe) and alopecia etc... This dog has been fairly itchy since 12 weeks old. The first treatment included Cephalexin,paramite dips, and Benadryl. She responded Ok and the Benadryl controlled the pruritis for awhile. (skin scrape and DTM were negative at this time.) There were also a few fleas at the time, so we addressed that as well. The dog relapsed and seemed to be worse and this time a skin scrape produced multiple life stages of demodex. DTM is still negative. We started Iams F&P diet,Primor(owner said vomited Cephalexin) 480mg sid,and Atarax 50mg 1-2 tablets bid/tid. The dog weighs 42 pounds. The dog was also dipped in mitaban. Dog did fine until about the 10th day on medication, the owner noticed the dog seemed sleepy-previously had been fine. On Sat-she presented with the dog who was totally gorked and had not given any medication for 24 hours. On exam, the dog was extremely sedated-could walk but would wobble, slightly dilated pupils,H/R of about 80, and tremors of the head and skin when aroused and while sleeping. CBC was WNL ,SMA was also WNL. Bile Acids= Pre=19.7 and Post 29.6. We put the dog on fluids and supported and she slept until about Tuesday. She improved a little each day but was not able to go home until then. All clinical signs have resolved now, but the pruritis has returned and I am not sure what I should do. It is time for another mitaban dip and she has been off all medication since the sleeping episode. She also is not eating the diet. Suggestions? The only up side of the sleeping episode was the that the skin improved because the pruritis was totally controlled along with most other voluntary functions.LOL. Thanks

Was there a pyoderma?

Is the alt higher than the sap?

Diabetes 96-09-20 A2JW 9/11/96 -- 9 1/2 yr, Fe/S, DSH, 6.9lbs....Hx-New patient recently moved from New York to Texas. Anorectic for 2 days, hiding under bed, Vomiting several episodes over last 3 days, lethargic, and not grooming. Water drinking and urination unknown Weight 11.0lbs 10/95 in New York. PE - T-101.2, significant clinical dehydration, small palpable kidneys. BUN 43.5 (14-36) GLU 252.1 (54-145) Na 147.2 (150-165) Cl 108.7 (112-129) WBC 19.1 (5.0-18.9) U/A - Glucose - 1000mg/dl Blood - 4+ All other lab values within normal limits including T4. Tenative Dx - Non-ketoacidotic Diabetes Mellitus, clinical dehydration Tx - IV fluids for rehydration, antibiotics, the following AM began Glucotrol XL(Glipizide) 5mg po 10:00am. At 4:00pm GLU 58 (54-145), BUN 14.9(14-36), Na 148.7 (150-165), K 4.03 (3.7-5.8), Cl 118.8 (112-129). Patient sent home with Glucotrol XL 5mg sid, antibiotics, unsweet metamucil added to diet. Weekly re-cks. Doing great, eating well. Vomited one time 9/18/96 pm. 9/19/96 GLU 61.2 (54-145). I am going to discontinue Glucotrol and continue weekly re-cks and GLU. Questions.. 1) Could this have been a stress hyperglycemia? 2) Other possible conditions that would cause these signs including weight loss with above lab values. Patient is doing well now and has regained 0.5 lbs in past week. Thanks for your thoughts, Wall

Presumed stress response?

Sounds plausible, any lumbar pain?

Diabetes 96-09-20 A2JW 9/11/96 -- 9 1/2 yr, Fe/S, DSH, 6.9lbs....Hx-New patient recently moved from New York to Texas. Anorectic for 2 days, hiding under bed, Vomiting several episodes over last 3 days, lethargic, and not grooming. Water drinking and urination unknown Weight 11.0lbs 10/95 in New York. PE - T-101.2, significant clinical dehydration, small palpable kidneys. BUN 43.5 (14-36) GLU 252.1 (54-145) Na 147.2 (150-165) Cl 108.7 (112-129) WBC 19.1 (5.0-18.9) U/A - Glucose - 1000mg/dl Blood - 4+ All other lab values within normal limits including T4. Tenative Dx - Non-ketoacidotic Diabetes Mellitus, clinical dehydration Tx - IV fluids for rehydration, antibiotics, the following AM began Glucotrol XL(Glipizide) 5mg po 10:00am. At 4:00pm GLU 58 (54-145), BUN 14.9(14-36), Na 148.7 (150-165), K 4.03 (3.7-5.8), Cl 118.8 (112-129). Patient sent home with Glucotrol XL 5mg sid, antibiotics, unsweet metamucil added to diet. Weekly re-cks. Doing great, eating well. Vomited one time 9/18/96 pm. 9/19/96 GLU 61.2 (54-145). I am going to discontinue Glucotrol and continue weekly re-cks and GLU. Questions.. 1) Could this have been a stress hyperglycemia? 2) Other possible conditions that would cause these signs including weight loss with above lab values. Patient is doing well now and has regained 0.5 lbs in past week. Thanks for your thoughts, Wall

Do you have a t4 on the cat?

Were the urine samples brought in in a container of the owner's?

Problem DM 96-02-12 J I am about to beat my head against the wall cannot get this damn dog to response to the insulin. he is acting real good still PU/PD, eating real well in clinic, This is what I have done so far consulted with Purdue and they suggested to switch to NPH. Which is what i did today: 26 gave 15units 9am 300, 10.30 172, 1.0 369, 4. 400; 2-7 10U 9am 363, 11. 377, 1, 370. 2-8 20U 9.283, 10. 345, 11. 357, 5. 370, 2-9 25U 9. 346, 1. 339, 4. 342, Send home for weekend No insulin Today NPH longer needle 35U 9. 339, 12, 333, 4. 316. He is receiving SID Insulin afraid to give BID will not be here to monitor if he goes hypo, I don't think Iam missing an underlying problem. Please help owner stated if counld not get regulated will Euth. Thanks

Did i understand your message correctly that the dog received no insulin over the weekend?

Is the dog currently clinical for this infection (and if not, was it at any point during the treatment course)?

Polyuria/polydipsia/Doby pup 96-02-23 C I am having a perplexing problem with a 6 month old Doby puppy. Puppy was bred by me and has been healthy to this point. Historically, the puppy had vomiting, fever, anorexia 10 days ago. Puppy was presented to regular vet. who treated with amoxicillin, also some delta albaplex for 3 days. Lab work at that time revealed mild azotemia and mildly elevated creatinine. Otherwise lab was supposed to be ok. (I didn't receive copies of lab unfortunately). 3 days later second lab revealed normal renal tests. Puppy improved clinically, but developed pronounced polyuria/polydipsia. Owner reported insatiable thirst, with puppy drinking 1-2 gallons a day, and would drink more if allowed. Urinations nearly uncontrollable according to owner, with dribbling, nocturia and extremely frequent voiding of large quantities of dilute urine. Puppy also demonstrated cyclic fever in the 103-104 range and muscle tremors, particularly in rear legs. P.E 2-21-96.: Wt 70 lb, good body condition, BAR. EENT-HL-ABD OK, temp on presentation 101. I encouraged my buyer to see our local internist. He took abdominal rads with the only abnormality an arguably small liver. He was suspicious of portocaval shunt, and advised owner to begin cottage cheese and green bean, etc. low protein diet, and lactulose. He advised owner to return for bile acid tests with me. I repeated CBC, chem screen, and drew pre and 2 hr post-prandial bile acids. I also collected cath'ed urine sample. Lab results: Normal CBC and Chem screen with exception of 272 alk. phos.(n=20-200) and 367 cholesterol. Bile acids pre and post prandial were 6umol/L (pre norm=0-10, post 0-15). U/A showed dilute urine (s.g.=1.007) clear, yellow, no wbcs, or significant. sediment. C/S pending. Serum osmolality is pending. I called owner tonight, visit was yesterday (2-22) and puppy is marginally better. My differential diagnoses include pyelonephritis, Diabetes indipidus (probably nephrogenic), renal medullary washout-post renal insult, pyschogenic polydipsia....Am I missing anything? Any suggestions? As this is one of my pups, I may not be the most objective person. I apologize for the length of this post.

Did the pu/pd develop after the delta-albaplex?

So she just got a new percorten injection last night?

