Intravenous administration of levothyroxine for treatment of suspected myxedema coma complicated by severe hypothermia in a dog.

A 7-year-old male English Coonhound with suspected myxedema coma complicated by severe hypothermia and metabolic abnormalities was treated with a combination of active external and core rewarming techniques, i.v. and oral administration of levothyroxine, supplemental oxygen, and administration of fluids (0.9% NaCl solution). Myxedema coma develops as a consequence of severe hypothyroidism and is characterized by a hypometabolic, stuporous state. Myxedema coma is associated with a high mortality rate, and most reported cases have involved Doberman Pinschers. Intravenous administration of levothyroxine can be used successfully in combination with oral administration to restore normal metabolic function and assist in warming and thermoregulation, although dosages should be conservative to avoid adverse cardiovascular effects.

Pericardial effusion and cardiac tamponade secondary to brodifacoum toxicosis in a dog.

Hemorrhage resulting from ingestion of anticoagulant rodenticides may be evident at any traumatized site or in any body cavity. It is important for clinicians to include coagulopathies among the differential diagnoses for pericardial effusion and to evaluate clotting function before routine pericardiocentesis is performed.

Rickets caused by excessive renal phosphate loss and apparent abnormal vitamin D metabolism in a cat.

Rickets was diagnosed in a 1-year-old cat with a history of weakness, osteopenia, and recurrent fractures. Processes causing rickets include vitamin D deficiency caused by inadequate, nutrition, lack of exposure to sunlight, defective metabolism of parent vitamin D to active metabolites, inherited vitamin D receptor defects, hypoparathyroidism, chronic renal failure, renal loss of phosphate, or malabsorptive states resulting from gastrointestinal or hepatic diseases. On the basis of analysis of serum 25-hydroxyvitamin D3 and 1,25-dihydroxyvitamin D2 and D3 concentrations, serum biochemical analysis, and urinary fractional clearance of electrolytes, the causes of rickets in our cat, were most compatible with a combination of excessive loss of phosphorus via the kidneys and deficient or abnormal hepatic 25-hydroxylation of vitamin D. Calcifediol treatment and twice daily administration of phosphate salts resulted in clinical improvement and increases in mineralization of the skeleton, as evidenced on radiographic evaluation.

Diagnosis and treatment of systemic hypertension.

Systemic hypertension is often observed in dogs and cats with chronic renal failure and other metabolic and endocrinological abnormalities. High systemic arterial blood pressure has been associated with chronic renal failure, ocular injury, neurologic complications, and cardiovascular changes. Recent advances in our knowledge of the prevalence and consequences of systemic hypertension dictate that proper diagnosis and treatment of this problem should become a component of routine therapy for many of our patients.

Plasma renin activity and angiotensin I and aldosterone concentrations in cats with hypertension associated with chronic renal disease.

OBJECTIVE: To determine plasma renin activity (PRA), angiotensin I (Ang I), and aldosterone (ALDO) values in clinically normal cats and hypertensive cats with renal disease, and the relation of renin-angiotensin-aldosterone activation in response to treatment with beta-blockers or angiotensin-converting enzyme inhibitors. ANIMALS: 5 normotensive healthy control cats and 12 Untreated hypertensive cats with chronic renal disease. PROCEDURE: Untreated hypertensive cats received either propanolol (n = 6) or enalapril (n = 6) as initial antihypertensive treatment. PRA and baseline plasma Ang I and ALDO concentrations were measured prior to treatment. The difference in Ang I values at 2 hours (Ang I generated) and at time 0 (baseline Ang I) was divided by 2 to give the PRA value. Values for PRA, Ang I, and ALDO were obtained from 5 clinically normal, normotensive cats, and compared with those of hypertensive cats. RESULTS: Mean +/- SD PRA and baseline Ang I concentration were not significantly different between normotensive and hypertensive cats. Mean ALDO concentration was significantly (P = 0.0235) higher in hypertensive cats with renal disease (186.18 +/- 145.15 pg/ml), compared with that in normotensive controls (51.1 +/- 16.76 pg/ml). Eight hypertensive cats with ALDO concentration > 2 SD above the mean concentration in control cats had low (n = 3), normal (n = 4), or high (n = 1) PRA, suggesting variable activation of the renin-angiotensin-aldosterone axis in the hypertensive state. Overall, enalapril was effective long-term monotherapy in only 1 of 6 cats, and propranolol was ineffective as long-term monotherapy. CLINICAL RELEVANCE: Evaluation of the renin-angiotensin-aldosterone system in cats with hypertension associated with renal disease may lead to greater understanding of the pathophysiologic mechanisms of this disorder. In addition, identification of biochemical markers in hypertensive cats may permit selection of appropriate antihypertensive drugs. Propranolol and enalapril were ineffective antihypertensive agents in most cats of this study.

Treatment of systemic hypertension in cats with amlodipine besylate.

Amlodipine besylate, a calcium channel blocker, was used to treat (mean +/- standard deviation [SD], 127 +/- 68 days) 12 cats with systemic hypertension. Amlodipine was administered orally at a dosage of 0.625 mg per cat (range, 0.08 to 0.23 mg/kg body weight; mean dose +/- SD, 0.17 +/- 0.04 mg/kg body weight) once daily as a single agent. Average indirect systolic blood pressure measurements in the 12 cases decreased significantly from 198 to 155 mmHg during amlodipine treatment. Significant changes in body weight and serum creatinine and potassium concentrations were not detected. Amlodipine appears to be a safe and effective oral treatment for systemic hypertension in cats when used chronically once daily as a single agent.

