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phenylpropanolamine & heart dis. 94-09-26

Is he coughing?

Is his weight stable?

phenylpropanolamine & heart dis. 94-09-26

Also, does the moderate cardiomegaly come from the lateral or the dv radiograph?

Possible myasthenia?

phenylpropanolamine & heart dis. 94-09-26

Does this dog have a heart murmur?

What site is this owner using?

feline rear limb weakness 94-01-24 RobertsA 'Opus' is an overweight, 6 year, spayed female indoor cat who was presented because the owner noticed that she 'thumped' for the past 1 1/2 weeks when she came down the stairs. She then noticed that she walked in a squatting position. Physical exam was normal except obesity and that Opus was 'fallen down in her hocks'. She was developing thickening along the posterior tarsal surface indicating she had been in this condition possibly longer that normal. There was no pain evident and I believe neuro is OK (not my strong suit). Radiographs were normal. The stifles can be overextended indicating weak ligaments. Baseline lab work was normal except Alk Phos 42 and alt of 160 and 8% monocytes with 8700 WBC. T4 was 2.8 (normal). I put cat on Tumil-K. Any ideas where to go? Thanks

Any exposure to organophosphates?

What's her current bcs?

resistant Cushings 93-10-19 L I have an 8 year old Chihuahua with Cushings. He failed Nizoral. After 2 weeks of 50 mg/kg/day of Lysodren his post ACTH cortisol was still 18 mcg/dl (It was 36 pre-TX and 51 after 1 week of Lysodren!). After 2 weeks of weekly Lysodren followed by another 10 days of daily Lysodren, his post stim was 17. However when he is on daily Lysodren, his skin develops new patches of inflamed, open calcinosis cutis--it is so severe I am afraid to give more loading dose so we decreased the Lysodren to 25 mg/kg daily and continued another 3 weeks. He then had a stim test result of 8 pre, 19.5 post. I have done multiple ultrasounds and the adrenals always look symmetric, about 2 cm diameter. The liver is huge but otherwise abdomen is normal (SAP was about 3500, now up to 4500). At that point, I submitted an endogenous ACTH which was 395 at KSU. We increased the Lysodren to 30 mg/kg daily for 2 weeks and the recheck stim is pending. Have you ever had a pituitary Cushings that you couldn't control with Lysodren? I have discussed pituitary radiation with the owner but I am afraid his skin would disintegrate if we actually were able to suddenly lower the cortisol. (Of course I am worried he is a good candidate for macroadenoma-induced neuro signs if we don't!) I have never had such a resistant case--I have to believe the endog ACTH value is reliable since his cortisol levels weren't suppressed at the time. I don't think we've radiographed his chest; maybe he has an ACTH-secreting malignancy? Comments?

Is the medication in date?

How is cholesterol?

resistant Cushings 93-10-19 L I have an 8 year old Chihuahua with Cushings. He failed Nizoral. After 2 weeks of 50 mg/kg/day of Lysodren his post ACTH cortisol was still 18 mcg/dl (It was 36 pre-TX and 51 after 1 week of Lysodren!). After 2 weeks of weekly Lysodren followed by another 10 days of daily Lysodren, his post stim was 17. However when he is on daily Lysodren, his skin develops new patches of inflamed, open calcinosis cutis--it is so severe I am afraid to give more loading dose so we decreased the Lysodren to 25 mg/kg daily and continued another 3 weeks. He then had a stim test result of 8 pre, 19.5 post. I have done multiple ultrasounds and the adrenals always look symmetric, about 2 cm diameter. The liver is huge but otherwise abdomen is normal (SAP was about 3500, now up to 4500). At that point, I submitted an endogenous ACTH which was 395 at KSU. We increased the Lysodren to 30 mg/kg daily for 2 weeks and the recheck stim is pending. Have you ever had a pituitary Cushings that you couldn't control with Lysodren? I have discussed pituitary radiation with the owner but I am afraid his skin would disintegrate if we actually were able to suddenly lower the cortisol. (Of course I am worried he is a good candidate for macroadenoma-induced neuro signs if we don't!) I have never had such a resistant case--I have to believe the endog ACTH value is reliable since his cortisol levels weren't suppressed at the time. I don't think we've radiographed his chest; maybe he has an ACTH-secreting malignancy? Comments?

Any reason why it might not be as active as expected?

What should the cat weigh?

Amitraz/Preventic 94-04-19 W I don't know what the current company 'line' is regarding toxicity of Amitraz collars(Preventic), but it used to be 'don't be overly concerned if your dog eats a collar and gets sick'. When the collars first were available I put them on my daughter's 2 Dobermans. Within a few days the dogs decided to eat each others collar. She lives 100 miles away, so one of the dogs ended up in an emergency clinic, and recovered. I called Virbac and talked to their veterinarian. He assured me that intensive therapy was unnecessary.....no big deal. He even sent me a copy of a memo he had written saying the same thing. Of course I know better now. I think the original Preventic collars I bought are still sitting on the shelf.

Consuming amitraz collars seems to occur reasonably often! what do you suppose is attractive about these particular collars that dogs want to eat them?

How much does she weigh and how many calories are in a can of this diet?

? from E-mail1 94-07-13 ER Vet Had some questions from E-mail that I thought were appropriate for this board.

Can anyone help?

Bid i assume, correct?

?Haws Syndrome in dog? 94-05-05

Re:?haws syndrome in dog?

What diet is the dog on?

insulin supply? 93-11-14

What question did you have about human ul?

Were the adrenals enlarged on ultrasound?

insulin kinetics feline 93-12-03 GKBDVM I need some help on insulin absorption kinetics. I inherited a poorly controlled diabetic cat, who was on 3 units of Beef pork ultra Lente. We decided not to continue with beef pork when they needed a refill, so we started Humulin-U. With beef pork at 3 units, the cat was between 250 and 300 at 7 hours post injection. We have stabilized diet, but cannot get glucose below 350 with, now up to 7 units. Since I know that she did respond to 3 units of beef pork, but was not on high enough dosage, I am assuming that the absorption of the Humulin-U was delayed. Nelson and Feldman describe this as a problem with Humulin u and suggest beef pork or Humulin Lente. Anyone have suggestions. I plan on stopping Humulin U and beginning with 3 units of Humulin Lente. I don't think this cat is cushingoid due to the response to Beef pork.

How does a glucose curve look?

What does the owner do if she doesn't eat her meal all at once?

glucagon 93-12-07 L I have a dog with possible early glucagonoma. Who runs glucagon assays? Thanks as always

What clinical signs id the dog displaying?

Are his triglycerides high enough to cause this?

glucagon 93-12-07 L I have a dog with possible early glucagonoma. Who runs glucagon assays? Thanks as always

Any evidence for liver disease?

Is him eating the totality?

Feline Diabetic/Cushings 94-01-18 RHLDVM Sascha is a 16 year old neutered male domestic shorthair. He has been treated successfully for diabetes with PZI insulin bid for several years. Periodic rechecks previously were normal with good blood glucose levels. Those levels started increasing several months ago as PZI became unavailable and we converted him to Ultralente. The dose of Ultralente needed continual increases and blood sugar stayed up. Suspicious of Cushings: Lo dose Dex Test: Pre: 5.8, Post: 2.4 = kind of in the grey area. Insulin response test: gave 10units Humulin Ultralente and tested blood sugar over the next 9 hours. Results: Pre: 631.0mg/dl; 1 thru 8 hour post:651.0, 671.6, 665.0, 655.6, 631.5, 605.2, 577.2, 591.1. While there is some lowering at 6-8 hours there is strong insulin resistance. Next did an ACTH response just to be a little more sure: Pre: 6.8, Post: 18.0 OK I think there's enough evidence to assume Cushings. Now what?..... My books and telephone consults say locate an adrenal tumor via U/S & perform unilateral adrenalectomy, but what if no tumor as is probable? References give little information on treatment of feline diabetic/Cushingoid. Our lab specialists tell me that Lysodren & Ketoconazole are not safe or effective in cats. Saschsa is a great cat & acts very healthy. I'd like to see him get his maximum allotment of years. Any suggestions? p Le Vine (RHLDVM)

How did you do your ldds test and what dose of dex did you give?

What is his bcs?

New info on diabetes! 94-02-15

From whom did this 'study' come?

Is this a spayed female?

Hyperthyroid, cushingoid diabetic 94-03-27 GKBDVM Penny Lane is a 13 yr old DSH with Hx of allergic skin disease on her belly, confirmed by multiple biopsies.. I was unable to figure what was causing, food trials unsuccessful, consulted dermatologist at Tufts. Pred did not control, but 2 mg triamcinolone q 48 hours has worked well and hair is regrowing for the first time in 2 yrs. Cat was dx hyperthyroid at about 2 mo ago, and is well controlled on Tapazole while owner decides whether or not to cut thyroids. Presented Pu/PD and 1#( of 13) wt loss on Saturday. Blood glucose is 230 in office(+/-10) which I repeated 3 times. Urine glucose is between 500 and 1000. My first thought is that the Triamcinolone has caused the rise in glucose, but 1. Isn't the renal threshold for glucose 500 mg/dl. Why are we spilling. Cat has no documented renal dz, 1/25/94 sp.g. was>1.045. 2. Chem at time of t4 (1/25/95) had glucose at 330, which I assumed was sampling stress, especially as cat was not pu/pd and had high urine Sp.G. 3. UA shows only glucose, no secondary infections etc, now sp.g of 1.020 pres. due to glucose diuresis/ 4. I have begun triam at 1 mg in pm for 1 week then stop, also begun high fiber diet for NIDDM. Is there a better way than this to drop steroids? Have we created just a Cushing like problem, (as bl glucose is above normal but low, or is this cat developing diabetes? Any and all comments welcome.