Polyuria/polydipsia/Doby pup 96-02-23 C I am having a perplexing problem with a 6 month old Doby puppy. Puppy was bred by me and has been healthy to this point. Historically, the puppy had vomiting, fever, anorexia 10 days ago. Puppy was presented to regular vet. who treated with amoxicillin, also some delta albaplex for 3 days. Lab work at that time revealed mild azotemia and mildly elevated creatinine. Otherwise lab was supposed to be ok. (I didn't receive copies of lab unfortunately). 3 days later second lab revealed normal renal tests. Puppy improved clinically, but developed pronounced polyuria/polydipsia. Owner reported insatiable thirst, with puppy drinking 1-2 gallons a day, and would drink more if allowed. Urinations nearly uncontrollable according to owner, with dribbling, nocturia and extremely frequent voiding of large quantities of dilute urine. Puppy also demonstrated cyclic fever in the 103-104 range and muscle tremors, particularly in rear legs. P.E 2-21-96.: Wt 70 lb, good body condition, BAR. EENT-HL-ABD OK, temp on presentation 101. I encouraged my buyer to see our local internist. He took abdominal rads with the only abnormality an arguably small liver. He was suspicious of portocaval shunt, and advised owner to begin cottage cheese and green bean, etc. low protein diet, and lactulose. He advised owner to return for bile acid tests with me. I repeated CBC, chem screen, and drew pre and 2 hr post-prandial bile acids. I also collected cath'ed urine sample. Lab results: Normal CBC and Chem screen with exception of 272 alk. phos.(n=20-200) and 367 cholesterol. Bile acids pre and post prandial were 6umol/L (pre norm=0-10, post 0-15). U/A showed dilute urine (s.g.=1.007) clear, yellow, no wbcs, or significant. sediment. C/S pending. Serum osmolality is pending. I called owner tonight, visit was yesterday (2-22) and puppy is marginally better. My differential diagnoses include pyelonephritis, Diabetes indipidus (probably nephrogenic), renal medullary washout-post renal insult, pyschogenic polydipsia....Am I missing anything? Any suggestions? As this is one of my pups, I may not be the most objective person. I apologize for the length of this post.

Is the dog still on an ab?

You could try a short course and closely monitor the glucose?

Juvenile diabetes 96-03-14 DMcguffin1 16 week old G Shep F Presented for continued V/D after tx for parvo at another hosp.Dog was cachetic and had palp intuss. Hypoprotenemic(3 mg/dl),sl azotemic and hyperglcemic.Post sx and plasma transfusion dog was improved and ate w/o vomiting. Liver bx-compat w/ anorexia and stomach showed ulcerative gastritis(fibeglass insulation was poss. ingested too). Now dog has ketoacidotic DM. Any correlation to Multiple gi and hepatic probs or does this dog really have bad luck? p

Was the pancreas at all inflammed looking or involved in the intussusception area such that it might have been damaged during the surgery?

E.g. he truly got 0.01 mg/kg of dex iv?

Diabetic dog/rear limbs weak 96-04-05

How well regulated is the dog on bid nph?

How much should he weigh?

Diabetic dog/rear limbs weak 96-04-05

Is the dog just showing weakness, no pain to rear end or walking to suggest djd or lumbosacral dz?

How is the cat doing clinically?

Diabetic dog/rear limbs weak 96-04-05

Are there any neuro deficits (esp hopping, may be more sensitive to picking up subtle long track effects by loss of postural responses)?

What is this cat's specific gravity?

Liver,Diabetic Dog 96-06-05 PKVET 12 yr old schnauzer with diabetes on 5 units insulin bid. Has recently had several episodes of pu/pd but when insulin was checked at hospital had good control with levels between 100 and 220. We did a bile acids and his levels were 50 which our top levels are 20 (his sgpt was elevated at 256) we also did a acth stim because his al k phos has been at 500 (top is 160) and it fell within normal range would actigal be a good drug for him or should we look elsewhere he has also had a 2 lb wt loss thanks

How is his appetite?

It could also have become positive at 8 hours if she was very nervous while there at the clinic...was she?

Liver,Diabetic Dog 96-06-05 PKVET 12 yr old schnauzer with diabetes on 5 units insulin bid. Has recently had several episodes of pu/pd but when insulin was checked at hospital had good control with levels between 100 and 220. We did a bile acids and his levels were 50 which our top levels are 20 (his sgpt was elevated at 256) we also did a acth stim because his al k phos has been at 500 (top is 160) and it fell within normal range would actigal be a good drug for him or should we look elsewhere he has also had a 2 lb wt loss thanks

What diet is the dog receiving?

Did you have a catheter placed?

Liver,Diabetic Dog 96-06-05 PKVET 12 yr old schnauzer with diabetes on 5 units insulin bid. Has recently had several episodes of pu/pd but when insulin was checked at hospital had good control with levels between 100 and 220. We did a bile acids and his levels were 50 which our top levels are 20 (his sgpt was elevated at 256) we also did a acth stim because his al k phos has been at 500 (top is 160) and it fell within normal range would actigal be a good drug for him or should we look elsewhere he has also had a 2 lb wt loss thanks

Is it possible he's not getting enough calories?

How long since she's had a urine culture?

Immune-Anemia 96-06-20 VISIOUSVET 8 year old Yorkie male with history of being on 10 mg of Pred SID for 1 months. The client said her previous veterinarian had continued with this dose for allergeries when skin testing and other routes of control failed. Today the dog was presented with a severe anemia(PCV-13 and RBC of 2.5)., lethargic, but eating OK. Coombs Positive and blood glucose of 415. No loss of weight as of yet, but the UA did show 2+Ketones and 4+ Glucose. Liver and kidney enzymes along with rest of SMA-16 were normal. Where should I start with this patient? I do have a tick screen pending. Could the diabetes be related to an autoimmune problem too? The dog weighs 16 pounds and I tonight I gave 15 mg of prednisone, 15 mg of Imuran, and 250 mg of Tetracycline. Thanks for any help,

Is there any real evidence of hemolysis?

Any other abnormalities on lab work?

Diabetes on pred 96-02-13 M I am treating a 13 year old cat with prednisone for a confirmed (MRI) cerebral tumor. After one year she has started spilling sugar in the urine. Her BG was only 215. She is PU/PD. Her neuro signs are mostly controlled--circles sometimes. Should I treat her with insulin? I am worried about becoming hypoglycemic with just a slightly elevated BG. I forgot to mention that this cat had ketones in his urine. Thanks, MK

As far as the steroids do you think the cat would do all right on every other day steroids?

Should i wait to see if his glucose is going to creep higher?

Hypothyroid diabetic 96-02-21 DrJWV What is the relationship between thyroid hormone levels and insulin regulation. I have a diabetic lab who is giving me trouble in regulating its DM and her thyroid levels are very low. Do I get her thyroid regulated first or keep fussing with the DM? Thanks for the help. DrJWV

Is she insulin resistant?

Could you post the entire lab work including normal reference ranges for us?

Hypothyroid diabetic 96-02-21 DrJWV What is the relationship between thyroid hormone levels and insulin regulation. I have a diabetic lab who is giving me trouble in regulating its DM and her thyroid levels are very low. Do I get her thyroid regulated first or keep fussing with the DM? Thanks for the help. DrJWV

Is she on thyroid medication now?

What should he weigh?

OFA Thyroid Registry 96-03-19

4.) the diagnosis of 'true' hypothyroidism is not clear cut....there is a large grey area.....will we be giving prelimenary clearances to affected animals?......is hypothyriodism a disease even suitable for a registry based on giving clearances?

How much prednisone is he on?

OFA Thyroid Registry 96-03-19

How many breeders will send in info on their affected animals....will it be enough representation to reduce hypothyroidism?

Did she have adequate access to food and water at her original home?

Reflex hypergylcemia? 96-03-21 M I am treating a 7 year old Schnauzer (16 pounds) with 10 units of NPH Humulin insulin BID. The dog is generally doing well however I am concerned that reflex hyperglycemia is occuring. Two recent serial BG's have been performed. In January, the results weRe: 0-435 2 hours-139 4-63 8-376 10-347 In March: 0-428 2-88 4-54 6-160 8-255 10-228 The dog is not showing signs of hypoglycemia. Do you think that I should lower his insulin dramatically to see if he has reflex hyperglycemia or should I just leave things be since the patient has been doing well? Also, will fructosamine levels give me more information? Thank you. Mitch

, how is the dog doing in the hospital during these curves?

Did you test for microfilaria?

Reflex hypergylcemia? 96-03-21 M I am treating a 7 year old Schnauzer (16 pounds) with 10 units of NPH Humulin insulin BID. The dog is generally doing well however I am concerned that reflex hyperglycemia is occuring. Two recent serial BG's have been performed. In January, the results weRe: 0-435 2 hours-139 4-63 8-376 10-347 In March: 0-428 2-88 4-54 6-160 8-255 10-228 The dog is not showing signs of hypoglycemia. Do you think that I should lower his insulin dramatically to see if he has reflex hyperglycemia or should I just leave things be since the patient has been doing well? Also, will fructosamine levels give me more information? Thank you. Mitch

Is it eating similar amounts of food as it does at home?

What should she weigh?