Systemic hypertension and its management.

The pathophysiology of hypertension in dogs and cats, the methods available to monitor blood pressure, and the signs and treatment of hypertension are reviewed. Clinical signs of hypertension are usually referable to target organ damage, most notably in ophthalmic, renal, and cardiovascular tissues, which have a rich arteriolar supply. Blood pressure should be measured in any animal with renal disease, hyperthyroidism, hyperadrenocorticism, retinal detachment or hemorrhage, hyphema, or echocardiographically determined cardiac hypertrophy. All cats with acquired cardiac murmur should also be evaluated for hypertension. Antihypertensive medication should be administered if the indirect blood pressure in cats is consistently over 170/100 mmHg, or if the indirect blood pressure in dogs is greater than 180/100 mmHg.

Hypotensive shock syndrome associated with acute Babesia canis infection in a dog.

A Doberman Pinscher contracted babesiosis after receiving a fresh blood transfusion from a Greyhound blood donor. Hypotensive shock syndrome was suspected on the basis of arterial hypotension, weakness, and pyrexia in the absence of detectable hemolysis and within hours of detection of low numbers of circulating Babesia canis organisms. Treatment with imidocarb dipropionate appears to have been effective in eliminating circulating B canis organisms and clinical disease. The blood donor, recently acquired from a race track, was healthy and lacked any abnormalities on initial laboratory evaluation; however, its serum antibody titer for B canis was > 1:5,000; B canis organisms were later identified on blood smears after the dog had been splenectomized and treated with corticosteroids at an immunosuppressive dosage. This case draws attention to a potential problem in current screening practices for infectious diseases of retired racing Greyhounds intended for use as blood donors.

Clinical features of salmonellosis in cats: six cases (1981-1986).

Of 6 cats with salmonellosis, only cats 1, 4, and 5 manifested clinical signs of gastroenteritis. In cats 2 to 5, salmonellosis was characterized by fever, a left-shifted leukogram, and vague nonspecific signs of illness. Salmonellae were isolated from blood and feces of cats 1 to 4, and from extraintestinal sites as part of a mixed gram-negative bacterial flora in cats 5 and 6. Of 4 cats with Salmonella bacteremia, cats 2, 3, and 4 were successfully treated with trimethoprim-sulfadiazine, amoxicillin, and/or chloramphenicol; treatment with cephapirin was ineffective in 3 cats. In some cats, salmonellosis was observed as a chronic febrile illness without specific gastrointestinal signs or as a localized tissue infection.

Central nervous system infection associated with anaerobic bacteria in two dogs and two cats.

Central nervous system (CNS) infection caused by anaerobic bacteria (including Bacteroides, Fusobacterium, Peptostreptococcus, and Eubacterium) was diagnosed in two dogs and two cats. In one dog there was extensive meningomyeloencephalitis, presumably the result of hematogenous spread of bacteria from lung abscesses and bacterial endocarditis. Subdural empyema of unknown origin was found in a second dog and two cats. Clinical signs in all four animals included mental depression and focal neurologic deficits, without fever.

Effects of body position and ventilation/compression ratios during cardiopulmonary resuscitation in cats.

Eighteen cats were anesthetized and were randomly assigned to 2 groups (9 cats/group). Cardiopulmonary resuscitation (CPR) was performed on each cat, with the cat in dorsal (group 1) or lateral (group 2) recumbency, by administering 5 external cardiac compressions/1 interposed (diastolic) ventilation (American Heart Association [AHA] technique; n = 3 cats/technique), simultaneous compression and ventilation (SCV; n = 3 cats/technique), or SCV with 1 interposed (diastolic) ventilation every tenth compression (SCV/DV; n = 3 cats/technique). Fourteen of the 18 cats were resuscitated. Central aortic and venous pressures were determined concurrently with lead II electrocardiography. Arterial blood samples were collected during the base-line period (after pressure fluctuations had stabilized, with the cats spontaneously breathing room air), 2.5 minutes after the onset of arrest (defined as the cessation of aortic pressure fluctuations), and after 10 minutes of CPR. Arterial blood gas values during the base-line period or during the period of arrest were not significantly different between group-1 and group-2 cats. After CPR, arterial pH and bicarbonate values were not significantly different between groups or between technique categories. The PaCO2 values were significantly lower in cats resuscitated by SCV or by SCV/DV than in cats resuscitated by AHA (P less than 0.05). The PaO2 values were significantly (P less than 0.001) higher in group-2 cats than in group-1 cats and were significantly (P less than 0.001) different between each technique category, with cats resuscitated by AHA having the lowest PaO2 and cats resuscitated by SCV/DV having the highest PaO2. Body position, CPR technique, sex, weight, or arterial blood gas values after CPR were not predictors of successful resuscitation.

Endocarditis caused by Corynebacterium sp in a dog.

Mitral valve bacterial endocarditis, caused by Corynebacterium sp, was diagnosed in a dog. The bacteria had characteristics unlike those commonly recognized for most species of Corynebacterium. The primary source of bacteremia was suspected to be a pilonidal cyst of the sacrum. The dog was treated with a first-generation cephalosporin for 6 weeks, and the pilonidal cyst was surgically removed. Physical examination 1 year after initial examination revealed no abnormalities other than a cardiac murmur. On echocardiographic examination 1 year after treatment, the vegetative lesion was still present; however, chamber dimensions had returned to normal. Wall thickness and contractility remained increased.