Is the hyperthyroidism controlled on the tapazole?

The owner moves the injections around on her body every day?

If it walks like a duck? 94-03-15 ICUT Jacque, a 10 year old poodle with diabetes mellitus dxed 3 weeks ago, seen by one of my associates. Dog is also pot-bellied, thin haircoat. Difficult to regulate-with insulin dosages not yet approaching unit/lb. ACTH response test done with initial lab work. Pre=6.9 Post 17.9 Our lab normals (pre 1-10) (post 10-20). Would LDD suppression be indicated now? Or is there enough evidence to go ahead and start treating Cushings?

But, do you have increased ap enzyme?

How much does this dog weigh?

Re: Chromium and insulin 94-04-01

Fact or fiction?

What were the physical exam findings?

Big, Greasy, Dandruffy Cats 94-04-05

Are you sure your big fat cat isn't just lazy and not grooming?

What exactly did the stim look like in january?

Mixing Insulins 94-07-28

How is the dog doing on the current regimen?

Are the calories the same each day?

Switching insulin 94-09-02 GGJVet I have a cat that has had it's DM controlled fairly well on UL insulin. The owner has been having trouble getting UL and wants to know what 'other' insulin he can use ( as fate would have it, the owner is a diabetic, so he knows his insulin). Can he use Humulin? Should he give the same # of units as he was with UL? Please let me know how to best handle the transition.

Insulin-what now?

Are the eyes red or light sensitive?

Switching insulin 94-09-02 GGJVet I have a cat that has had it's DM controlled fairly well on UL insulin. The owner has been having trouble getting UL and wants to know what 'other' insulin he can use ( as fate would have it, the owner is a diabetic, so he knows his insulin). Can he use Humulin? Should he give the same # of units as he was with UL? Please let me know how to best handle the transition.

If it is so, would lente or human ultralente be the best substitute for a dog?

Was the ldds performed at reference lab or in house?

Diabetes 94-08-16

When you say there has been 'no response' how do you define that?

Perhaps doing the trial and seeing that the cat is not appropriately regulated will convince them to continue insulin therapy?

Diabetes 94-08-16

Symptoms still present?

The steroids in the eyes can cause insulin resistance (not just the lack of control of the cushing's)--any chance of using topical nsaids instead?

Diabetes 94-08-16

Checking blood glucose values, and if so, when?

Any sign of that?

Diabetes 94-08-16

Are you doing glucose curves?

Could you post pictures from that aspirate here, for us to evaluate?

Diabetes 94-08-16

Which type of insulin are you using, animal source or humulin?

What kind of insulin is he on?

Diabetes 94-08-16

Insulin given once or twice a day?

Any other advice?

Diabetes 94-08-16

What diet is the dog currently receiving?

Not sure if that ends up saving more money or spending more to get the cat regulated?

anorexic diabetic 94-08-23 Lboggs Was presented with a male, neutered, Siamese cat 3 weeks ago for weight loss (13 lbs to 10.5 lbs). Owner mentioned an increase of water consumption for the last several months. Blood work showed glucose - 614, mild K decrease. Glucosuria. No ketones. Cat was put on a trial of glipizide. Water consumption subjectively decreased. Blood glucose after 1 week - 415. Net week, cat presented for anorexia, lethargy. Blood work: BG - 400, mild BUN elevation, Mild decrease in K and Na, Mild increase in ALT. Cat was put on iv fluids, force fed, given slowly increasing doses of insulin (ending with 2.5 U bid of NPH). Blood glucose varied from 230 to 360 between doses. Cat began eating on its own after 7 s. Eating very well by 9. Owner was given instructions on insulin administration. Discharged from hospital. The next the cat quit eating and became severely depressed. Glucose - 36. Had pharmacist redilute new insulin vial. Watched owner's insulin administration - no problems seen. Put on iv fluids. Began force feeding. After 2 s, cat still anorexic. Blood glucose staying between 200 and 335. Liver enzymes normal. K - 5.8 Na - 155 WBC- 4300 HCT- 23.0 fT4- 0.6 Ultrasound exam- NAF Liver aspirate- no evidence of hepatic lipidosis. The cat vomits occasionally (0 - 1 X ). Normal BM. Normal mentation. Why doesn't this cat want to eat? Where do we go from here?

Also is there any evidence of a urinary tract infection?

This is available online at www.youngagainpetfoods.com  will she eat canned food?

Diabetic Cat 94-08-31

What diet is the cat on?

The rest of the panel looks ok?

Feline Juvenile Diabetes 94-09-28 Kingstowne I have a one year old DSH that has just not been right since spaying 2 months ago. Blood work reveals a glucose of 424 and elevations of ALT and SAP and a low normal PCV. The urine is positive for glucose but not ketones. Has anyone had experience with a juvenile diabetic? Thanks,

Any other significant findings on physical or labs?

Have signs of cushing's disease improved/normalized on current trilostane dose and with current acth stim results?

Feline DM, possible Cushings? 94-10-03 HlywdVet 10 yr old MN DSH, 10 lbs. Persistent hyperglycemia (~500) with glycosuria. Mature neutrophilia, lymphopenia, eosinophilia, normal serum enzyme levels and electrolytes. Nonrepsonsive to 21u Humulin NPH BID. Pre ACTH 10, Post ACTH 17. Normal thoracic and abdominal radiographs. Abdominal ultrasound not done. Further diagnostic and therapeutic options greatly appreciated.

When was the post-acth stim sample taken?

Only the canned version of the dm, right?

Diabetic poodle 94-09-30 KSBVET A 12 yo spayed female poodle presented with BG at 586. She had been on 1 unit NPH insulin for 6 months, unchecked during this time by another hospital. She is ketoacidotic. Plan is to start on fluids, R insulin and get the dog to eat. Two questions . She has a very thin hair coat and looks all the world like a cushingoid. Liver enzymes are elevated, but I think that a long term unregulated diabetic would have this type of panel. If I wanted to do a LDDS - when would it be safe for the dog? Also I am concerned about the possibility that she has been Cushingoid from the start and long term use of insulin that she may not have needed could be causing a compounding Somogyi effect. The owner reported that the dog crashed on 2 u of insulin. The dog weighs 4 kg. Also, she has eaten hot dogs for her entire life, and won't eat anything else. I think that I can fix that problem over time. Maybe I'll put w/d in a sausage casing! Input appreciated.

What is her urine specific gravity?

Was the acth stim done using synacthen/cortrosyn?

Greggs Diabetic... 93-10-26

Are you checking the blood sugar at 2 hour intervals?

Are the 'lytes being run in-house?

Wt loss, hypok+ cat 93-12-18 GKBDVM The following case is a 11+ yr old DLH with neg retrovirus screen. Hx of wt loss of about 2# over last few weeks in spite of good appetite. Cat is thin with a grade 3/6 systolic murmur, normal EKG. UA, >1.030, pH 6, prot 2-3+ sedi negative. Blood work 7000 WBC with 37% PMN, 43 lymph, 3 mon, 17 eos. Stool pending. Chemistries WNL except alt 100 (n,68) normal CPK, ast 57(n,45), K+=3.2 (n=3.7-4.9)and glucose 258. T4 is normal 2.6 Questions? Any hints here? why the hypokalemia, is this cat unable to absorb?.( or is there some borderline diabetes situation here, there is no visible stress to this cat, was purring in office, so I am concerned with whether the glucose was real or not.? Do I need a Prot/creat ratio or is the 2-3+ protein ok with urine SG>1.030? DDx includes IBD, renal loss of prot, DM willing to consider others from collective minds. I have placed cat on K+ supplement orally and will recheck next week.

What about the cardiac murmur?

Discontinue the otomax and start baytril otic with daily ear cleanings?

Wt loss, hypok+ cat 93-12-18 GKBDVM The following case is a 11+ yr old DLH with neg retrovirus screen. Hx of wt loss of about 2# over last few weeks in spite of good appetite. Cat is thin with a grade 3/6 systolic murmur, normal EKG. UA, >1.030, pH 6, prot 2-3+ sedi negative. Blood work 7000 WBC with 37% PMN, 43 lymph, 3 mon, 17 eos. Stool pending. Chemistries WNL except alt 100 (n,68) normal CPK, ast 57(n,45), K+=3.2 (n=3.7-4.9)and glucose 258. T4 is normal 2.6 Questions? Any hints here? why the hypokalemia, is this cat unable to absorb?.( or is there some borderline diabetes situation here, there is no visible stress to this cat, was purring in office, so I am concerned with whether the glucose was real or not.? Do I need a Prot/creat ratio or is the 2-3+ protein ok with urine SG>1.030? DDx includes IBD, renal loss of prot, DM willing to consider others from collective minds. I have placed cat on K+ supplement orally and will recheck next week.

What do you think is causing that?

Did you check her blood pressure?

Wt loss, hypok+ cat 93-12-18 GKBDVM The following case is a 11+ yr old DLH with neg retrovirus screen. Hx of wt loss of about 2# over last few weeks in spite of good appetite. Cat is thin with a grade 3/6 systolic murmur, normal EKG. UA, >1.030, pH 6, prot 2-3+ sedi negative. Blood work 7000 WBC with 37% PMN, 43 lymph, 3 mon, 17 eos. Stool pending. Chemistries WNL except alt 100 (n,68) normal CPK, ast 57(n,45), K+=3.2 (n=3.7-4.9)and glucose 258. T4 is normal 2.6 Questions? Any hints here? why the hypokalemia, is this cat unable to absorb?.( or is there some borderline diabetes situation here, there is no visible stress to this cat, was purring in office, so I am concerned with whether the glucose was real or not.? Do I need a Prot/creat ratio or is the 2-3+ protein ok with urine SG>1.030? DDx includes IBD, renal loss of prot, DM willing to consider others from collective minds. I have placed cat on K+ supplement orally and will recheck next week.