Another Cushings Question!! 96-05-16 CATS6DR I have a question regarding steroid use and Cushings. I know that steroids will elevate the Alkaline Phosphatase and Urine Creatinine/Cortisol to give false readings, but how long after steroid withdrawl will it take for the Alk Phos to come back to normal levels? I have a dog that was on prednisone for allergies 2 months ago and hasn't had any since. Now however, he has an elevated Alk Phos (4 x normal) and slightly elevated ALT (2x) and I am wondering if I should be checking a UCC and looking in the direction of Cushings or if it is still the steroids interfering with the liver enzymes. Thanks Jan

Is the ucc test a more sensitive indicator of cushings?

What did the cbc look like?

Another Cushings Question!! 96-05-16 CATS6DR I have a question regarding steroid use and Cushings. I know that steroids will elevate the Alkaline Phosphatase and Urine Creatinine/Cortisol to give false readings, but how long after steroid withdrawl will it take for the Alk Phos to come back to normal levels? I have a dog that was on prednisone for allergies 2 months ago and hasn't had any since. Now however, he has an elevated Alk Phos (4 x normal) and slightly elevated ALT (2x) and I am wondering if I should be checking a UCC and looking in the direction of Cushings or if it is still the steroids interfering with the liver enzymes. Thanks Jan

Have you had any dogs get gastrointestinal side effects from this drug?

Do you know if anyone has ever looked for end-organ damage in this dog (usually evidence of hypertensive retinopathy)?

Diabetic Cat 96-06-04 GiraffeDVM I have a 8 year old intact male cat with diabetes. He has started chewing on the end of his tail. We have tried to get him to stop by getting his blood glucose under control. At this time his levels are good, but he still attacks his tail aggressively. We collared him to stop the licking of his tail and now he has started attacking his front feet and nails. I know that cats and people get a peripheral neuropathy that normally gets better once the blood glucose gets regulated. My husband's neuropathy seemed to get better with the addition of inostitol to his diet. Any ideas or suggests to help this cat.

Is the cat showing signs of pruritus or problems at the site of the insulin injections?

Or?

Diabetic neuropathy? 96-06-06 Thayv I have a diabetic case that seems to be a bit of a puzzler. This is an 11 year old MN DSH who has been on insulin for the past 5 months. The owner boarded him for a few days for a family emergency and asked that we examine him because he had not been steady on his feet. He had lost about 1 lb. since his last visit. On exam, he seemed 'down' in his hocks and unable to put full weight on his hindlegs. He looks just like other cases of diabetic neuropathy that I have seen. But whenever we do glucose curves on him, he seems very well controlled and in fact this time, his blood glucose was at 94, 12 hours after his last insulin injection. We had to decrease his treatments to once a day for now (though he does not like to eat well when he stays with us). The owner describes that he eats a lot and still has shown PU/PD at home before this visit, yet our checks do not show a need to increase insulin. I repeated lab work and had a T4 done and all was normal. I was thinking about testing his long term control with either glycolated Hg or fructosamine. Does this seem reasonable? I'm not sure what to think of this neuropathy appearance. It is hard to balance his history, exam, and test results. Thanks,

Is the k and cpk normal in this cat?

Has she had her urine cultured?

Diabetic neuropathy? 96-06-06 Thayv I have a diabetic case that seems to be a bit of a puzzler. This is an 11 year old MN DSH who has been on insulin for the past 5 months. The owner boarded him for a few days for a family emergency and asked that we examine him because he had not been steady on his feet. He had lost about 1 lb. since his last visit. On exam, he seemed 'down' in his hocks and unable to put full weight on his hindlegs. He looks just like other cases of diabetic neuropathy that I have seen. But whenever we do glucose curves on him, he seems very well controlled and in fact this time, his blood glucose was at 94, 12 hours after his last insulin injection. We had to decrease his treatments to once a day for now (though he does not like to eat well when he stays with us). The owner describes that he eats a lot and still has shown PU/PD at home before this visit, yet our checks do not show a need to increase insulin. I repeated lab work and had a T4 done and all was normal. I was thinking about testing his long term control with either glycolated Hg or fructosamine. Does this seem reasonable? I'm not sure what to think of this neuropathy appearance. It is hard to balance his history, exam, and test results. Thanks,

Any neuro deficits?

Why would the blood pressure go up after starting her medications?

Monocytosis With Neutropenia 96-05-26 Cwarn 6 yr old terrier spayed diabetic on insulin for 2 yrs. Now acutely sick persistent fever 104, glucose level ok, 3000wbc 80%monocytes, 8% neuts. Neutropenia with compensatory monocytosis? Is this a myeloproliferative disease? No response to ABs.

What ab's was the dog on?

She's not on a raw diet?

Monocytosis With Neutropenia 96-05-26 Cwarn 6 yr old terrier spayed diabetic on insulin for 2 yrs. Now acutely sick persistent fever 104, glucose level ok, 3000wbc 80%monocytes, 8% neuts. Neutropenia with compensatory monocytosis? Is this a myeloproliferative disease? No response to ABs.

Any problems on the ua?

How many calories/meal does he currently get?

Normal K,But Signs Of HypoK 97-02-15 WarmVet 12 y/o cat seen for recent weakness which is episodic. Hx of intermittant vomiting and cow pie stool. Borderline renal function which has been managed with home cooked low-protien diet for ~2yrs. Also has had a Hx of ileus in the past, worse last month. Since themn cat has deteriorated. Was thoroughly worked up before I saw the case with normal cbc, K+4.95 (3.5-5.8) hypernatremia 167.5 (150-165), megacolon on radiographs,norm spine and thorax, isosthenuric usg and neg sediment.Blood lead and cholinesterase activity normal. On P.E. cat is very weak with cp deficits all 4 limbs, norm reflexes, and deep pain. not painful anywhere. Ate well this am per owner.. good femoral pulses present, mild distended abdomen, remainder of pe wnl. QUESTIONS? If serum K+ doesn't necc reflect intracellular K+ levels and with the Hx of mild borderline kidney dz, would it be prudent to start K+ supp? Was planning on sending out another profile to a diff ref lab but our lab work doesn't go out til monday! If this cat had a norm K+ could I make it worse by suppl at 4meq/day (8#cat) Is there another more reliable indicator of the true K+rather than serum? Also If I started thiamine supp would oral suppl be effective? would it destry any hopes of a dx if started now? Would really appreciate any help with this kitty case. Thanks much

Have you thought about ibd?

U40 syringes?

Normal K,But Signs Of HypoK 97-02-15 WarmVet 12 y/o cat seen for recent weakness which is episodic. Hx of intermittant vomiting and cow pie stool. Borderline renal function which has been managed with home cooked low-protien diet for ~2yrs. Also has had a Hx of ileus in the past, worse last month. Since themn cat has deteriorated. Was thoroughly worked up before I saw the case with normal cbc, K+4.95 (3.5-5.8) hypernatremia 167.5 (150-165), megacolon on radiographs,norm spine and thorax, isosthenuric usg and neg sediment.Blood lead and cholinesterase activity normal. On P.E. cat is very weak with cp deficits all 4 limbs, norm reflexes, and deep pain. not painful anywhere. Ate well this am per owner.. good femoral pulses present, mild distended abdomen, remainder of pe wnl. QUESTIONS? If serum K+ doesn't necc reflect intracellular K+ levels and with the Hx of mild borderline kidney dz, would it be prudent to start K+ supp? Was planning on sending out another profile to a diff ref lab but our lab work doesn't go out til monday! If this cat had a norm K+ could I make it worse by suppl at 4meq/day (8#cat) Is there another more reliable indicator of the true K+rather than serum? Also If I started thiamine supp would oral suppl be effective? would it destry any hopes of a dx if started now? Would really appreciate any help with this kitty case. Thanks much

Questions?

Do the owners always give the insulin so late in the morning?

Cushing's Cat? 97-02-13 RNIXON4824 Hi everyone. Have a 14 year old female intact dsh presents with thin, broken haircoat and thin translucent skin. Multiple areas of alopecia over body. Has been like this for quite some time(4-96) first noted in chart. Skin biopsy revealed 'follicular atrophy, mild to moderate with mild dermal and adnexal atrophy 'with the comment that this is suggestive of an endocrine dermatosis. #1 ddx Cushings. Cat is Felv/Fiv negative,t4, free t4 normal, all else ok on cbc,chem and ua except for persistently high liver values ALKP 171 (1-40) ALT 373 (10-100) AST 141 (10-100). Gluc-190 (Liver values about the same in April). Ran two Acth responses. First using standard Acth gel at 2.2 u/kg im . Results: Pre-3.6 1hr-2.2 2hr-1.4 YIKES? Re ran with Cortrosyn-fasted overnight .125mg iv pre-2.4 30 min.- 9.5 60 min.- 9.6 90 min-10.3 Feline normal response is 4.5-15 for lab. Where do we go from here? Thanks in advance for your help. Donna (Doug's associate)

What about sex hormone responsive dermatoses?

