Pathophysiology

Clinical signs associated with portosystemic shunts commonly involve the nervous system, gastrointestinal tract, and urinary tract. General clinical signs include poor growth rate, weight loss, fever, and anesthetic or tranquilizer intolerance. Neurologic dysfunction is seen in most animals with PSS and includes lethargy and depression, ataxia, seizures, behavioral changes, and blindness. Head pressing, circling, and development of a head tilt have also been reported. Gastrointestinal clinical abnormalities include anorexia, vomiting, and diarrhea. Some dogs have no apparent signs or present with signs of cystitis or urinary tract obstruction. Many cats have hypersalivation and some have unusual copper colored irises.

Abnormalities found on hemograms of animals with PSS include leukocytosis, anemia, and microcytosis. Most animals with congenital PSS have normal coagulation profiles. Biochemical abnormalities associated with PSS include decreases in blood urea nitrogen, protein, albumin, glucose, and cholesterol; and increases in serum alanine aminotransferase and alkaline phosphatase. Increase in alkaline phosphatase is most likely from bone growth, since cholestasis is not usually a problem in animals with shunts. Cats with PSS usually have normal albumin concentrations. Urinalysis abnormalities include low urine specific gravity and ammonium biurate crystalluria. At magnifications of 400x or more, ammonium biurate crystals often have a spikey, thornapple or starfish shape and golden color. Because of increased urinary excretion of ammonia and uric acid, dogs and cats may also develop uroliths. Urate uroliths are often radiolucent and therefore may not be detectable on survey radiographs unless they are combined with struvite. Abnormal urine sediment suggestive of cystitis (hematuria, pyuria, and proteinuria) has been described in animals with PSS and may be associated with crystalluria or urolithiasis.

Hepatic histologic changes in animals with PSS include generalized congestion of central veins and sinusoids, lobular collapse, bile duct proliferation, hypoplasia of intrahepatic portal tributaries, proliferation of small vessels and lymphatics, diffuse fatty infiltration, hepatocellular atrophy, and cytoplasmic vacuolization. These pathology changes can also be seen in dogs with hepatic microvascular dysplasia that do not have single congneital shunts. Pathologic changes may be present in the central nervous system, especially in encephalopathic animals.

All information on this page is courtesy of the University of Tennessee Veterinary Medicine Website