Could it be related?

Have you done skin scrapings?

Pu/Pd 94-03-20 LJMT Well, I tried to figure this out without help but I just keep getting more tangled up. I have a 6.5 yr old F/s Shar-Pei with a history of recurrent Familial Shar-Pei Fever who has been on colchicine for 2 years since her littermate w/ FSF died of systemic amyloidosis. Current CC: severe polydipsia w/ polyuria and nocturnal incontinence. Lab work at presentation revealed a mildly dehydrated (hct=58, TP=7.2) dog with SG of 1015 and when I did equation for serum osmolality = 254 (>280 N). Dog was nonazotemic, normal creatinine, normal phos, etc etc on profile and urine cortisol to creatinine ratio was normal. No evidence of diabetes mellitus. Urine protein/creatinine ratio= 0.23 (N). Told owner not to restrict access to water (she had before 1.5hr car trip to me.) SG=1006 at reck. Okay... She probably has medullary amyloidosis +/- interstitial nephritis (most common findings at necropsy... glomerular involvement is very variable). She may have nephrogenic diabetes insipidus or medullary washout. Do I do a water deprivation test w/ ADH administration in a patient who very likely has occult renal disease? Do I do a renal biopsy in a patient in which a biopsy dx isn't going to change my Rx's? U/S guided renal biopsies are difficult when what I need is the medulla. Gen. Anes/Laparotomy for biopsy might compromise a patient already on the edge. And has anyone ever looked at whether renal biopsy can accelerate the progression of chronic renal failure? (Can you tell I really HATE to cut!) Should I do a Hickey-Hare Test (hypertonic saline admin.)? Should I attempt DDAVP admin by owner at home for a few days then remeasure SG? But if I've got medullary washout, this won't tell me anything? So, I'm not sure what to do and I'm not sure what order I'm not sure what to it in :) Thanks!

Have you cultured the urine?

Is he performing full bg curves at home as well?

Cushings, cataracts and renal dz 94-07-22 VMDatSEA I have a 15-yr-old fem. sp. min poo with 18 mo Hx of mild renal compromise (Creat. 2.3, BUN 40). Dog recently had dexameth suppression test results consistent with PDH. Dog has bilat. mature cataracts, and owner wants to improve dog's quality of life by having cataract removed. Dog is stable, very perky. My concern is not so much with risk of Surgery, but with whether it is advisable to treat Cushing's Dz in this dog with Lysodren. Any advice would be appreciated. Thanks.

Is the dog a diabetic?

Have you cultured the urine?

Cushing's? 94-10-05

What was the 8 hour post ldds value?

Neuro exam is normal?

Re: Grey top glucose values 94-01-06 PDP1 The answer is statistical probability -- and I don't know - 1. in 15 minutes I don't think RBC's in the tube would do much to the glucose concentration -- and you proved this with an n of 1 :) so I think that in the best of all worlds all tubes should give the same number. 2. Different anticoagulants will affect the result of the assay and you might find that the GREY TOP (Fluoride) tubes (even with the same known concentration of glucose) give a predictably lower result 3. The numbers you give are NOT very different -- you must remember that a NUMBER is NOT a NUMBER when looking at lab test results -- there are SO MANY FACTORS that come into play from sample handing and acquisition to how the assay is run to the anticoagulant used that the NUMBER you get is an ESTIMATE f the true value. The more you repeat the test and AVERAGE your results the more you can believe your ESTIMATE. But for your purposes I would not worry about the range you got -- you have more than enough info to make the same clinical judgement from each sample =================== Great question and great to see how you approached it!!! And who says medicine is an art and not a science........ Scott you are obviously a GREAT CLINICAL SCIENTIST.

Does anyone else have that experience?

Are the cats in this house indoor, outdoor, or a combination?

Re: Grey top glucose values 94-01-06 PDP1 The answer is statistical probability -- and I don't know - 1. in 15 minutes I don't think RBC's in the tube would do much to the glucose concentration -- and you proved this with an n of 1 :) so I think that in the best of all worlds all tubes should give the same number. 2. Different anticoagulants will affect the result of the assay and you might find that the GREY TOP (Fluoride) tubes (even with the same known concentration of glucose) give a predictably lower result 3. The numbers you give are NOT very different -- you must remember that a NUMBER is NOT a NUMBER when looking at lab test results -- there are SO MANY FACTORS that come into play from sample handing and acquisition to how the assay is run to the anticoagulant used that the NUMBER you get is an ESTIMATE f the true value. The more you repeat the test and AVERAGE your results the more you can believe your ESTIMATE. But for your purposes I would not worry about the range you got -- you have more than enough info to make the same clinical judgement from each sample =================== Great question and great to see how you approached it!!! And who says medicine is an art and not a science........ Scott you are obviously a GREAT CLINICAL SCIENTIST.

And when running serial glc tests to try to curve a diabetic...how long can you safely hold the blood (in red or grey tops?) in the 'fridge til my lab picks up?

Ehbdo from pancreatitis?

Eosinophilic Plaques in Cats 94-07-14 DrDVet Anything new, unpublished re: this nemesis of a dermatopathy? I have an Abyssinian that has gone the gamet with Tx's and is still chronically affected. I'd appreciate any and all ideas.

I have no personal experience with this but it should be non-toxic so why not give it a try?

What labwork do you have on him - chem, t4, urine culture, pli/gi panel?

Re: chromium levels and obese cat 95-05-28 DocCat Greg, You did see a summary of Hazel Carney's 'Serum Chromium Values in Clinically Normal and Clinically Obese Cats' in the AAFP Newsletter...A summary of this summary: Healthy obese cats have significantly(p=0.0255) lower serum chromium levels than healthy normal weight cats...(Normal weight levels were 1 ppb to 13 ppb with mean of 5.7 ppb) (Obese cats had 1 ppb to 8 ppb with mean of 2.93 ppb) Louisiana Veterinary Medical Diagnostic Labs, P O Box 25070, Baton Rouge, LA 70894....phone: 504-346-3193...cost about $15/sample...need one ml of serum Suggested dose of chromium picolinate (200 mcg/tablet) was start at 200 mcg/day...can give in divided dose with food There is considerable information of chromium and its affect on glucose metabolism in the human literature....chromium is very safe since the FDA suspects up to 90% of the people in the USA may be deficient in chromium....you may want to monitor the blood glucose level initially, and some cases of hypoglycemia have been reported with humans...but overall, people take up to 1000 mcg/day (body builders) without any problems....the average dose taken is usually 400-600 mcg/day.

Interesting, eh?

What is the cat's diet?

Winstrol? 97-03-12 VetACH I am not a big user of this stuff (like NEVER), but am considering using it in a recovering aortic thrombus kitty with some muscle atrophy and a crappy appetitite. Does anyone have any input on this use or on their clinical experiences with it in general? This cat is also on 30mg Cardizem CD s.i.d. and 81mg aspirin q. 3d. and is making good clinical improvement.

What is with this 'outbreak' of thromboembolism?

Using u40 syringes?

Winstrol? 97-03-12 VetACH I am not a big user of this stuff (like NEVER), but am considering using it in a recovering aortic thrombus kitty with some muscle atrophy and a crappy appetitite. Does anyone have any input on this use or on their clinical experiences with it in general? This cat is also on 30mg Cardizem CD s.i.d. and 81mg aspirin q. 3d. and is making good clinical improvement.

Now...the big q...how could this interfer with the cat's vascular status?

Absolutely sure that there is no exposure to steroids, including topicals on eyes, ears or skin?

Winstrol? 97-03-12 VetACH I am not a big user of this stuff (like NEVER), but am considering using it in a recovering aortic thrombus kitty with some muscle atrophy and a crappy appetitite. Does anyone have any input on this use or on their clinical experiences with it in general? This cat is also on 30mg Cardizem CD s.i.d. and 81mg aspirin q. 3d. and is making good clinical improvement.

Before i go, though...what about cyproheptadine?

What is this guy's bp?

Winstrol? 97-03-12 VetACH I am not a big user of this stuff (like NEVER), but am considering using it in a recovering aortic thrombus kitty with some muscle atrophy and a crappy appetitite. Does anyone have any input on this use or on their clinical experiences with it in general? This cat is also on 30mg Cardizem CD s.i.d. and 81mg aspirin q. 3d. and is making good clinical improvement.

Is his inappetance and muscle loss due to anemia?

Did you start him on relion nph or humulin nph?

Re: Canine Hypertrophic CM 95-03-27 CORVET Paul, Let's look at this piece by piece. From your description it sounds like this dog is between 5 and 10 kg. Correct? If so the LV and RV chamber sizes are normal. The septal thickness is also within normal limits but the free wall is markedly thickened. This pattern of thickening makes aortic stenosis very unlikely and systemic hypertension also unlikely (although systemic hypertension in man can sometimes show up with just septal thickening). So what's left? Hypertrophic cardiomyopathy is a possibility. It's rare in the dog. Hormonal stimulation of hypertrophy (growth hormone, thyroid hormone) are possibilities. None of these are likely but could occur. A tumor of the LV free wall is also a possibility. Again, not likely but could occur. So we have an unusual presentation with a bunch of zebras for rule-outs. Should make it interesting. Can you measure blood pressure? Any other evidence of hormonal stimulation like evidence of diabetes, etc.? Is the thickening localized or is the echogenicity of the free wall different from the rest of the heart? As to how this relates to the dog's clinical signs, obviously it could be causing it or this could be an incidental finding. Do you hear any rhythm abnormality? What does the dog's ECG look like? It's hard to imagine that free wall hypertrophy alone could cause an outflow tract obstruction and so syncope. Consequently giving a beta blocker probably wouldn't do much from this standpoint. However, if the dog has a ventricular arrhythmia a beta blocker might help. If, on the other hand, it has a supraventricular tachyarrhythmia a beta blocker or a calcium channel blocker might help. Obviously a good neurological exam is in order also. Let us know what you think and/or find. Mark

With regards to the possible pressure problem, can you measure blood pressure in this dog?