Have you done radiographs recently to be sure there isn't right middle lung lobe collapse?

Re: Glycosuria 97-01-20

Anyone else familiar with this?

Have you measured fasted cholesterol and triglycerides in this dog?

Pu/Pd Case 97-01-03 GRIZDVM I have been working on a perplexing case and need some help. There is a lot of stuff here so I will try to stick to the relevant details. 12/26 10 year old spayed female mixed breed dog presented for pu/pd. also decreased appetite. lethargic. pe-alert. good condition. hydration wnl. no significant physical findings. labwork-urine specific gravity of 1.002. pcv 53.7 normal wbc albumin 2.3 (2.5-4.4) calcium 8.3 (9.1-12.4) chloride 94 (107-121) sodium 131 (140-155) potassium normal bun and creatinine normal total protein 5.5 (5.4-8.1) considered renal/hepatic/adrenal disease/diabetes insipidus. plan was to have owner return dog for a few random urine samples to see if the specific gravity became fixed. 12/30 dog returned-now ill. more lethargic; vomited twice. exam-dehydrated. pcv-60% urine specific gravity 1.005 sodium decreased to 106. potassium 5.8 glucose 142 calcium 7.6 bun and creatinine normal. because of the low sodium was concerned about a hypoadrenal crisis but the increased blood glucose did not make sense. preformed an ACTH stim. started on 0.9% nacl. treated with dexamethasone after the ACTH stim. treated at emergency clinic over the weekend;; they said the dog perked up each time it was given dex/pred (we were tapering the dose). ACTH stim showed HYPERadrenal (post ACTH cortisol 28.3) dog does not look hyperadrenal clinically and the sap is normal. continued on fluids; dog started eating but still lethargic and somewhat weak. started diarrhea which has improved with bland diet. 1/2/97 clinical picture-hydration normal and good appetite but weak. pcv 35% albumin 2.1 calcium 7.2 sodium 142 potassium 3.4 This dog really looked hypoadrenal on 12/30. I am confused as to what else would cause the sodium to drop that low. Could whatever is causing the low albumin be the primary problem? I would appreciate any help with this case! Thanks!

Do these tumors commonly cause multiple endocrine abnormalities?

Can you also show this video to your client?

Pu/Pd Case 97-01-03 GRIZDVM I have been working on a perplexing case and need some help. There is a lot of stuff here so I will try to stick to the relevant details. 12/26 10 year old spayed female mixed breed dog presented for pu/pd. also decreased appetite. lethargic. pe-alert. good condition. hydration wnl. no significant physical findings. labwork-urine specific gravity of 1.002. pcv 53.7 normal wbc albumin 2.3 (2.5-4.4) calcium 8.3 (9.1-12.4) chloride 94 (107-121) sodium 131 (140-155) potassium normal bun and creatinine normal total protein 5.5 (5.4-8.1) considered renal/hepatic/adrenal disease/diabetes insipidus. plan was to have owner return dog for a few random urine samples to see if the specific gravity became fixed. 12/30 dog returned-now ill. more lethargic; vomited twice. exam-dehydrated. pcv-60% urine specific gravity 1.005 sodium decreased to 106. potassium 5.8 glucose 142 calcium 7.6 bun and creatinine normal. because of the low sodium was concerned about a hypoadrenal crisis but the increased blood glucose did not make sense. preformed an ACTH stim. started on 0.9% nacl. treated with dexamethasone after the ACTH stim. treated at emergency clinic over the weekend;; they said the dog perked up each time it was given dex/pred (we were tapering the dose). ACTH stim showed HYPERadrenal (post ACTH cortisol 28.3) dog does not look hyperadrenal clinically and the sap is normal. continued on fluids; dog started eating but still lethargic and somewhat weak. started diarrhea which has improved with bland diet. 1/2/97 clinical picture-hydration normal and good appetite but weak. pcv 35% albumin 2.1 calcium 7.2 sodium 142 potassium 3.4 This dog really looked hypoadrenal on 12/30. I am confused as to what else would cause the sodium to drop that low. Could whatever is causing the low albumin be the primary problem? I would appreciate any help with this case! Thanks!

Or can her problems be explained exclusively by acth deficiency?

What was the phosphorous level?

Atypical Mycobacteriosis? 97-01-16 ENDONUT I have a 10 year old MN DSH with inguinal weeping ulcerative skin lesions of 1 month duration. These lesions tend to wax and wane and can be extremely exudative. A biopsy and acid fast staining has shown pyogranulomatous dermatitis with no acid fast organisms seen. A routine culture yielded heavy growth of enterobacter cloacae and was not cultured due to expense for mycobacterium. The cat has had recently become diabetic during the course of these lesions and is being managed on 3 units of Ultralente BID. Currently the cat has been on enrofloxacin at 2.5 mg/kg TID for 2 weeks with no response. Given the clinical picture and biopsy results, I feel atypical mycobacterial infection is most likely. I have since change the dose to 5 mg/kg BID of the enrofloxacin and added doxycycline at 5 mg/kg BID. 1. Do you agree with this assessment? 2. If so, what do you feel works best therapeutically? 3. If there will be a response, when should we expect one? This lesion appears too extensive to be surgically removed. Thanks for your input. p DACVIM, Melbourne, FL

Did they do special stains?

Any other issues that might cause insulin resistance?

Re: fatty liver/pancreatitis 97-02-17 K9DOC Dave: Oh dear... sounds like the proverbial rock and the hard place. :( Ideally, it would be best to have a jejunostomy tube in this cat thus bypassing the stomach and duodenum altogether. Failing in that, we do need to address the lipidosis so I'd recommend feeding, by tube if necessary. Use a low fat diet to avoid as much pancreatic stimulation as possible. Modest protein now for the same reason... if all goes well you can increase the protein content to assist in mobilizing the fat from the liver. I'd have to give a guarded prognosis for this cat given these two concurrent (and conflicting) problems.

Gondii?

Do you have a full recent curve (bg q 2hrs over 12 hours)?

Feline Semi-plantegrade Walk 97-02-26 R I was presented with a 15 yrold F/S cat. The owners contend the cat has had a abnormal gait most of its life- very similar to a cow's sickled-hock. I radiographed the cat and found: 1. mild hip dysplasia, 2. narrowed disc space at L 6-7, and suspect lumbo-sacral degenerative stenosis. Has anyone seen LSDS in a cat and what were your treatments. The owner will definitely decline surgery as an option. The cat blood picture and urine ruled out diabetes mellitus. Thanks

Anyone else have some ideas?

;) has he just had this one set of bloodwork done since his initial presentation for inappetance?

Figuring protein/carbo req. 97-02-06 TULSADVM This may be a stupid question but here goes...Is there a current method as in humans where you can take an individual animal and figure there lean body mass/body fat percentage in order to figure their protein/carbohydrate/fat needs so you could make a homemade diet? I don't have any nutrition texts as yet. Thanks, Kerry Jones, DVM

Does this get to your point?

Any idea which one?

Stimulating cat appetite 97-03-03 FTAnHosp Any suggestions/tricks as to how to get old cats with diagnosed problems to eat?

What is your particular situation?

The owner is neither over- nor under-shaking the insulin (we scare them so much sometimes about not over-shaking it that they fail to reconstitute it well and inject diluent); well, since vetsulin came back on the market, the new label requires us to vigorously shake it the first time the bottle is opened, then it should be shaken each time the bottle is used, to keep it looking continuously milky...is this being done?

PUPD epileptic dog 97-02-11 SAHDVM Daisy is a 6 year old epileptic FS Dalmation on phenobarbitol. She is very PUPD, her water consumption was 140 ml/kg/day and her urine specific gravity was 1.000. Her labwork showed an alk phos of 256, We did a modified water deprivation test where she concentrated to a specific gravity of 1.028 after about 30 hours and an 8% body weight loss. Her final urine osmolality was 858 and serum osmolality was 302. I interpreted this as psychogenic diabetes inspidus and recommended tapering water consumption SLOWLY down to what would be about 80 ml/kg/day-she has been receving this much water for a couple of weeks. I think the owners have been good about complying but she is still hyposthenuric-1.000. Any ideas on where to proceed? Ts, Marti

How long and what dose of phenobarb has the dog been on?

Do you think this owner would be amenable to home glucose monitoring?

