Diseases of the Liver

 

PORTOSYSTEMIC SHUNTS (Update)

Portosystemic shunts are reported less commonly in cats than in dogs. Portosystemic shunts are either single or multiple vascular communications with the portal circulation that bypass the liver to join the systemic circulation. Portosystemic shunts may be congenital, which is the most common type, or acquired. Acquired PSSs, which are extremely rare in cats, develop secondary to portal hypertension and are associated with diseases such as cirrhosis, chronic cholangiohepatitis, hepatic neoplasia, and arteriovenous fistulas. Portal hypertension may result in the formation of multiple extrahepatic shunts, which were previously nonfunctional remnant vessels of the portal system. Congenital PSSs, which are emphasized in the following discussion, are usually single large vessels that may be classified as intrahepatic or extrahepatic. Intrahepatic shunts usually result from failure of the ductus venosus to close shortly after birth. The ductus venosus is a fetal vascular channel that connects the umbilical vein with the caudal vena cava. Congenital intrahepatic PSSs are most commonly reported in large breed dogs but are occasionally reported in cats. In cats, congenital extrahepatic PSSs, are the most common type of shunt, especially portocaval shunts, but also include hypoplasia of the portal vein with collateral PSS and portoazygous shunts.

Shunting of the portal circulation prevents nutrients and hepatotrophic factors from reaching the liver and precludes hepatic removal of toxins and bacteria from the portal circulation. As a result, most cats with PSSs have a small atrophic liver and clinical signs of HE. In fact, PSSs are the most common cause of HE in cats. (For discussion of the pathogenesis and manifestations of HE, see Hepatic Encephalopathy).   The most common clinical signs are behavioral changes, ptyalism, depression, aggression, dementia, blindness, and seizures. Signs of neurologic dysfunction often wax and wane and may be associated with eating, especially a high-protein meal. Exaggerated responses to sedatives and prolonged recovery from anesthesia are sometimes observed. Signs of HE are often apparent at a very young age, but age of diagnosis of PSS ranges from 2 months to 4 years.  Vague signs, such as anorexia, polyphagia, diarrhea, intermittent vomiting, polydipsia, and lower urinary tract signs, may also be present.

Physical examination is often unremarkable, except for a smaller than normal body size and neurologic deficits. Copper color of the iris has been associated with the presence of PSS in some cats. A few cats have had large kidneys, systolic murmurs,and cardiac malformations.

Tentative diagnosis is based on subtle abnormalities found on routine hematologic and biochemical tests and urinalysis. Hematologic abnormalities may include erythrocytic microcytosis and poikilocytosis, a nonspecific change in erythrocyte shape associated with liver disease. Microcytosis is present in approximately -50 percent of cats with PSS. The pathogenesis is unknown, but iron deficiency is not involved .

Serum biochemical abnormalities associated with PSS include mildly increased ALT, AST, and ALP activity, normal to decreased BUN, hypocholesterolemia, and rare hypoalbuminemia. Serum bilirubin is usually normal. The values for liver enzymes range from normal to twice normal, which may be attributable to poor hepatic perfusion and hypoxia-induced hepatocyte injury, or to the associated lesions of bile duct hyperplasia and periportal fibrosis that are found in some cats with PSS. In young growing animals, increases in ALP may be due to the bone isoenzyme.

Normal to decreased BUN concentrations have been attributed to a decreased conversion of ammonia to urea by the liver. A low BUN is present in about 65 percent of cats with PSS. Hydration status, diet, renal function, and fluid therapy may also affect serum urea concentration; thus, low BUN is not specific for liver disease or PSS. Cholesterol is synthesized by the liver and absorbed from the intestinal tract and is low in the serum of 67 percent of cats with PSS. Hypoalbuminemia is an uncommon finding in cats with PSS. Urine may be dilute and ammonium biurate crystals or calculi may be found in the urine of cats With PSS. Ammonium urate uroliths may be visible radiographically if they contain other mineral components as well. Microhepatica, a common radiographic finding in dogs with PSS, is seen less consistently in cats.

Historical, physical, hematologic, and biochemical findings are usually sufficiently suggestive ofPSS to warrant liver function testing (see under Diagnostic Evaluation of Liver Disease). Fasting hyperammonemia is specific for hepatic insufficiencybut is an insensitive test. Fasting SBA concentrations may also be normal in cats with PSS, particularly if the cat has been anorectic or h eld off foodfor a prolonged period. Postprandial SBA concentration is usually markedly abnormal in cats with PSS and is the screening test of choice.

Definitive diagnosis of PSS requires contrast portography (See Illus); the technique is described in Contrast Portography. Although the shunt vessel may be visualized or suspected based on ultrasonographic evaluation, contrast portography is preferred for localization of the shunt prior to surgical exploration and ligation of the shunt vessel. Rectal portal scintigraphy using technetium-99m pertechnetate is available at some referral institutions for noninvasively confirming the presence of a shunt, but this procedure does not provide reliable anatomic identification of the location of the shunt.

Surgical ligation is considered the treatment of choice for long-term improvement or elimination of clinical signs associated with PSS. A complete description of the surgical procedures and management of PSS may be found here. Medical management is discussed elsewhere (see under Hepatic Encephalopathy).

 

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Illus. (A) Lateral and (B) ventrodorsal radiographs of the abdomen during contrast mesenteric portography in a cat with a single extrahepatic portacaval shunt. The catheter is positioned in the mesenteric vein; contrast media outlines the mesenteric vein, portal vein, shunt (arrowhead), and caudal vena cava. The cat was a 1-year-old male domestic shorthair cat with signs of stunted growth, aggressive behavior changes, and urate urolithiasis. (From Johnson, with permission.)

Pathogenesis and Pathophysiology - Diagnosis - Treatment

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