The owner can accurately measure and then inject the insulin each time?

Homeopathy! 95-03-15

I presume this preparation is given orally?

Did lyddie belle have one or two palpable thyroid nodules?

Homeopathy! 95-03-15

How do 'immunostimulatory' proteins escape digestion in the stomach acid?

Can you post the entire bg curve?

Homeopathy! 95-03-15

How are they absorbed across the intestinal wall?

I'm guessing this is fall 2015, not 2014?

blood gases 95-03-19 Lboggs I need help! Will someone help me go through the logic in these blood gases? Diabetic/renal failure cat. Decompensated after dental work (and belongs to one of our receptionists) Signalment: Looks like hell Objective: Severe dehydrate. Emaciated. Normal heart and lung sounds. Normal abdominal palpation. Purulent discharge from nose and eyes. BUN >450, Creat 12, Glucose 818, Phos 18, WBC 23,000. Urine - no ketones, Glucose >1000, SG 1.015. 8:17 am: pH 7.02, pCO2 45, pO2 48 (I am absolutely positive this IS an arterial sample), HCO3 11.4 So, it is a metabolic acidosis without compensation. Is this cat not panting because it's too weak? Why is the pO2 so low? Is the dehydration causing poor lung perfusion? Decided to correct the dehydration and O2 deficit before doing anything else. After 300 ml NaCl and O2 hood for 2 hours.... 10:21 am: Venous sample: pH 7.01, pCO2 40, pO2 45, HCO3 9.9. Was too busy to look up much at the time. Protocol with the bypass machine calls for slow bolus of 2 mEq/kg bicarb when the pH is this low, so I gave 7 mEq bicarb. Later looked up the formula (base deficit X .9 X wt kg)...... correcting HCO3 to 15 would have called for 13 mEq --- 1/2 as bolus, 1/2 in fluids. So my guess was pretty close. 12:36 am: Venous sample: pH 7.07, pCO2 52, pO2 49, HCO3 14.6. The HCO3 looks better, but the pCO2 is higher. This is still a primary metabolic acidosis, but is also a respiratory acidosis. Why? Why is this cat not blowing off CO2? It was still on 100% O2. What would have been the best course of action here? I gave 7 mEq of bicarb. Was that overdoing it in light of the HCO3 level? Was I trying to correct the acidosis to rapidly? 3:38 pm: Arterial sample: pH 7.12, pCO2 40, pO2 75, HCO3 14.4. The pO2 is still very low for an animal on 100% O2. Hydration status seemed pretty good at this point.....why still poor oxygenation? I put 7 mEq in the fluids at this point. 8:27 am (next day): Arterial sample: pH 7.34, pCO2 26, pO2 81, HCO3 13.8. I was happy to leave well enough alone at this point. Please help me muddle through this.....most of this is new thought process and the neurons are all crackling and popping trying to learn new firing patterns :)

Wonder what the pao2 is in the aorta?

What brand is the owner's glucometer?

blood gases 95-03-19 Lboggs I need help! Will someone help me go through the logic in these blood gases? Diabetic/renal failure cat. Decompensated after dental work (and belongs to one of our receptionists) Signalment: Looks like hell Objective: Severe dehydrate. Emaciated. Normal heart and lung sounds. Normal abdominal palpation. Purulent discharge from nose and eyes. BUN >450, Creat 12, Glucose 818, Phos 18, WBC 23,000. Urine - no ketones, Glucose >1000, SG 1.015. 8:17 am: pH 7.02, pCO2 45, pO2 48 (I am absolutely positive this IS an arterial sample), HCO3 11.4 So, it is a metabolic acidosis without compensation. Is this cat not panting because it's too weak? Why is the pO2 so low? Is the dehydration causing poor lung perfusion? Decided to correct the dehydration and O2 deficit before doing anything else. After 300 ml NaCl and O2 hood for 2 hours.... 10:21 am: Venous sample: pH 7.01, pCO2 40, pO2 45, HCO3 9.9. Was too busy to look up much at the time. Protocol with the bypass machine calls for slow bolus of 2 mEq/kg bicarb when the pH is this low, so I gave 7 mEq bicarb. Later looked up the formula (base deficit X .9 X wt kg)...... correcting HCO3 to 15 would have called for 13 mEq --- 1/2 as bolus, 1/2 in fluids. So my guess was pretty close. 12:36 am: Venous sample: pH 7.07, pCO2 52, pO2 49, HCO3 14.6. The HCO3 looks better, but the pCO2 is higher. This is still a primary metabolic acidosis, but is also a respiratory acidosis. Why? Why is this cat not blowing off CO2? It was still on 100% O2. What would have been the best course of action here? I gave 7 mEq of bicarb. Was that overdoing it in light of the HCO3 level? Was I trying to correct the acidosis to rapidly? 3:38 pm: Arterial sample: pH 7.12, pCO2 40, pO2 75, HCO3 14.4. The pO2 is still very low for an animal on 100% O2. Hydration status seemed pretty good at this point.....why still poor oxygenation? I put 7 mEq in the fluids at this point. 8:27 am (next day): Arterial sample: pH 7.34, pCO2 26, pO2 81, HCO3 13.8. I was happy to leave well enough alone at this point. Please help me muddle through this.....most of this is new thought process and the neurons are all crackling and popping trying to learn new firing patterns :)

Do you have these values?

What is his bcs?

blood gases 95-03-19 Lboggs I need help! Will someone help me go through the logic in these blood gases? Diabetic/renal failure cat. Decompensated after dental work (and belongs to one of our receptionists) Signalment: Looks like hell Objective: Severe dehydrate. Emaciated. Normal heart and lung sounds. Normal abdominal palpation. Purulent discharge from nose and eyes. BUN >450, Creat 12, Glucose 818, Phos 18, WBC 23,000. Urine - no ketones, Glucose >1000, SG 1.015. 8:17 am: pH 7.02, pCO2 45, pO2 48 (I am absolutely positive this IS an arterial sample), HCO3 11.4 So, it is a metabolic acidosis without compensation. Is this cat not panting because it's too weak? Why is the pO2 so low? Is the dehydration causing poor lung perfusion? Decided to correct the dehydration and O2 deficit before doing anything else. After 300 ml NaCl and O2 hood for 2 hours.... 10:21 am: Venous sample: pH 7.01, pCO2 40, pO2 45, HCO3 9.9. Was too busy to look up much at the time. Protocol with the bypass machine calls for slow bolus of 2 mEq/kg bicarb when the pH is this low, so I gave 7 mEq bicarb. Later looked up the formula (base deficit X .9 X wt kg)...... correcting HCO3 to 15 would have called for 13 mEq --- 1/2 as bolus, 1/2 in fluids. So my guess was pretty close. 12:36 am: Venous sample: pH 7.07, pCO2 52, pO2 49, HCO3 14.6. The HCO3 looks better, but the pCO2 is higher. This is still a primary metabolic acidosis, but is also a respiratory acidosis. Why? Why is this cat not blowing off CO2? It was still on 100% O2. What would have been the best course of action here? I gave 7 mEq of bicarb. Was that overdoing it in light of the HCO3 level? Was I trying to correct the acidosis to rapidly? 3:38 pm: Arterial sample: pH 7.12, pCO2 40, pO2 75, HCO3 14.4. The pO2 is still very low for an animal on 100% O2. Hydration status seemed pretty good at this point.....why still poor oxygenation? I put 7 mEq in the fluids at this point. 8:27 am (next day): Arterial sample: pH 7.34, pCO2 26, pO2 81, HCO3 13.8. I was happy to leave well enough alone at this point. Please help me muddle through this.....most of this is new thought process and the neurons are all crackling and popping trying to learn new firing patterns :)

Risky?

Could have a uti (not simple cystitis but pyelonephritis)---we should culture the urine (maybe you did?

blood gases 95-03-19 Lboggs I need help! Will someone help me go through the logic in these blood gases? Diabetic/renal failure cat. Decompensated after dental work (and belongs to one of our receptionists) Signalment: Looks like hell Objective: Severe dehydrate. Emaciated. Normal heart and lung sounds. Normal abdominal palpation. Purulent discharge from nose and eyes. BUN >450, Creat 12, Glucose 818, Phos 18, WBC 23,000. Urine - no ketones, Glucose >1000, SG 1.015. 8:17 am: pH 7.02, pCO2 45, pO2 48 (I am absolutely positive this IS an arterial sample), HCO3 11.4 So, it is a metabolic acidosis without compensation. Is this cat not panting because it's too weak? Why is the pO2 so low? Is the dehydration causing poor lung perfusion? Decided to correct the dehydration and O2 deficit before doing anything else. After 300 ml NaCl and O2 hood for 2 hours.... 10:21 am: Venous sample: pH 7.01, pCO2 40, pO2 45, HCO3 9.9. Was too busy to look up much at the time. Protocol with the bypass machine calls for slow bolus of 2 mEq/kg bicarb when the pH is this low, so I gave 7 mEq bicarb. Later looked up the formula (base deficit X .9 X wt kg)...... correcting HCO3 to 15 would have called for 13 mEq --- 1/2 as bolus, 1/2 in fluids. So my guess was pretty close. 12:36 am: Venous sample: pH 7.07, pCO2 52, pO2 49, HCO3 14.6. The HCO3 looks better, but the pCO2 is higher. This is still a primary metabolic acidosis, but is also a respiratory acidosis. Why? Why is this cat not blowing off CO2? It was still on 100% O2. What would have been the best course of action here? I gave 7 mEq of bicarb. Was that overdoing it in light of the HCO3 level? Was I trying to correct the acidosis to rapidly? 3:38 pm: Arterial sample: pH 7.12, pCO2 40, pO2 75, HCO3 14.4. The pO2 is still very low for an animal on 100% O2. Hydration status seemed pretty good at this point.....why still poor oxygenation? I put 7 mEq in the fluids at this point. 8:27 am (next day): Arterial sample: pH 7.34, pCO2 26, pO2 81, HCO3 13.8. I was happy to leave well enough alone at this point. Please help me muddle through this.....most of this is new thought process and the neurons are all crackling and popping trying to learn new firing patterns :)

What is the base excess reported by the blood gas analyzer?