PUPD epileptic dog 97-02-11 SAHDVM Daisy is a 6 year old epileptic FS Dalmation on phenobarbitol. She is very PUPD, her water consumption was 140 ml/kg/day and her urine specific gravity was 1.000. Her labwork showed an alk phos of 256, We did a modified water deprivation test where she concentrated to a specific gravity of 1.028 after about 30 hours and an 8% body weight loss. Her final urine osmolality was 858 and serum osmolality was 302. I interpreted this as psychogenic diabetes inspidus and recommended tapering water consumption SLOWLY down to what would be about 80 ml/kg/day-she has been receving this much water for a couple of weeks. I think the owners have been good about complying but she is still hyposthenuric-1.000. Any ideas on where to proceed? Ts, Marti

Any recent phenobarb blood levels?

Can anybody help me on this one?

Re: Weird musc. addendum 97-02-10 Toxoplasma John- This sounds like a real tough case! I am unsure what to make of the ulcerated tongue also. The response to steroids makes me worry about neoplastic or inflammatory diseases of the CNS. Any retinal changes? It may be worth a CSF tap with follow up toxo titers on serum and CSF collected at the same time. What type of toxo test was it? If you do a CSF tap, a biopsy of the tongue might provide some additional info. Let us know what you find,

Any help?

Do you think the owner can feed just canned hypoallergenic diet?

Insulin Selection 97-02-13 HPuck My client wishes to change Insulin and has run out of BP ultralente insulin. The dog weighs 17lb and is presently taking 20u UID. She refuses to bring the dog in for a curve @ this time. Choices Humulin u/l, B/Pork Lente, or Pure Pork Lente. She will not give more than UID. Recent profile showed all else OK. Our feeling is the U/L insulin but I was not aware that Lilly made an all Pork Insulin.

Now what dose to use?

Is the owner feeding the cat an infinite amount of food rather than a defined amount that is appropriate for the cat's weight?

Insulin Selection 97-02-13 HPuck My client wishes to change Insulin and has run out of BP ultralente insulin. The dog weighs 17lb and is presently taking 20u UID. She refuses to bring the dog in for a curve @ this time. Choices Humulin u/l, B/Pork Lente, or Pure Pork Lente. She will not give more than UID. Recent profile showed all else OK. Our feeling is the U/L insulin but I was not aware that Lilly made an all Pork Insulin.

What were the results of the last curve and what dose of insulin was the dog on at that time?

Was anemia characterized as regenerative or non-?

Insulin Resistance? 97-02-21 FourDocs How long would it take after an OHE for progesterone and estrogens' effect on mammary gland tissue to subside? The reason for the question is that I have an 8 yr. old Sheperd (in heat 4 weeks ago) that seems to be insulin resistant. The ovaries both grossly looked active when I spayed the dog the other day. I heard Dr. Peterson speak at a seminar and he said he always spays any intact female diabetic ASAP due to a proposed growth hormone related peripherial insulin resistance that is occasionally seen in some dogs. I have no idea how common this is or if it is having ANY effect in THIS dog but, if it were true, I was wondering how long I might expect for the repro. hormones to decrease to a level where they would not be having any affect on the mammary tissue( which I understand is the most likely source of the growth hormone like substance). Mike

Is this a recently diagnosed diabetic?

Does this seem logical?

Insulin Resistance? 97-02-21 FourDocs How long would it take after an OHE for progesterone and estrogens' effect on mammary gland tissue to subside? The reason for the question is that I have an 8 yr. old Sheperd (in heat 4 weeks ago) that seems to be insulin resistant. The ovaries both grossly looked active when I spayed the dog the other day. I heard Dr. Peterson speak at a seminar and he said he always spays any intact female diabetic ASAP due to a proposed growth hormone related peripherial insulin resistance that is occasionally seen in some dogs. I have no idea how common this is or if it is having ANY effect in THIS dog but, if it were true, I was wondering how long I might expect for the repro. hormones to decrease to a level where they would not be having any affect on the mammary tissue( which I understand is the most likely source of the growth hormone like substance). Mike

What dosage of insulin is it receiving?

Surgery still not an option?

Lab With Cushing's/DM? 97-03-03 Jebbie1 was just presented with an 8 yo intact male lab. ADR. Cortrosyn test very suggestive of cushing's and the bg is >400mg/dl. I am initiating lysodren induction with pred supplementation. I am letting the possible diabetes go for now until I have a chance to get a response to the lysodren. I plan on rechecking the bg 4 days into induction to see if I should use insulin to make the patient feel better until the dust settles. Have I missed anything or is there any suggestions on how to improve my approach in this case. Do you suggest using pred during induction? Are you afraid as I am that aggressive pursuit of the hyperglycemia with insulin during the induction could result in a severe hypoglycemic episode? this patient is being tx'd on an outpatient basis.

Why do you suspect cushing's in this patient?

The owner is able to reconstitute the insulin well each time?

Diabetes and Domitor? 99-05-20 I was wondering if domitor (in combo with ket and torb) is safe to use to sedate a regulated diabetic cat for a dental prophy. My thought is that since you can reverse it, you can get them up and eating a bit sooner than using other anesthetics that I have. Any thoughts/suggestions would be appreciated. Thanks.

Re:diabetes and domitor?

At 1 1/2 years of age or at 9 months of age?

Diabetes and Domitor? 99-05-20 I was wondering if domitor (in combo with ket and torb) is safe to use to sedate a regulated diabetic cat for a dental prophy. My thought is that since you can reverse it, you can get them up and eating a bit sooner than using other anesthetics that I have. Any thoughts/suggestions would be appreciated. Thanks.

What sort of protocol and management did you have in mind for him?

Have bile acids been performed?

Ketoacidosis or Ketosis 97-03-23 Mtbooker We have had a few DKA type emergencies lately and I have what I feel like is a stupid question but--if you don't have access to blood gas measurements, HCO3 etc. is there a good way to spot the acidosis in a patient that is hyperglycemic and ketotic? I know there is a depression in sodium with acidosis--anything else? Enlightenment appreciated.

Why did you ask the question?

Thoughts on testing for addison's?

Diabetic cat w/diarrhea 97-03-16 DrKAT17653 Shablee is an 11 year old M(c) DSH who has had a sensitive bowel since kittenhood. He first made our acquaintance in 1993, and was on Viokase at that time (I have no clue how or if he was actually diagnosed with EPI). Became diabetic in March of '96 after dexamethasone treatment for back injury (Dx'd and Tx'd elsewhere); also, at this time, owner discontinued Viokase (I don't know why). After cat presented to me, I thought we should give it a couple of weeks to see if hyperglycemia was CCS induced. 6 weeks after conclusion of CCS Tx, hyperglycemia persists, we started on glucotrol - poor response - put on ultralente, 3u qd. After 2 months, stabilized at 11 to 14 units qd. (cat weighed 7kg). GI problem started in 11/96 when cat treated for lethargy, anorexia and fever with doxycycline 100mg qd; probiocin dispensed at same time to try to mitigate GI flora problems. Cat developed colitis anyway. tried Tylan powder, owner resumed Viokase, bowel problem went away. Cat had severe hypoglycemic episode (29 mg/dl 10 hours post-insulin inj!) in 12/96. Took off insulin for a couple of weeks before sugar started to rise again. Started back at 5u; now seems stable at 7u BID (still on ultralente - think we may have been doing a Somogyi thing at high doses SID). BUT, cat has had persistent diarrhea. We have tried metronidazole 125mg bidx7, centrine 1/2 bidx3..and any number of foods. Centrine slows cat down from 4 to 2 episodes runny stools per day, otherwise no help. We sent TLI/cobalamin/folate test to Dave Williams @ Purdue.... TLI 42 (17-49) cobalamin 150 (200-1680) folate 16.9 (13.4-38) Test interpretation: low cobalamin consistent with EPI, SIBO or 'disease affecting the distal small intestine' We have been giving this cat weekly vitamin B12 injections since the beginning of February, have repeated metronidazole for 2 weeks, and we have tried centrine out of desperation, but all to no avail. Cat is still on viokase (tablets) and owner is putting Tylan in capsules to get it on board (cat will not eat food if Tylan in or on it). Cat's current diet = 1/8 can Eukanuba LB bid, Science Diet lite + WD ad lib. Owner states she is using older batches of Science diet lite, as newer formulation has more copper sulfate (?). Cat will not eat CNM-EN, diarrhea worsened when on CNM-OM. Prefers dry food. We suspect this cat has IBD (no bowel trouble at all while on CCS), and would put it on theraputic trial of pred in a heartbeat if it were not diabetic. Any alternative therapies for IBD in cats? We are all getting a bit frustrated. I love kitties! ;-)

Have you tried hills wd?

Did you culture the urine?

