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Hepatobiliary Disease 1163
injury (Thornburg et al, 1984, 1985, 1986, 1996). Breeds that
VetBooks.ir are currently thought to have primary copper-associated hep-
atopathies include Skye terriers (Haywood et al, 1988;
McGrotty et al, 2003), West Highland white terriers (Thorn-
burg et al, 1996), Doberman pinschers (Specti et al, 1998),
Dalmatian dogs (Webb et al, 2002) and Labrador retrievers
(Hoffman et al, 2006).
The liver diseases in these dogs are distinct from copper tox-
icosis in Bedlington terriers in that hepatic copper concentra-
tions are generally lower and do not always increase with age.
Other factors may be responsible for hepatic damage in some
breeds.The exceptions might be Doberman pinschers and Dal-
matian dogs because they tend to accumulate hepatic copper in
concentrations similar to Bedlington terriers, suggesting defects
in hepatic copper excretion (Mandigers, 2005).
Cholangitis in Cats Figure 68-9. Cirrhotic liver from an eight-year-old female Doberman
Cholangitis (i.e., inflammation of the biliary ducts, especially pinscher with chronic hepatitis. (Photograph courtesy Dr. Susan
Johnson, The Ohio State University, Columbus.)
the intrahepatic ducts and the surrounding liver tissue) is the
most common feline inflammatory liver disease (Gagne et al,
1999; Armstrong et al, 1997; Day, 1995). The World Small vascular dysplasia) is a second congenital vascular anomaly
Animal Veterinary Association Liver Pathology Standardiza- occurring in dogs, but rarely in cats. This anomaly is a conse-
tion Working Group categorized the two most common forms quence of portal vein hypoperfusion that results in hepatic
of cholangitis into neutrophilic and lymphocytic forms (2006). arterialization in the portal triad and the development of
Bacterial infection from enteric bacteria (especially Escherichia microscopic intrahepatic shunts. Commonly affected breeds
coli) ascending through the bile ducts is thought to be the cause include cairn terriers, Yorkshire terriers and Maltese (Scher-
of most neutrophilic forms, whereas immunologic mechanisms merhorn et al, 1996). Affected dogs have abnormal bile acid
may be involved in the lymphocytic type. Chronic cholangitis concentrations and variable liver enzymes but rarely have
may progress to biliary cirrhosis. clinical signs. A less common variant of portal vein hypopla-
Many cats with cholangitis develop significant cholestasis sia associated with fibrosis in the portal triads results in por-
and may have sludged or inspissated bile, causing partial or tal hypertension, ascites and PSS (Christiansen et al, 2000;
complete biliary obstruction (Armstrong et al, 1997; Day, Bunch et al, 2001).
1995). Concurrent cholecystitis, pancreatitis and inflammatory Clinical signs of HE usually predominate in patients with
bowel disease are common in feline cholangitis patients PSS (Box 68-1). Polydipsia and polyuria are also commonly
(Armstrong et al, 1997; Day, 1995). seen. Ammonium urate and other purine uroliths occur in
some animals because of high urinary excretion of ammonia
Portosystemic Shunts in Dogs and Cats and uric acid (Chapter 39). Stunted growth or failure to gain
PSS are vascular communications between the portal and sys- weight may occur in young animals with congenital shunts.
temic venous circulation. PSS can be either congenital or ac- Surgical closure is the treatment of choice for congenital PSS
quired. Congenital shunts can be further subdivided into intra- but not for acquired PSS. Dietary management is the corner-
hepatic shunts, occurring mostly in large-breed dogs or extra- stone of successful case management and prevention of HE in
hepatic shunts, occurring mostly in smaller dog breeds and cats. the pre- and immediate postoperative phase and in partially
Intrahepatic shunts are the remnant of a ductus venosus that closed shunts (Meyer and Rothuizen, 1996).
did not completely close after birth. Extrahepatic shunts are
seen as anomalous embryonic vessels between the portal vein Neoplasia
and the systemic circulation (mostly to caudal vena cava or azy- The most commonly encountered hepatic malignancies in dogs
gos vein) (Moon, 1990; Lamb, 1998; Center, 1996b). A hered- and cats are metastases, lymphoma, hemangiosarcoma, hepato-
itary basis for congenital shunts has been established in Irish cellular carcinoma and cholangiocarcinoma (Cullen and Popp,
wolfhounds (Meyer et al, 1995) and a number of other breeds 2002).The appearance may be localized or diffuse. Because the
have a significant risk for development of congenital shunts, liver has such a tremendous reserve capacity, tumors, especially
supporting a hereditary etiology. Acquired PSS may develop as localized malignancies may be undetected for long periods. In
multiple shunts in response to portal hypertension caused by advanced stages,tumors may be visible or palpable during phys-
cirrhosis or other causes (e.g., tumors or portal vein thrombo- ical examination. Severe liver dysfunction with icterus, coagu-
sis). Both congenital and acquired PSS are more common in lopathies and portal hypertension may occur especially in dif-
dogs than in cats. fusely distributed malignancies (e.g., malignant lymphoma and
Primary portal vein hypoplasia (also referred to as micro- hemangiosarcoma).