Was the dog diabetic first?

diabetic regulation problem 95-04-24

Is the lente recombinant human, or beef/pork, or beef?

If this is potentially diabetes insipidus, what do you recommend next?

Lufenuron 95-05-10 DVM I am sure I have seen this discussed here.......but I can't seem to put my hands on it. So I will ask. My sister has a 13yo m/n orange tabby that is diabetic. Any contraindications regarding lufenuron and diabetics? :)

Could you check with the ciba-geigy rep if they have heard any anecdotal or other reports of problems?

Large or small volume?

Re: DM, prerenal azotemia, hepat 95-08-09 Hypurr Ken, Yikes! This kitty was in tough shape! Good thing he came to see you. How's he doing today? What was his serum K+ at originally and on follow-up? I am very puzzled here and having a hard time getting a handle on this one. I hope that Alice or Chris or Dave or Duncan or, or, or ..... can see the forest for the trees here. Okay, we've got an obese, young adult, indoor NM cat in collapse with azotemia (I would call that a prerenal AND a renal azotemia, as the USG was 1.029), apparent hepatocellular injury and cholestasis, hyperglycemia and glucosuria, whose head is hanging (after therapy). Radiographically, no abnormalities are found. FeLV/FIV negative. He is started on insulin (type and amount and frequency?), fluids (type?) and IV KCl. He improves clinically and his insulin type and dose are changed to 3 units of NPH BID SC. His azotemia resolves (I would still be concerned about early renal insufficiency, although I confess that I am confused about how glucosuria affects urine SG....); repeat chemistries also show a resolution of the elevated liver enzymes, and his blood glucose has improved, even becoming normal. Potassium is low (value?). Appetite is fair and head is (still) hanging. It is great that you have used both the oral as well as IV KCl supplementation. :-) My questions are too many and my thoughts, confused/confusing. What is his T4? (I ask because of the elevated liver enzymes.) Did your lab run a gamma gt? I wonder about what degree of hepatic lipidosis is occurring....has to be some in an obese cat with an acute onset of inappetence/anorexia. What were the serum K+ levels? Did you get an amylase and lipase? Do you still have some serum in order to send some to Dave William's lab for a feline TLI? An abdominal ultrasound *might* be helpful wrt assessing the character of the pancreatic tissue and surrounding areas. I believe that with severe stress hyperglycemia, the renal threshold can be overwhelmed resulting in glucosuria. I don't know why we don't see it more often, though, as we do see so many cats with stress hyperglycemia. Is your lab running fructosamine levels or glycosolated hemoglobin? These would check is he was in fact diabetic prior to this incident. We don't (or at least *I* don't) know if this was a diabetic episode, the diagnosis of diabetes requiring the persistence of hyperglycemia and glycosuria. Fraid this gal has a wide open diagnostic list on this cat..... Maybe this was a case of a peracute pancreatitis who was lucky that his people noticed and that *you* are his doctor! I know we can and should say the latter. >M>

Did the kitty have any signs prior to this crash?

What does the cat weigh?

Re: Hypertension, Norvasc, Diabetes 95-08-12 K9DOC Lauren: Tough case, one of those where you have 3 balls up in the air juggling at once.... changing meds is sort of like trying to even up a chair by sawing a little off one leg at a time. If the cat needs pred for the IBD it is apparently going to have clinical diabetes mellitus. I'd recommend starting insulin therapy at a conservative level (1-2 units NPH BID) for starters and adjusting as needed from there to control BG and symptomatology. From the BP report, the Norvasc seems to be controlling the hypertension pretty well and I don't believe the drug is contributing to the diabetes although it may be increasing the azotemia somewhat. At this level of Creat, it's not likely to be clinically significant at this time but this should be watched. You've done a very nice job with management of all this cat's problems so far. Let's see what others think too.

May i ask why you chose norvasc (amlodipine) over enalapril in this case?

Has she had a urine culture yet?

Diabetes and Ovaban 95-08-15 Texvet A relief vet at my hospital prescribed a reducing dosage of Ovaban over a 6 week period beginning June 10 th for a 5 year old male cat with inappropriate urination behavior. The cat returned Saturday with a complaint of defecating in the front hallway of the home. The cat had loss 2.5 lbs (it is still 13 lbs) since that time. I did a UA and had mega glucose and some ketones. The basic profile showed a blood glucose of 415 and moderate elevation of liver enzymes. Should I treat this cat with insulin or 'monitor' it for a while and see with it spontaneously resolves. It has been off of Ovaban for 2 weeks. Larry

Is he eating okay?

So who knows?

Diabetes and Ovaban 95-08-15 Texvet A relief vet at my hospital prescribed a reducing dosage of Ovaban over a 6 week period beginning June 10 th for a 5 year old male cat with inappropriate urination behavior. The cat returned Saturday with a complaint of defecating in the front hallway of the home. The cat had loss 2.5 lbs (it is still 13 lbs) since that time. I did a UA and had mega glucose and some ketones. The basic profile showed a blood glucose of 415 and moderate elevation of liver enzymes. Should I treat this cat with insulin or 'monitor' it for a while and see with it spontaneously resolves. It has been off of Ovaban for 2 weeks. Larry

Have they resolved?

Do you think that he is reasonably well controlled?

Diabetes and Ovaban 95-08-15 Texvet A relief vet at my hospital prescribed a reducing dosage of Ovaban over a 6 week period beginning June 10 th for a 5 year old male cat with inappropriate urination behavior. The cat returned Saturday with a complaint of defecating in the front hallway of the home. The cat had loss 2.5 lbs (it is still 13 lbs) since that time. I did a UA and had mega glucose and some ketones. The basic profile showed a blood glucose of 415 and moderate elevation of liver enzymes. Should I treat this cat with insulin or 'monitor' it for a while and see with it spontaneously resolves. It has been off of Ovaban for 2 weeks. Larry

Did the relief vet do a u/a initially?

Is she moving the injections around on his body every day?

Diabetes and Ovaban 95-08-15 Texvet A relief vet at my hospital prescribed a reducing dosage of Ovaban over a 6 week period beginning June 10 th for a 5 year old male cat with inappropriate urination behavior. The cat returned Saturday with a complaint of defecating in the front hallway of the home. The cat had loss 2.5 lbs (it is still 13 lbs) since that time. I did a UA and had mega glucose and some ketones. The basic profile showed a blood glucose of 415 and moderate elevation of liver enzymes. Should I treat this cat with insulin or 'monitor' it for a while and see with it spontaneously resolves. It has been off of Ovaban for 2 weeks. Larry

Are kitty's people open to the idea of neutering him once he is better?

How long ago did he become diabetic?

Diabetes and Ovaban 95-08-15 Texvet A relief vet at my hospital prescribed a reducing dosage of Ovaban over a 6 week period beginning June 10 th for a 5 year old male cat with inappropriate urination behavior. The cat returned Saturday with a complaint of defecating in the front hallway of the home. The cat had loss 2.5 lbs (it is still 13 lbs) since that time. I did a UA and had mega glucose and some ketones. The basic profile showed a blood glucose of 415 and moderate elevation of liver enzymes. Should I treat this cat with insulin or 'monitor' it for a while and see with it spontaneously resolves. It has been off of Ovaban for 2 weeks. Larry

Please let us know?

Have you done skin scrapings?

Re: Diabetic Cat 95-08-23 Ozvet Bill, Looks like a hypoglycemia-induced hyperglycemia (Somogyi) problem--that is, too much insulin. I would back off the insulin dose to 2 or 3 units q12h, stick with free choice w/d, and recheck a glucose curve in 3-5 s. Interesting, please keep us posted.

Are you, in fact, seeing a rebound due to too much insulin?

Has the cat continued to lose weight?

DSH with Hyperglobulinemia 95-08-28 PBvet I have recently seen a 7 year old, neutered male DSH (Toby), who has been seen here for FBA 2 months ago-given delvosterone for that and Tiguvon. He has presented again with a marked plantigrade hindlimb stance, weight loss (eating well) some polydipsia (never used to drink water, but now does), chy but widespread alopecia esp. ventrum. Temperature normal, bright but listless compared to his former self. He is an indoor cat primarily in a single cat household. Palion of abdomen revealed no abnormal masses, kidneys smooth and normal size. I took some bloods and sent away for biochem and hematology which have come back showing a marked hyperglobulinemia, slightly elevated urea and creatinine, liver enzymes all normal, calcium slightly elevated. Hematology shows a low hemoglobin (8.3g/dl) and a low MCHC (27.3g/dl) but PCV and others are WNL. A lymphopenia (26%) was also present (stress?). The comment was made that red cells showed marked rouleaux formation. No Haemobartonella was seen. I admit that I have not tested for FeLV/FIV, but will be doing so as soon as the shop opens again tomorrow (we've had a 'bank holiday weekend' and this was my last client in on Friday). I was sure (almost) that the cat would turn out to be diabetic, but glucose is WNL(not done urine, just blood). Any of you feline practitioners have any insights that might guide me (aside from the importance of assessing viral status-slap hand!). TIA, P

Also, as i recall, tiguvon is an organophosphate?