Ulcer/Pain/Complications 97-03-29 MLPVETDIVE I have a complicated case due to several medical problems & an owner that is unable to have surgery performed. This is a 13 yr old male neutered American Eskimo who is diabetic, hypothyroid, atopic, borderline Cushing (Consistent high ALP but ACTH & dexamethason tests are negative for this), and is blind due to mature cataracts from the diabetes. Also has arthritis in both stifles. He is on insuling, soloxine, pred at lowest dose possible to control itching(only choice we have-owner can't do allergy testing, antihistamines don't work, & it is not a food allergy). And then most recently has been diagnosed with early kidney disease(creat=2.0 with normal being 1.3). S.G was 1.031 but there was glucose in the urine. Well the presenting problem is a non-healing corneal ulcer on right eye for 6 weeks. I know the diabetes & pred are all complicating the healing but I have no other choice. I also know that surgical debridement is the way to help heal this but this is not an option for this client. Is currently on Optimmune, adequan in artifical tears, atropine, & chloramphenicol ophto. Have also tried gentocin ophto. and every time he is in we try to debride the ulcer with a swab. Nothing has worked. The ulcer is not getting worse either. The dog is in a lot of pain from the eye. The owner is wanting to know if we can use anything else for pain? Any advise on this case? I also wanted to know if carprophen who help with its better analgesic effects. I know that one must be careful with NSAIDS with renal disease but which is the lesser of 2 evils. Hard for me to answer. Also about 3 years ago we had an ulcer occur and it took about 3-4 months of treatment and it did heal.

If you don't feel comfortable doing the procedure on a standing animal, is there an ophthalmologist to whom you can refer this patient?

Does the dog look cushingoid to you?

Changing Insulin 97-03-06 LondonDVM A cat who has been 'poorly regulated' on and off on NPH 7.5 units bid has come to me in a near diabetic coma, no ketones, BUN high, creat normal, high glucose. After 11 injections of Regular insulin hourly, the glucose has been normal all day...cat BAR and happy. I am not feeding him as I suspect he has pancreatitis, is on dextrose/half strength saline and ampicillin. He also has gingivitis...when his glucose climbs again, is it better to : 1. Continue the insulin he was on? Along with the antibiotics? 2. Change to 30% Regular 70% NPH mixture? And would it be a lower dose, and would I dilute it with saline or 'proper'diluent...and is there any big difference between Novolin and Humilin? 3. He also has hyperlipidemia, and is very thin...would medical Weight control or w/d be a poor food choice...I want calories but low fat. Right now he eatsPerformatirin (I think this is just in Pet Value in Ontario). Any comments? He is going home orrow assuming things continue to improve. Thanks, Kristina

What were numbers for bun and cr?

Ldds?

Changing Insulin 97-03-06 LondonDVM A cat who has been 'poorly regulated' on and off on NPH 7.5 units bid has come to me in a near diabetic coma, no ketones, BUN high, creat normal, high glucose. After 11 injections of Regular insulin hourly, the glucose has been normal all day...cat BAR and happy. I am not feeding him as I suspect he has pancreatitis, is on dextrose/half strength saline and ampicillin. He also has gingivitis...when his glucose climbs again, is it better to : 1. Continue the insulin he was on? Along with the antibiotics? 2. Change to 30% Regular 70% NPH mixture? And would it be a lower dose, and would I dilute it with saline or 'proper'diluent...and is there any big difference between Novolin and Humilin? 3. He also has hyperlipidemia, and is very thin...would medical Weight control or w/d be a poor food choice...I want calories but low fat. Right now he eatsPerformatirin (I think this is just in Pet Value in Ontario). Any comments? He is going home orrow assuming things continue to improve. Thanks, Kristina

Has the bun returned to normal after being on fluids?

Was there an active urine sediment too?

Changing Insulin 97-03-06 LondonDVM A cat who has been 'poorly regulated' on and off on NPH 7.5 units bid has come to me in a near diabetic coma, no ketones, BUN high, creat normal, high glucose. After 11 injections of Regular insulin hourly, the glucose has been normal all day...cat BAR and happy. I am not feeding him as I suspect he has pancreatitis, is on dextrose/half strength saline and ampicillin. He also has gingivitis...when his glucose climbs again, is it better to : 1. Continue the insulin he was on? Along with the antibiotics? 2. Change to 30% Regular 70% NPH mixture? And would it be a lower dose, and would I dilute it with saline or 'proper'diluent...and is there any big difference between Novolin and Humilin? 3. He also has hyperlipidemia, and is very thin...would medical Weight control or w/d be a poor food choice...I want calories but low fat. Right now he eatsPerformatirin (I think this is just in Pet Value in Ontario). Any comments? He is going home orrow assuming things continue to improve. Thanks, Kristina

What are the current clinical signs?

Have they done parr (lymphoma pcr) also?

Re: Insulin choice 97-03-27 Hypurr Patsy, Your duration of effect of the NPH is at least 11 hours from what you have posted, meaning that her glucose level didn't get back to its original 361 after 12 hours....I think that sticking with the NPH is a safe bet here. Generally I ask the client's to increase the dose to 4 units BID for one week, record the water intake, urine output, food consumption, activity level and any other comments BID, we call tham after a week and I may adjust the dose again based on what the client reports and how comfortable I am with their attentiveness. BG curves every 10-14 days, as a general rule, are adequate. Good luck! Cheers! >M>

Does that make sense?

What site does the owner use for bg collection?

Anorectic Diabetic Cat 97-04-17 HEATHVET I have been treating CJ (10yo MN DSH) for about 1+ years. He has been diabetic for about 4 years. He initially regulated well but has had episodes of GI distress- seems painful in abdomen after he eats off and on. Owner reports this has gone on for years. The cat has been as high as 7 un Humulin U SID in the past but was at 2 units when I started seeing him.We have done Chem screens and Acth stim and amylase lipase looking for a reason for this cats anorexia (all WNL). He is bright and alert, vomiting has not been a problem. Films of the abodomen not revealing. I gave him some barium about 2 weeks ago and thought the barium spent a little too much time in the small intestine but no dilated loops or obvious obstuctive pattern. Stools are firm and much larger than I would expect for no more than he is eating. I have had the cat at my house for about a week because the owner doesn't know what to do about the insulin. He is on about 1 1/2 un Humulin U now. I have checked him daily for the last 5 days. He will be 350 to 400 8am about 150 whenI have checked at noon (not every day) and between 85 and 95 at 4pm. I haven't checked later than that. He eats some turkey and tuna and juice off canned chicked but not much else. My feeling is that there is something else going on in this cats gut. I ultrasounded him several times this week and feel that the douodenum is wider than normal but am not absolutely sure what I am seeing. A human US tech came over and confirmed its not lymph node and it looked like something in the lumen of the gut to her. I have mentioned biopsy to the owner but they are reluctant to do surgery. Would this cat be better regulated if insulin was divided BID and could the wide swings contribute to anorexia.THe cat has lost about 2 pounds since the first of the year. Hes at about 10.4 now. I hope this isn't too vague of a HX. Both the owner and the cat are about to give me fits so I appreciate any input that anyone has. Thanks.

Is this mass purely luminal and not infiltrating and disrupting the gi layers?

Is her weight stable?

Re: When should I be happy? 97-04-26 ENDONUT Irv, I would ignore specific gravities and go off of clinical signs. How did you work the dog up for PU/PD? This central DI is most likely acquired. Any history of head trauma or neurologic deficits? p

Have you tried discontinuing the ddavp and seeing if water consumption picks up again?

Ua- neg glu but trace ketones?

Diabetic Cat w/Diarrhea 97-03-16 DrKAT17653 I am going to try to post this in both GI and Endocrine boards......Shablee is an 11 year old M(c) DSH who has had a sensitive bowel since kittenhood. He first made our acquaintance in 1993, and was on Viokase at that time (I have no clue how or if he was actually diagnosed with EPI). Became diabetic in March of '96 after dexamethasone treatment for back injury (Dx'd and Tx'd elsewhere); also, at this time, owner discontinued Viokase (I don't know why). After cat presented to me, I thought we should give it a couple of weeks to see if hyperglycemia was CCS induced. 6 weeks after conclusion of CCS Tx, hyperglycemia persists, we started on glucotrol - poor response - put on ultralente, 3u qd. After 2 months, stabilized at 11 to 14 units qd. (cat weighed 7kg). GI problem started in 11/96 when cat treated for lethargy, anorexia and fever with doxycycline 100mg qd; probiocin dispensed at same time to try to mitigate GI flora problems. Cat developed colitis anyway. tried Tylan powder, owner resumed Viokase, bowel problem went away. Cat had severe hypoglycemic episode (29 mg/dl 10 hours post-insulin inj!) in 12/96. Took off insulin for a couple of weeks before sugar started to rise again. Started back at 5u; now seems stable at 7u BID (still on ultralente - think we may have been doing a Somogyi thing at high doses SID). BUT, cat has had persistent diarrhea. We have tried metronidazole 125mg bidx7, centrine 1/2 bidx3..and any number of foods. Centrine slows cat down from 4 to 2 episodes runny stools per day, otherwise no help. We sent TLI/cobalamin/folate test to Dave Williams at Purdue.... TLI 42 (17-49) cobalamin 150 (200-1680) folate 16.9 (13.4-38) Test interpretation: low cobalamin consistent with EPI, SIBO or 'disease affecting the distal small intestine' We have been giving this cat weekly vitamin B12 injections since the beginning of February, have repeated metronidazole for 2 weeks, and we have tried centrine out of desperation, but all to no avail. Cat is still on viokase (tablets) and owner is putting Tylan in capsules to get it on board (cat will not eat food if Tylan in or on it). Cat's current diet = 1/8 can Eukanuba LB bid, Science Diet lite + WD ad lib. Owner states she is using older batches of Science diet lite, as newer formulation has more copper sulfate (?). Cat will not eat CNM-EN, diarrhea worsened when on CNM-OM. Prefers dry food. We suspect this cat has IBD (no bowel trouble at all while on CCS), and would put it on theraputic trial of pred in a heartbeat if it were not diabetic. Any alternative therapies for IBD in cats? We are all getting a bit frustrated. I love kitties! ;-)

How is the fecal cytolgy?

