The pathophysiology and laboratory diagnosis of congenital portosystemic shunts in dogs

Abstract

Congenital portosystemic shunts generally arise as single vascular anomalies that cause the portal blood to bypass the liver and enter the systemic venous circulation directly. The liver is primarily affected, as it is deprived of perfusion by portal hepatotrophic factors such as insulin, glucagon, and amino acids. There is progressive hepatic atrophy, and as a consequence, dysfunction.

Hepatic encephalopathy can result from increased levels of ammonia and gamma-aminobutyric acid within the systemic circulation. Variably toxic amines, captans and short chain fatty acids may act as false neurotransmitters. Hypoglycaemia will exacerbate the effects of these substances. Increased concentrations of ammonia and uric acid in the urine predispose to the precipitation of ammonium biurate crystals and the formation of calculi.

Haematological changes include anaemia, microcytosis, hypoproteinaemia, leucocytosis, and coagulation abnormalities. Gastrointestinal effects are common. They may be displayed as anorexia, vomiting, ptyalism, pica, diarrhoea, or polyphagia. Most dogs are less than 1 year of age at initial presentation.

Diagnosis from a laboratory viewpoint will involve a consideration of the history, clinical findings, haematology, serum biochemistry and urinalysis. If the findings are suggestive of a congenital portosystemic shunt, the demonstration of elevated fasting or, more consistently, post-prandial serum bile acid concentrations, and subsequent histological examination of a liver biopsy will provide a definitive diagnosis.