Again, maybe we shouldn't be taking cats off meds?

DSH with Hyperglobulinemia 95-08-28 PBvet I have recently seen a 7 year old, neutered male DSH (Toby), who has been seen here for FBA 2 months ago-given delvosterone for that and Tiguvon. He has presented again with a marked plantigrade hindlimb stance, weight loss (eating well) some polydipsia (never used to drink water, but now does), chy but widespread alopecia esp. ventrum. Temperature normal, bright but listless compared to his former self. He is an indoor cat primarily in a single cat household. Palion of abdomen revealed no abnormal masses, kidneys smooth and normal size. I took some bloods and sent away for biochem and hematology which have come back showing a marked hyperglobulinemia, slightly elevated urea and creatinine, liver enzymes all normal, calcium slightly elevated. Hematology shows a low hemoglobin (8.3g/dl) and a low MCHC (27.3g/dl) but PCV and others are WNL. A lymphopenia (26%) was also present (stress?). The comment was made that red cells showed marked rouleaux formation. No Haemobartonella was seen. I admit that I have not tested for FeLV/FIV, but will be doing so as soon as the shop opens again tomorrow (we've had a 'bank holiday weekend' and this was my last client in on Friday). I was sure (almost) that the cat would turn out to be diabetic, but glucose is WNL(not done urine, just blood). Any of you feline practitioners have any insights that might guide me (aside from the importance of assessing viral status-slap hand!). TIA, P

Same as spotton?

Can you post the actual curves for 12/9 and 12/17?

Lactulose and Hypercalcemia? 95-09-07 JGug We've been treating a constipated DSH 14 yr old m/c with lactulose at 1 cc bid. In early August he developed diabetes mel. and was started on Humulin U sid (that's going well). After an episode of constipation that required hospitalization, enemas, etc, his lactulose dose was increased to 5ml bid-TID to effect. (He weighs 19.7#) About a week later he re-presented for depression and loss of appetite. Was not constipated, having regular, sl softish to firm stools, his diabetes was loosely controlled (191). We treated him for mild dehydration with LRS while awaiting bloodwork, switched from lactulose to Vetasyl 'just in case.' He perked up (got mean again!) and started to eat. But his bloodwork showed a Ca level of 16.5 (corrected to 16). We repeated a Ca and found it was 13.5 (8.10-11.6) on our VetTest after 1 day of LRS, so we started saline diuresis and went hunting for cause: renal fx fine, films NSF. A Cat Doctor friend of mine heard this history and said he had seen at least a half dozen cats on lactulose, esp at higher doses (5cc bid), develop hypercalcemia. His sick patients also presented for vague lethargy, inappetence. He says he sees it often enough that he now routinely checks a chem 10 days after starting lactulose at hi doses. Have any of you seen this? Does anyone have an explanation of why this might occur? Thanks to you all!

*could he have been mildly ketoacidotic when he presented with the soft-stools, depression and loss of appetite?

Do you have a glucose curve or just the spot check on panel?

Lactulose and Hypercalcemia? 95-09-07 JGug We've been treating a constipated DSH 14 yr old m/c with lactulose at 1 cc bid. In early August he developed diabetes mel. and was started on Humulin U sid (that's going well). After an episode of constipation that required hospitalization, enemas, etc, his lactulose dose was increased to 5ml bid-TID to effect. (He weighs 19.7#) About a week later he re-presented for depression and loss of appetite. Was not constipated, having regular, sl softish to firm stools, his diabetes was loosely controlled (191). We treated him for mild dehydration with LRS while awaiting bloodwork, switched from lactulose to Vetasyl 'just in case.' He perked up (got mean again!) and started to eat. But his bloodwork showed a Ca level of 16.5 (corrected to 16). We repeated a Ca and found it was 13.5 (8.10-11.6) on our VetTest after 1 day of LRS, so we started saline diuresis and went hunting for cause: renal fx fine, films NSF. A Cat Doctor friend of mine heard this history and said he had seen at least a half dozen cats on lactulose, esp at higher doses (5cc bid), develop hypercalcemia. His sick patients also presented for vague lethargy, inappetence. He says he sees it often enough that he now routinely checks a chem 10 days after starting lactulose at hi doses. Have any of you seen this? Does anyone have an explanation of why this might occur? Thanks to you all!

What was his serum phosphorus?

The owner is gently rolling the nph until it's fully reconstituted?

Seizures 95-11-22 SASDVM I have a 4 yr. old, obese, Norwegian Elkhound ient that has seizures and is not being controlled with Phenobarbital. She weighs 80 lbs and I have increased her dosage (in increments) from 50 mg BID to 100 mg BID. She is still having seizures and is also PU/PD and polyphagic!! I plan to add KBr and slightly decrease her Phenobarbital at this point. The owner is sure she is becoming hypoglycemic so is not feeding strictly r/d. The husband is a diabetic and so they have the ability to test her blood glucose during a seizure which they may try to do. Previous CBC and Profiles have been normal and her most recent Phenobarb level was 30 on 11/20/95 while taking 100 mg. BID. Several concerns are: 1. The dog has what appears to be a fluid filled cyst on top of her head that seems to wax and wane on a 28-30 day schedule which coincides with the dogs seizure activity. Any possible connection? 2. I had the owners give 10 mg of diazepam starting around the time that the seizures were expected to try to prevent them. This appeared to delay the seizure but instead of having one moderate seizure the dog had 3-4 mild seizures and now is on a different 30 day cycle. Any thoughts will be appreciated, especially concerning the fluid filled cyst which enlarges over the 30 days then starts to drain and go down just prior to a seizure!!!!!! p

What would you guess the dog should really weigh?

Frustrating case, but i think you have a lot of great ideas for how to approach this! when was sasha's incontinence first diagnosed?

Seizures 95-11-22 SASDVM I have a 4 yr. old, obese, Norwegian Elkhound ient that has seizures and is not being controlled with Phenobarbital. She weighs 80 lbs and I have increased her dosage (in increments) from 50 mg BID to 100 mg BID. She is still having seizures and is also PU/PD and polyphagic!! I plan to add KBr and slightly decrease her Phenobarbital at this point. The owner is sure she is becoming hypoglycemic so is not feeding strictly r/d. The husband is a diabetic and so they have the ability to test her blood glucose during a seizure which they may try to do. Previous CBC and Profiles have been normal and her most recent Phenobarb level was 30 on 11/20/95 while taking 100 mg. BID. Several concerns are: 1. The dog has what appears to be a fluid filled cyst on top of her head that seems to wax and wane on a 28-30 day schedule which coincides with the dogs seizure activity. Any possible connection? 2. I had the owners give 10 mg of diazepam starting around the time that the seizures were expected to try to prevent them. This appeared to delay the seizure but instead of having one moderate seizure the dog had 3-4 mild seizures and now is on a different 30 day cycle. Any thoughts will be appreciated, especially concerning the fluid filled cyst which enlarges over the 30 days then starts to drain and go down just prior to a seizure!!!!!! p

How long after giving a pb tab was the blood drawn for the blood level?

Are you using a high protein low carb diet?

Seizures 95-11-22 SASDVM I have a 4 yr. old, obese, Norwegian Elkhound ient that has seizures and is not being controlled with Phenobarbital. She weighs 80 lbs and I have increased her dosage (in increments) from 50 mg BID to 100 mg BID. She is still having seizures and is also PU/PD and polyphagic!! I plan to add KBr and slightly decrease her Phenobarbital at this point. The owner is sure she is becoming hypoglycemic so is not feeding strictly r/d. The husband is a diabetic and so they have the ability to test her blood glucose during a seizure which they may try to do. Previous CBC and Profiles have been normal and her most recent Phenobarb level was 30 on 11/20/95 while taking 100 mg. BID. Several concerns are: 1. The dog has what appears to be a fluid filled cyst on top of her head that seems to wax and wane on a 28-30 day schedule which coincides with the dogs seizure activity. Any possible connection? 2. I had the owners give 10 mg of diazepam starting around the time that the seizures were expected to try to prevent them. This appeared to delay the seizure but instead of having one moderate seizure the dog had 3-4 mild seizures and now is on a different 30 day cycle. Any thoughts will be appreciated, especially concerning the fluid filled cyst which enlarges over the 30 days then starts to drain and go down just prior to a seizure!!!!!! p

Have you checked her for cushing's disease?

Was cortrosyn used?

Seizures 95-11-22 SASDVM I have a 4 yr. old, obese, Norwegian Elkhound ient that has seizures and is not being controlled with Phenobarbital. She weighs 80 lbs and I have increased her dosage (in increments) from 50 mg BID to 100 mg BID. She is still having seizures and is also PU/PD and polyphagic!! I plan to add KBr and slightly decrease her Phenobarbital at this point. The owner is sure she is becoming hypoglycemic so is not feeding strictly r/d. The husband is a diabetic and so they have the ability to test her blood glucose during a seizure which they may try to do. Previous CBC and Profiles have been normal and her most recent Phenobarb level was 30 on 11/20/95 while taking 100 mg. BID. Several concerns are: 1. The dog has what appears to be a fluid filled cyst on top of her head that seems to wax and wane on a 28-30 day schedule which coincides with the dogs seizure activity. Any possible connection? 2. I had the owners give 10 mg of diazepam starting around the time that the seizures were expected to try to prevent them. This appeared to delay the seizure but instead of having one moderate seizure the dog had 3-4 mild seizures and now is on a different 30 day cycle. Any thoughts will be appreciated, especially concerning the fluid filled cyst which enlarges over the 30 days then starts to drain and go down just prior to a seizure!!!!!! p

How long have they noticed it, has there been a history of trauma, does the skull pale normally?