Have you tried adequan in this kitty?

Diabetic Cat w/Diarrhea 97-03-16 DrKAT17653 I am going to try to post this in both GI and Endocrine boards......Shablee is an 11 year old M(c) DSH who has had a sensitive bowel since kittenhood. He first made our acquaintance in 1993, and was on Viokase at that time (I have no clue how or if he was actually diagnosed with EPI). Became diabetic in March of '96 after dexamethasone treatment for back injury (Dx'd and Tx'd elsewhere); also, at this time, owner discontinued Viokase (I don't know why). After cat presented to me, I thought we should give it a couple of weeks to see if hyperglycemia was CCS induced. 6 weeks after conclusion of CCS Tx, hyperglycemia persists, we started on glucotrol - poor response - put on ultralente, 3u qd. After 2 months, stabilized at 11 to 14 units qd. (cat weighed 7kg). GI problem started in 11/96 when cat treated for lethargy, anorexia and fever with doxycycline 100mg qd; probiocin dispensed at same time to try to mitigate GI flora problems. Cat developed colitis anyway. tried Tylan powder, owner resumed Viokase, bowel problem went away. Cat had severe hypoglycemic episode (29 mg/dl 10 hours post-insulin inj!) in 12/96. Took off insulin for a couple of weeks before sugar started to rise again. Started back at 5u; now seems stable at 7u BID (still on ultralente - think we may have been doing a Somogyi thing at high doses SID). BUT, cat has had persistent diarrhea. We have tried metronidazole 125mg bidx7, centrine 1/2 bidx3..and any number of foods. Centrine slows cat down from 4 to 2 episodes runny stools per day, otherwise no help. We sent TLI/cobalamin/folate test to Dave Williams at Purdue.... TLI 42 (17-49) cobalamin 150 (200-1680) folate 16.9 (13.4-38) Test interpretation: low cobalamin consistent with EPI, SIBO or 'disease affecting the distal small intestine' We have been giving this cat weekly vitamin B12 injections since the beginning of February, have repeated metronidazole for 2 weeks, and we have tried centrine out of desperation, but all to no avail. Cat is still on viokase (tablets) and owner is putting Tylan in capsules to get it on board (cat will not eat food if Tylan in or on it). Cat's current diet = 1/8 can Eukanuba LB bid, Science Diet lite + WD ad lib. Owner states she is using older batches of Science diet lite, as newer formulation has more copper sulfate (?). Cat will not eat CNM-EN, diarrhea worsened when on CNM-OM. Prefers dry food. We suspect this cat has IBD (no bowel trouble at all while on CCS), and would put it on theraputic trial of pred in a heartbeat if it were not diabetic. Any alternative therapies for IBD in cats? We are all getting a bit frustrated. I love kitties! ;-)

Do you think it has small or large bowel diarrhea?

How low did his hct drop?

Re: Diabetes 97-04-21 K9DOC I have found the ultralente to be much less predicatable and reliable than NPH. Have you done glucose curves in your office and that is how you know that you get good glucose control for 7 hours? Maybe try once daily insulin. It's difficult to measure less than 1 unit, and even that's tough to do accurately for most owners even with a microdose syringe. I don't know that glipizide is a good option for this cat.

I aggree with about not using glipizide for this kitty...it is much harder to regulate cats with it, is not without possible side effects (as everything else is, too, eh?

Can you post her most recent cbc/chem/ua?

Re: hypokalemia and....hypoMg? 97-04-22 Hypurr Mark, I am aware only minimally of muscular weakness caused by hypoMg, and that low Mg can occur with chronic renal insufficiency, malnutrition, dialysis, diuresis, diarrhea and diabetic ketoacidosis. I *suspect* that on a diet of c/d, malnutrition shouldn't be involved, but you might want to post on the Hill's folder or give Hill's a call...they are always very helpful. I also imagine that the hypokalemia is the main problem, and that continuing with the oral potassium supplementation is the route to go. It may take longer than 2 weeks for the hypokalemia to correct itself. Now, what is the underlying cause of the hypokalemia, and how to work that up further? It can be secondary to nephropathy, as you have so correctly looked for, BUT, hypoK can also be the primary problem (nutritional) with nephropathy following behind. Dr DiBartola discovered this about 10 years ago. A fractional excretion is an easy and inexpensive, non invasive place to start. From his excellent text on fluid therapy, here is his list of causes of hypokalemia: DECREASED INTAKE: abberant diet; admin of K-free fluids (eg dextrose in water or 0.9% NaCl) TRANSLOCATION FROM ECF -> ICF: alkalemia; insulin/glucose-containing fluids; catecholamines; hypothermia?; hypokalemic periodic paralysis of burmese INCREASED LOSS: Gastrointestinal (FE of K 4-6%):="" vomiting="" of="" sach="" contents;="" diarrhea=""> Urinary: (FE of K > 4-6%): chronic renal failure; diet-induced hypokalemic nephropathy; distal (type I) RTA; proximal (type II) RTA after NaHCO3) treatment; postobstructive diuresis; dialysis; mineralocorticoid excess (hyperadrenocorticism, primary hyperaldosteronism (adenoma, hyperplasia)) Drugs: loop diuretics (furosemide, ethacrynic acid); thiazide diuretics (chlorothiazide, hydrochlorothiazide); amphotericin B; penicillins Here is something from the database: Disorders Of Potassium, Phosphorus, and Magnesium in Critical Illness compend contin="" educ="" pract="" vet="" 19[1]:41-49;83="" jan'97="" review="" article="" 32="" refs="">/compend> Douglass K. Macintire, DVM, MS Department of Small Animal Surgery and Medicine, College of Veterinary Medicine, Auburn University, Alabama Potassium, phosphorus, and magnesium are important for normal metabolic and cellular functions. Serum concentrations of these primarily intracellular ions are normally maintained within a narrow range by strict homeostatic mechanisms. Critically ill animals are prone to total body depletion or retention of these substances. These disorders must be corrected cautiously, with frequent monitoring to avoid severe side effects. Hypokalemia often results from decreased intake, excessive losses (e.g. from renal disease, diarrhea, or vomiting), or translocation of potassium into cells (e.g., from initiation of insulin therapy). Hyperkalemia can result from hypoadrenocorticism, acute oliguric renal failure, urethral obstruction, or massive cellular destruction. Hypophosphatemia often occurs early in the treatment of malnutrition or diabetes. Hyperphosphatemia often results from renal failure. The importance of hypomagnesemia in critically ill patients has recently been recognized. (Author Abstract) Hope this helps! Please keep us posted! Cheers! >M>

How about ksu?

What exactly are the results of the ldds tests that you have done?

