Gallbladder perforation associated with cholelithiasis and cholecystitis in a dog.

A four-year-old female Japanese akita was admitted with icterus, ascites and chronically elevated serum bilirubin and liver enzymes. Abdominal ultrasonography revealed a diffusely thickened, hyperechoic gallbladder wall with a focal defect, hepatic lymphadenopathy and a large volume of anechoic fluid within the peritoneal space. Diagnosis of biliary tract rupture with bile peritonitis was based on the findings of bile and suppurative exudate in peritoneal aspirates. A perforated gallbladder and cholelithiasis were found on exploratory celiotomy, while histopathology revealed chronic suppurative cholecystitis. The dog recovered uneventfully after cholecystectomy. Although rare, the triad of cholelithiasis, cholecystitis and gallbladder perforation should be considered after detection of one of these conditions.

Chronic phenobarbital therapy reduces plasma benzodiazepine concentrations after intravenous and rectal administration of diazepam in the dog.

Disposition of diazepam (DZ) 2 mg/kg after single bolus intravenous (i.v.) and rectal (p.r.) administration before and after 30 day oral phenobarbital therapy was investigated in normal dogs. Adverse cardiovascular and neurologic effects for each drug, dosage and route of administration were evaluated. Plasma benzodiazepine concentrations were determined by fluorescence polarization immunoassay. This assay measured DZ and its active metabolites, oxazepam and nordiazepam to provide a total benzodiazepine concentration. Mean peak plasma concentrations after i.v. administration were 5963 and 5565 ng/mL, before and after phenobarbital treatment, respectively. After p.r. administration, mean peak concentrations were 629 ng/mL and 274 ng/mL and were reached within 30 min before and after phenobarbital treatment, respectively. The target concentration for potential seizure control (i.e. 150 ng/mL) was attained in five dogs in the post phenobarbital p.r. group with a median time to attainment of target concentration of 8 min. The administration of phenobarbital resulted in significantly lower areas under the plasma concentration vs. time curves (AUC) for both i.v. and p.r. administration. Similarly, there was a reduction in maximal plasma concentration, bioavailability (F), mean residence time, and time to target and peak concentrations in the postphenobarbital p.r. group, as compared to the prephenobarbital p.r. group. Adverse cardiovascular and neurologic effects were short-lived and were considered of minor clinical significance. Overall, chronic phenobarbital therapy in the dog reduces total benzodiazepine concentration after i.v. and p.r. administration presumably due to increased hepatic clearance of DZ and its metabolites oxazepam and nordiazepam. Despite this finding, administration of DZ rectally at 2 mg/kg may be a clinically useful alternative to i.v. administration to treat emergency seizures when i.v. therapy is not possible in dogs on chronic phenobarbital therapy.

Generalized tremors in dogs: 24 cases (1984-1995).

OBJECTIVE: To characterize clinical features, diagnostic evaluation, and treatment outcome for dogs with generalized tremors. DESIGN: Retrospective case series. ANIMALS: 12 white purebred and 12 nonwhite mixed-breed and purebred dogs. PROCEDURE: Medical records of dogs examined for tremors between January 1984 and July 1995 were reviewed. History, signalment, abnormalities on physical and neurologic examinations, results of diagnostic testing, and diagnosis were recorded for each dog. Results were divided into the following 3 categories on the basis of the cause of the tremors: inflammatory, noninflammatory, and idiopathic. Cause was determined by results of CSF analyses or a history of toxin exposure. RESULTS: The only noninflammatory cause of generalized tremors identified in these dogs was mycotoxin ingestion. Steroid-responsive tremor syndrome had developed in 22 of 24 dogs, half of which had abnormal results of CSF analyses. Most dogs were young adults between 1 and 5 years old. More than half of the dogs were nonwhite mixed-breeds and all weighed < 15 kg (33 lb). Eighty percent of the dogs responded to immunosuppressive treatment within 3 days. CLINICAL IMPLICATIONS: Inflammatory and noninflammatory causes for generalized tremors in dogs result in similar clinical signs, so a logical diagnostic and treatment approach is needed. Steroid-responsive tremor syndrome should be considered in small- to medium-breed, young adult dogs, regardless of coat color. A rapid and complete response to immunosuppressive treatment is expected.

Methylmalonic and malonic aciduria in a dog with progressive encephalomyelopathy.

A 12 week old female Labrador retriever dog with signs of progressive diffuse degeneration of the brain and spinal cord was found to have methylmalonic and malonic aciduria. Over a 5 month period, the dog developed neurologic signs compatible with disease of the central nervous system with predominant diffuse cerebral and right lateralizing brainstem deficits. Gross pathological examination of the brain showed that the lateral, third, and fourth ventricles of the brain were markedly enlarged and associated with white and grey matter atrophy. Syringomyelia and hydromyelia of the central canal into the dorsal funiculus of the spinal cord beginning at the level of the cervical intumescence and extending to the lumbar intumescence was also present. Significant biochemical abnormalities include methylmalonic and malonic aciduria, mild lactic and pyruvic aciduria. There was also accumulation of citric acid cycle intermediates including succinic, aconitic, and fumaric acids. Disordered fatty acid oxidation was suggested by increased excretion of adipic, ethylmalonic, suberic and sebacic acids. Neither ketoacidosis nor hyperammonemia were present, and serum cobalamin levels were normal. Overall, this dog demonstrates an inborn error of metabolism resulting in abnormal organic acid accumulation associated with a neurodegenerative disease.