Can you post the whole chem screen at the beginning?

Seizures 95-11-22 SASDVM I have a 4 yr. old, obese, Norwegian Elkhound ient that has seizures and is not being controlled with Phenobarbital. She weighs 80 lbs and I have increased her dosage (in increments) from 50 mg BID to 100 mg BID. She is still having seizures and is also PU/PD and polyphagic!! I plan to add KBr and slightly decrease her Phenobarbital at this point. The owner is sure she is becoming hypoglycemic so is not feeding strictly r/d. The husband is a diabetic and so they have the ability to test her blood glucose during a seizure which they may try to do. Previous CBC and Profiles have been normal and her most recent Phenobarb level was 30 on 11/20/95 while taking 100 mg. BID. Several concerns are: 1. The dog has what appears to be a fluid filled cyst on top of her head that seems to wax and wane on a 28-30 day schedule which coincides with the dogs seizure activity. Any possible connection? 2. I had the owners give 10 mg of diazepam starting around the time that the seizures were expected to try to prevent them. This appeared to delay the seizure but instead of having one moderate seizure the dog had 3-4 mild seizures and now is on a different 30 day cycle. Any thoughts will be appreciated, especially concerning the fluid filled cyst which enlarges over the 30 days then starts to drain and go down just prior to a seizure!!!!!! p

When you say it 'drains' do you mean literally opens to the outside and drains out fluid like a seroma or that it decreases in size without external drainage of fluid?

How many calories/day is he currently getting?

Seizures 95-11-22 SASDVM I have a 4 yr. old, obese, Norwegian Elkhound ient that has seizures and is not being controlled with Phenobarbital. She weighs 80 lbs and I have increased her dosage (in increments) from 50 mg BID to 100 mg BID. She is still having seizures and is also PU/PD and polyphagic!! I plan to add KBr and slightly decrease her Phenobarbital at this point. The owner is sure she is becoming hypoglycemic so is not feeding strictly r/d. The husband is a diabetic and so they have the ability to test her blood glucose during a seizure which they may try to do. Previous CBC and Profiles have been normal and her most recent Phenobarb level was 30 on 11/20/95 while taking 100 mg. BID. Several concerns are: 1. The dog has what appears to be a fluid filled cyst on top of her head that seems to wax and wane on a 28-30 day schedule which coincides with the dogs seizure activity. Any possible connection? 2. I had the owners give 10 mg of diazepam starting around the time that the seizures were expected to try to prevent them. This appeared to delay the seizure but instead of having one moderate seizure the dog had 3-4 mild seizures and now is on a different 30 day cycle. Any thoughts will be appreciated, especially concerning the fluid filled cyst which enlarges over the 30 days then starts to drain and go down just prior to a seizure!!!!!! p

Can you feel open fontanelles on this dog, i.e. a hydrocephalic with a meningocele?

Can you post the actual ultrasound report?

Seizures 95-11-22 SASDVM I have a 4 yr. old, obese, Norwegian Elkhound ient that has seizures and is not being controlled with Phenobarbital. She weighs 80 lbs and I have increased her dosage (in increments) from 50 mg BID to 100 mg BID. She is still having seizures and is also PU/PD and polyphagic!! I plan to add KBr and slightly decrease her Phenobarbital at this point. The owner is sure she is becoming hypoglycemic so is not feeding strictly r/d. The husband is a diabetic and so they have the ability to test her blood glucose during a seizure which they may try to do. Previous CBC and Profiles have been normal and her most recent Phenobarb level was 30 on 11/20/95 while taking 100 mg. BID. Several concerns are: 1. The dog has what appears to be a fluid filled cyst on top of her head that seems to wax and wane on a 28-30 day schedule which coincides with the dogs seizure activity. Any possible connection? 2. I had the owners give 10 mg of diazepam starting around the time that the seizures were expected to try to prevent them. This appeared to delay the seizure but instead of having one moderate seizure the dog had 3-4 mild seizures and now is on a different 30 day cycle. Any thoughts will be appreciated, especially concerning the fluid filled cyst which enlarges over the 30 days then starts to drain and go down just prior to a seizure!!!!!! p

Can you get an mri on the head to see what is going on?

I may be remembering incorrectly but doesn't pseudomonas have a fruity odor?

Seizures 95-11-22 SASDVM I have a 4 yr. old, obese, Norwegian Elkhound ient that has seizures and is not being controlled with Phenobarbital. She weighs 80 lbs and I have increased her dosage (in increments) from 50 mg BID to 100 mg BID. She is still having seizures and is also PU/PD and polyphagic!! I plan to add KBr and slightly decrease her Phenobarbital at this point. The owner is sure she is becoming hypoglycemic so is not feeding strictly r/d. The husband is a diabetic and so they have the ability to test her blood glucose during a seizure which they may try to do. Previous CBC and Profiles have been normal and her most recent Phenobarb level was 30 on 11/20/95 while taking 100 mg. BID. Several concerns are: 1. The dog has what appears to be a fluid filled cyst on top of her head that seems to wax and wane on a 28-30 day schedule which coincides with the dogs seizure activity. Any possible connection? 2. I had the owners give 10 mg of diazepam starting around the time that the seizures were expected to try to prevent them. This appeared to delay the seizure but instead of having one moderate seizure the dog had 3-4 mild seizures and now is on a different 30 day cycle. Any thoughts will be appreciated, especially concerning the fluid filled cyst which enlarges over the 30 days then starts to drain and go down just prior to a seizure!!!!!! p

Anyone else have any ideas?

What is the weight of the cat?

Nephrogenic diabetes insi 95-11-14 Schubvet Water dep test as per Feldman/Nelson restricted H2O intake three days, took till greater than 5% bw loss, urine osmolality at that time 284. No change in urine osmolality for 2 hrs after ADH.

Can severe glomerular nephritis (now resolved) result in diabetes insipidis?

Concerned about pancreatitis?

Nephrogenic diabetes insi 95-11-14 Schubvet Water dep test as per Feldman/Nelson restricted H2O intake three days, took till greater than 5% bw loss, urine osmolality at that time 284. No change in urine osmolality for 2 hrs after ADH.

Predispose a pet to glomerular nephritis?

Maybe apoquel?

diab: fallen & can't get up 96-01-18 MVYVET 12 year old F/S Samoyed. Has been a patient for about a year, dog is diabetic and owner has been giving 27 u NPH q 24 for years (on the days he remembers) and has steadfastly refused to hear about regulating her better. Big surprise, she's blind - cataracts plus some form of corneal dystrophy. Has had trouble with intermittent lameness and hindend weakness for over a year and has been on bute 200 mg bid or prn with presumptive dx of DJD. Owner called 1/15 saying dog was having hypoglycemic episode. She was out in the snow (loose on a job site, oy). He wasn't sure how long, thought she might be seizuring. He had given her a little karo, some cream and some chocolate. It sounded as though she were conscious so I told him to give her a good dose of karo and check back in 10 minutes. No better. She arrived seizuring, no other signs. Impossible to check pupils due to corneal abmornalities. Owner says he didn't think he got much karo into her ('she didn't swallow it') Blood Glucose (glucometer >400). T=104.2. I wasn't sure whether the seizures were diabetes related. Treated with iv diazepam and then on to pentobarb to control. Dipyrone for pyrexia and 25 mg Dexameth iv in case this was some sort of primary CNS (I know this complicates diabetic situation but it seemed like the thing to do at the time.) Started on Multisol R. Temp stayed > 104 for 24 hours so we started Doxycycline too (tick heaven here) Lab: CBC-WNL, Creat, GGT, ALT, TBil, TP, Glob, Ca, alb, amyl, all basically normal BUN- 57 (5-23), Phos 9.36 (2.5-5.5) , alkphos 1646 (0-400) Had lytes done by hospital Na=148, K=4.8, Cl=114, Co2=18.3 Dog is now well-regulated on 17 units of Lente, eating well, B & A. I have her on Doxycycline , Bute, Glycoflex. Problem is she can't stand up. She seems stronger each day and will sit up but even when we sling her up she can only support her weight for 30 seconds or so. Seems to knuckle on R hind although reflexes normal. I can't decide if this weakness is musculoskeletal , metabolic or CNS. If she weren't diabetic I'd use iv dex. I'm considering adequan. But I need her to be up and walking asap. Any suggestions on next steps or safe meds to try with diabetic? TIA, MGJ

Is the dog painful at all in the rear?