Re: hypokalemia and....hypoMg? 97-04-22 Hypurr Mark, I am aware only minimally of muscular weakness caused by hypoMg, and that low Mg can occur with chronic renal insufficiency, malnutrition, dialysis, diuresis, diarrhea and diabetic ketoacidosis. I *suspect* that on a diet of c/d, malnutrition shouldn't be involved, but you might want to post on the Hill's folder or give Hill's a call...they are always very helpful. I also imagine that the hypokalemia is the main problem, and that continuing with the oral potassium supplementation is the route to go. It may take longer than 2 weeks for the hypokalemia to correct itself. Now, what is the underlying cause of the hypokalemia, and how to work that up further? It can be secondary to nephropathy, as you have so correctly looked for, BUT, hypoK can also be the primary problem (nutritional) with nephropathy following behind. Dr DiBartola discovered this about 10 years ago. A fractional excretion is an easy and inexpensive, non invasive place to start. From his excellent text on fluid therapy, here is his list of causes of hypokalemia: DECREASED INTAKE: abberant diet; admin of K-free fluids (eg dextrose in water or 0.9% NaCl) TRANSLOCATION FROM ECF -> ICF: alkalemia; insulin/glucose-containing fluids; catecholamines; hypothermia?; hypokalemic periodic paralysis of burmese INCREASED LOSS: Gastrointestinal (FE of K 4-6%):="" vomiting="" of="" sach="" contents;="" diarrhea=""> Urinary: (FE of K > 4-6%): chronic renal failure; diet-induced hypokalemic nephropathy; distal (type I) RTA; proximal (type II) RTA after NaHCO3) treatment; postobstructive diuresis; dialysis; mineralocorticoid excess (hyperadrenocorticism, primary hyperaldosteronism (adenoma, hyperplasia)) Drugs: loop diuretics (furosemide, ethacrynic acid); thiazide diuretics (chlorothiazide, hydrochlorothiazide); amphotericin B; penicillins Here is something from the database: Disorders Of Potassium, Phosphorus, and Magnesium in Critical Illness compend contin="" educ="" pract="" vet="" 19[1]:41-49;83="" jan'97="" review="" article="" 32="" refs="">/compend> Douglass K. Macintire, DVM, MS Department of Small Animal Surgery and Medicine, College of Veterinary Medicine, Auburn University, Alabama Potassium, phosphorus, and magnesium are important for normal metabolic and cellular functions. Serum concentrations of these primarily intracellular ions are normally maintained within a narrow range by strict homeostatic mechanisms. Critically ill animals are prone to total body depletion or retention of these substances. These disorders must be corrected cautiously, with frequent monitoring to avoid severe side effects. Hypokalemia often results from decreased intake, excessive losses (e.g. from renal disease, diarrhea, or vomiting), or translocation of potassium into cells (e.g., from initiation of insulin therapy). Hyperkalemia can result from hypoadrenocorticism, acute oliguric renal failure, urethral obstruction, or massive cellular destruction. Hypophosphatemia often occurs early in the treatment of malnutrition or diabetes. Hyperphosphatemia often results from renal failure. The importance of hypomagnesemia in critically ill patients has recently been recognized. (Author Abstract) Hope this helps! Please keep us posted! Cheers! >M>

Can you measure his bp?

Why no curve?

Charlie with HAC and DM. 97-05-19 Petsdoc4 I have a very specific question about a very complicated case. We are currently treating a dog with Lysodren for Cushings and BID NPH insulin for diabetes. He's doing well in general but wets in the house late on Sat. and Sun. night (the only time he is inside for an extended period). He gets his lysodren on Monday. His blood glucose is fairly well regulated right now and as far as I can determine there is no difference in the routine on the weekends vs. the weekdays. Our theory is that perhaps the cortisol level is getting high toward the end of the week leading to these accidents. Is this possible? I will plan an ACTH stim test on Saturday if this is a possibility. Otherwise I won't waste the owners money (As you can imagine, she's already spent a bundle). Any alternate theories? LAB.

Do you have a urinalysis?

Is this dog also hyperlipidemic?

Charlie with HAC and DM. 97-05-19 Petsdoc4 I have a very specific question about a very complicated case. We are currently treating a dog with Lysodren for Cushings and BID NPH insulin for diabetes. He's doing well in general but wets in the house late on Sat. and Sun. night (the only time he is inside for an extended period). He gets his lysodren on Monday. His blood glucose is fairly well regulated right now and as far as I can determine there is no difference in the routine on the weekends vs. the weekdays. Our theory is that perhaps the cortisol level is getting high toward the end of the week leading to these accidents. Is this possible? I will plan an ACTH stim test on Saturday if this is a possibility. Otherwise I won't waste the owners money (As you can imagine, she's already spent a bundle). Any alternate theories? LAB.

Have you tried letting the dog out more frequently on the weekend?

How about albumin?

Gastric ulcers 97-06-01 Vetgroup I am treating an 8 year old Maltese with iatrogenic Addison's disease secondary to Lysodren. She is also a controlled diabetic. She receives DOCP every 20 days, and requires 1.25 mg of prednisone daily. She presented today with 5 days of anorexia. She has melena and a PCV of 15%. She has not received any NSAID's. Do you see gastric ulcers in controlled addisonian dogs? What else could do you think could have incited a gastric ulcer with this dog's history? I am treating her with tagamet and carafate. Thanks Vetgroup

What is the tp?

I'm not so sure i'd pursue the alt elevation, given that it's so mild, but the low albumin bothers me---are the skin lesions oozing?

Gastric ulcers 97-06-01 Vetgroup I am treating an 8 year old Maltese with iatrogenic Addison's disease secondary to Lysodren. She is also a controlled diabetic. She receives DOCP every 20 days, and requires 1.25 mg of prednisone daily. She presented today with 5 days of anorexia. She has melena and a PCV of 15%. She has not received any NSAID's. Do you see gastric ulcers in controlled addisonian dogs? What else could do you think could have incited a gastric ulcer with this dog's history? I am treating her with tagamet and carafate. Thanks Vetgroup

Any evidence for regeneration?

Can you post a couple of her current bg curves?

Route Of Fluids 97-05-03 NightVet Maybe you can help settle a debate - my boss and I sometimes disagree on the most safe and effective route of fluid administration in critical animals. For example, suppose you have an elderly cat with lymphoma (on prednisone etc), mild renal failure, and diabetes (just diagnosed - blood glucoses still up there a bit). Oh, and mild cardiomyopathy. He also has a PEG tube in. He comes in dehydrated, big surprise. So - the boss thinks that pushing water orally isn't going to help this guy, that it will just go right out his kidneys with the excess glucose until you get the blood glucose under control, therefor you need IV (or SQ) supplementation. This doesn't make sense to me, it seems like (since you can give him all the water you want to orally) that via the PEG tube would be adequate and maybe safer since IV fluids might overload his HCM heart. Does the intravascular volume increase as much (as with IVs) as with excessive oral intake, or do they absorb what they need and leave the rest in the GI tract? Jean

Is there left atrial dilation?

What should she weigh?

Route Of Fluids 97-05-03 NightVet Maybe you can help settle a debate - my boss and I sometimes disagree on the most safe and effective route of fluid administration in critical animals. For example, suppose you have an elderly cat with lymphoma (on prednisone etc), mild renal failure, and diabetes (just diagnosed - blood glucoses still up there a bit). Oh, and mild cardiomyopathy. He also has a PEG tube in. He comes in dehydrated, big surprise. So - the boss thinks that pushing water orally isn't going to help this guy, that it will just go right out his kidneys with the excess glucose until you get the blood glucose under control, therefor you need IV (or SQ) supplementation. This doesn't make sense to me, it seems like (since you can give him all the water you want to orally) that via the PEG tube would be adequate and maybe safer since IV fluids might overload his HCM heart. Does the intravascular volume increase as much (as with IVs) as with excessive oral intake, or do they absorb what they need and leave the rest in the GI tract? Jean

How thick is the wall?

(and body weight)?

Re: PU/PD and Hypo K+ 97-05-11

Do you have a globulin value?

I'm sort-of wondering if there are any visible sutures that we could remove at this point (as it seems like healing must be coming along pretty well) but i hate to do anesthesia again just to do that...since it seems like they're going to dissolve fairly soon anyway...what material is the suture material?

Re: PU/PD and Hypo K+ 97-05-11

Have you rechecked the cat's potassium while on supplement and adjusted it accordingly?

I guess that could explain the thickened area near pancreas, but would the stomach have that appearance?

Insulin Resistance? 97-05-22 LRDVM Currently trying to regulate an 11 yr old neutered male cat. He weighs 13.8 # as is taking 7 units of NPH U-100 in am, and 6 units in pm. We have used Lente, Ultrlente forms of insulin. His initial glucose curves seemed to demonstrate peak onset of action at about 4 hours with Lente, and with Ultralente at about 8 to 9 hours. Another feature of this case is any insulin we choose seems to work for a few days, then his BG begins to cliimb again. His BG last pm was 752 mg/dl prior to his evening dose of insulin. I am confident the client is handling the insulin correctly and injecting correcctly. Prior glucose curves have not even hinted at a Somogyi overswing. No history of corticosteroid use has been identified. I have read that cats aren't considered insulin resistant until they are getting 2.5 U/kg body weight of an intermediate or long acting insulin. Is that an SID or BID dose? This cat is currently getting 13 units total daily dose. It appears to me we need to further establish if this cat is truely insulin resistant by pushing his insulin dose a bit. If he is insulin resistant, the LDDST to R/O Cushings. Any help greatly appreciated.

Does the cat look like it has cushings or acromegaly?

What dose and type of insulin is she receiving?