Clinical and clinicopathologic abnormalities in young dogs with acquired and congenital portosystemic shunts: 93 cases (2003-2008).

OBJECTIVE: To determine whether clinical and clinicopathologic data could assist differentiation of congenital portosystemic shunts (CPSSs) from acquired portosystemic shunts (APSSs) in young dogs. DESIGN: Retrospective case series. ANIMALS: Dogs < 30 months of age with CPSSs (n = 62) or APSSs (31). PROCEDURES: Medical records from 3 referral centers identified 31 dogs with APSSs and 62 dogs with CPSSs diagnosed from July 2003 to July 2008. Signalment, clinical signs, physical examination, and clinicopathological data were recorded, and statistical analyses were performed to determine differences between groups. RESULTS: Univariable analysis showed APSS patients were older, heavier, and in poorer body condition, compared with CPSS patients. In CPSS patients, diarrhea was less prevalent, and neurologic signs were more prevalent. Ascites was more prevalent in APSS (Fisher exact test; OR, 50.2; 95% confidence interval [CI], 6.2 to 409.7), with no significant difference in albumin concentration between groups. The logistic regression model used to assess clinicopathological parameters showed lower Hct (OR, 1.42 × 10(-12); 95% CI, 1.42 × 10(-17) to 4.0 × 10(-6)), higher mean corpuscular volume (OR, 1.27; 95% CI, 1.08 to 1.50), and higher alanine aminotransferase concentrations (OR, 1.005; 95% CI, 1.001 to 1.009) were more likely in APSS patients. CONCLUSIONS AND CLINICAL RELEVANCE: Several clinicopathologic differences between dogs with congenital and acquired shunts were identified; however, assessed alone, these would be unlikely to enable differentiation between the 2 conditions. Awareness of the rarity of ascites in CPSS cases should prompt recognition of a likely diagnosis of APSS, allowing the veterinarian to target further diagnostics and counsel the owner appropriately.

Barium toxicosis in a dog.

CASE DESCRIPTION: A 2-year-old 14.9-kg (32.8-lb) neutered female Shetland Sheepdog was admitted to the University of Liverpool Small Animal Teaching Hospital for evaluation of acute collapse. CLINICAL FINDINGS: At admission, the dog was tachypneic and had reduced limb reflexes and muscle tone in all limbs consistent with diffuse lower motor neuron dysfunction. The dog was severely hypokalemic (1.7 mEq/L; reference range, 3.5 to 5.8 mEq/L). Clinical status of the dog deteriorated; there was muscle twitching, flaccid paralysis, and respiratory failure, which was considered a result of respiratory muscle weakness. Ventricular arrhythmias and severe acidemia (pH, 7.18; reference range, 7.35 to 7.45) developed. Intoxication was suspected, and plasma and urine samples submitted for barium analysis had barium concentrations comparable with those reported in humans with barium toxicosis. Analysis of barium concentrations in 5 control dogs supported the diagnosis of barium toxicosis in the dog. TREATMENT AND OUTCOME: Fluids and potassium supplementation were administered IV. The dog recovered rapidly. Electrolyte concentrations measured after recovery were consistently unremarkable. Quantification of plasma barium concentration 56 days after the presumed episode of intoxication revealed a large decrease; however, the plasma barium concentration remained elevated, compared with that in control dogs. CLINICAL RELEVANCE: To our knowledge, this case represented the first description of barium toxicosis in the veterinary literature. Barium toxicosis can cause life-threatening hypokalemia; however, prompt supportive treatment can yield excellent outcomes. Barium toxicosis is a rare but important differential diagnosis in animals with hypokalemia and appropriate clinical signs.