O had already declined referral)?

diab: fallen & can't get up 96-01-18 MVYVET 12 year old F/S Samoyed. Has been a patient for about a year, dog is diabetic and owner has been giving 27 u NPH q 24 for years (on the days he remembers) and has steadfastly refused to hear about regulating her better. Big surprise, she's blind - cataracts plus some form of corneal dystrophy. Has had trouble with intermittent lameness and hindend weakness for over a year and has been on bute 200 mg bid or prn with presumptive dx of DJD. Owner called 1/15 saying dog was having hypoglycemic episode. She was out in the snow (loose on a job site, oy). He wasn't sure how long, thought she might be seizuring. He had given her a little karo, some cream and some chocolate. It sounded as though she were conscious so I told him to give her a good dose of karo and check back in 10 minutes. No better. She arrived seizuring, no other signs. Impossible to check pupils due to corneal abmornalities. Owner says he didn't think he got much karo into her ('she didn't swallow it') Blood Glucose (glucometer >400). T=104.2. I wasn't sure whether the seizures were diabetes related. Treated with iv diazepam and then on to pentobarb to control. Dipyrone for pyrexia and 25 mg Dexameth iv in case this was some sort of primary CNS (I know this complicates diabetic situation but it seemed like the thing to do at the time.) Started on Multisol R. Temp stayed > 104 for 24 hours so we started Doxycycline too (tick heaven here) Lab: CBC-WNL, Creat, GGT, ALT, TBil, TP, Glob, Ca, alb, amyl, all basically normal BUN- 57 (5-23), Phos 9.36 (2.5-5.5) , alkphos 1646 (0-400) Had lytes done by hospital Na=148, K=4.8, Cl=114, Co2=18.3 Dog is now well-regulated on 17 units of Lente, eating well, B & A. I have her on Doxycycline , Bute, Glycoflex. Problem is she can't stand up. She seems stronger each day and will sit up but even when we sling her up she can only support her weight for 30 seconds or so. Seems to knuckle on R hind although reflexes normal. I can't decide if this weakness is musculoskeletal , metabolic or CNS. If she weren't diabetic I'd use iv dex. I'm considering adequan. But I need her to be up and walking asap. Any suggestions on next steps or safe meds to try with diabetic? TIA, MGJ

In the rear limbs are the patella and sciatic reflexes symmetrical?

When was the last culture?

diab: fallen & can't get up 96-01-18 MVYVET 12 year old F/S Samoyed. Has been a patient for about a year, dog is diabetic and owner has been giving 27 u NPH q 24 for years (on the days he remembers) and has steadfastly refused to hear about regulating her better. Big surprise, she's blind - cataracts plus some form of corneal dystrophy. Has had trouble with intermittent lameness and hindend weakness for over a year and has been on bute 200 mg bid or prn with presumptive dx of DJD. Owner called 1/15 saying dog was having hypoglycemic episode. She was out in the snow (loose on a job site, oy). He wasn't sure how long, thought she might be seizuring. He had given her a little karo, some cream and some chocolate. It sounded as though she were conscious so I told him to give her a good dose of karo and check back in 10 minutes. No better. She arrived seizuring, no other signs. Impossible to check pupils due to corneal abmornalities. Owner says he didn't think he got much karo into her ('she didn't swallow it') Blood Glucose (glucometer >400). T=104.2. I wasn't sure whether the seizures were diabetes related. Treated with iv diazepam and then on to pentobarb to control. Dipyrone for pyrexia and 25 mg Dexameth iv in case this was some sort of primary CNS (I know this complicates diabetic situation but it seemed like the thing to do at the time.) Started on Multisol R. Temp stayed > 104 for 24 hours so we started Doxycycline too (tick heaven here) Lab: CBC-WNL, Creat, GGT, ALT, TBil, TP, Glob, Ca, alb, amyl, all basically normal BUN- 57 (5-23), Phos 9.36 (2.5-5.5) , alkphos 1646 (0-400) Had lytes done by hospital Na=148, K=4.8, Cl=114, Co2=18.3 Dog is now well-regulated on 17 units of Lente, eating well, B & A. I have her on Doxycycline , Bute, Glycoflex. Problem is she can't stand up. She seems stronger each day and will sit up but even when we sling her up she can only support her weight for 30 seconds or so. Seems to knuckle on R hind although reflexes normal. I can't decide if this weakness is musculoskeletal , metabolic or CNS. If she weren't diabetic I'd use iv dex. I'm considering adequan. But I need her to be up and walking asap. Any suggestions on next steps or safe meds to try with diabetic? TIA, MGJ

Does the dog have good withdrawl and deep pain?

Could you post the complete histopath description?

diab: fallen & can't get up 96-01-18 MVYVET 12 year old F/S Samoyed. Has been a patient for about a year, dog is diabetic and owner has been giving 27 u NPH q 24 for years (on the days he remembers) and has steadfastly refused to hear about regulating her better. Big surprise, she's blind - cataracts plus some form of corneal dystrophy. Has had trouble with intermittent lameness and hindend weakness for over a year and has been on bute 200 mg bid or prn with presumptive dx of DJD. Owner called 1/15 saying dog was having hypoglycemic episode. She was out in the snow (loose on a job site, oy). He wasn't sure how long, thought she might be seizuring. He had given her a little karo, some cream and some chocolate. It sounded as though she were conscious so I told him to give her a good dose of karo and check back in 10 minutes. No better. She arrived seizuring, no other signs. Impossible to check pupils due to corneal abmornalities. Owner says he didn't think he got much karo into her ('she didn't swallow it') Blood Glucose (glucometer >400). T=104.2. I wasn't sure whether the seizures were diabetes related. Treated with iv diazepam and then on to pentobarb to control. Dipyrone for pyrexia and 25 mg Dexameth iv in case this was some sort of primary CNS (I know this complicates diabetic situation but it seemed like the thing to do at the time.) Started on Multisol R. Temp stayed > 104 for 24 hours so we started Doxycycline too (tick heaven here) Lab: CBC-WNL, Creat, GGT, ALT, TBil, TP, Glob, Ca, alb, amyl, all basically normal BUN- 57 (5-23), Phos 9.36 (2.5-5.5) , alkphos 1646 (0-400) Had lytes done by hospital Na=148, K=4.8, Cl=114, Co2=18.3 Dog is now well-regulated on 17 units of Lente, eating well, B & A. I have her on Doxycycline , Bute, Glycoflex. Problem is she can't stand up. She seems stronger each day and will sit up but even when we sling her up she can only support her weight for 30 seconds or so. Seems to knuckle on R hind although reflexes normal. I can't decide if this weakness is musculoskeletal , metabolic or CNS. If she weren't diabetic I'd use iv dex. I'm considering adequan. But I need her to be up and walking asap. Any suggestions on next steps or safe meds to try with diabetic? TIA, MGJ

Is anal tone ok and can the dog urinate and defecate normally?

Is the cat on the dry or canned form?

Von Willebrands question 95-11-22 CHAIMLIT Some advice please I 'm about to castrate a 7 month old 70lb Doberman and I recently ran a Von Willebrands test with VRA. The result was 1% (70-180%). 'This result indicates carrier range.' What's the significance of the 1% value? Do I need fresh frozen plasma and DDVAp prior to surgery? I don't have the equipment for a buccal bleeding time. Is that the' ideal' way to screen this? Thanks in advance and happy holi C. Litwin

Does you patient have any history of bleeding, for example associated with teeth loss or ear cropping?

Can you post the ultrasound report for 2/5 and the cytology report?

Von Willebrands question 95-11-22 CHAIMLIT Some advice please I 'm about to castrate a 7 month old 70lb Doberman and I recently ran a Von Willebrands test with VRA. The result was 1% (70-180%). 'This result indicates carrier range.' What's the significance of the 1% value? Do I need fresh frozen plasma and DDVAp prior to surgery? I don't have the equipment for a buccal bleeding time. Is that the' ideal' way to screen this? Thanks in advance and happy holi C. Litwin

The plan of attack?

Are you familiar with using calcitriol?

glipizide? 95-10-20 MVYVET I have a client with a 19 y.o. F/S Himalayan recently diagnosed as diabetic. Fasting blood glucoses ranging from 275 to >400. The owner is not willing to consider insulin injections. The cat won't eat WD. She is not obese but not particularly thin. We made the diagnosis on a profile drawn simply because the cat was yowling a lot at night. I was actually expecting her to be hyperthyroid but she's not. Only other abnormalities are a grade III/VI murmer and a BUN of 78 (creat. normal) Owners are interested in oral hypoglycemics to try to prolong her comfortable life and see if yowling resolves with tx. I have explained that glipizide works in less than 1/2 of cases and they're still interested. I read the literature on VIN but what I can't figure out is whether I could do this cat any HARM by trying it. I got the vague impression that, if it works, we might 'wear out' her remaining b-cells faster and end up in worse shape. Comments? Thanks, MGJ

What was the t4 level?

I'd put her on calcitriol (familiar with using this?

Re: Feline diabetes melitis 95-11-13 K9DOC Fred: How much does the cat weigh now? What Humulin type are you using? If NPH, most cats will regulate somewhere around 0.25 - 0.50 Unit/lb but some need a bit more. If Ultralente, many cats need up to or over 1 unit/lb to get regulated and frankly, because of its unpredicitability, I've stopped using the ultralente.

Oh yeah, what does your curve look like?

How is she doing clinically now?

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?

Did the timing of the exploratory seem apropriate?

Is he also diabetic?

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: -why did you run a fecal at the onset?

Have you changed your dose secondary to the weight gain?

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:- could there also have been more going on?

Is the cat pu/pd?

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?

What does your pathologist mean by 'hepatocellular degeneration'?

That he eats the same number of calories with each meal (how many calories/meal does he currently get?)   what should he weigh?

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?

Was there evidence at this point of hepatic lipidosis?

Medial, lateral, ventral medial etc?

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?

Sooner, later, not at all?

And the mornings of the curves, she's getting the insulin/food at home that morning, then she gets dropped off for you to start the curve?

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: what was his urine specific gravity?

What is going on here?

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?

Do we know for sure that arnie was in arf?

I'm not sure where your endocrine lab is in canada?

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?

Did the hetastarch cause severe dilution of alb and phos by pulling interstitial fluid into the blood vessels?

What is the actual value of the up:uc?

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?

Is there another cause of the severe hypophosphatemia?

What's the total protein?

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?

Any better ideas on the treatment of hypophosphatemia and iv hemolytic anemia?

How many calories/day does he currently get?