Diseases of the biliary tract

7.4.3.1 Cholecystitis

Pathogenesis

Cholecystitis and biliary mucocele are rare diseases in the dog.⁹⁵ Infection of the common bile duct through reflux from the duodenum is possible, though infection can also be hema­togenous.² The infectious agents often cultured in these pa­tients are E.

Symptoms

The most common symptoms of dogs with cholecystitis are upper abdominal pain, vomiting, and sometimes fever. Not all cases are associated with icterus. There may be occult blood loss from an affected blood vessel in the gallbladder causing anemia. In the case of gallbladder rupture, severe jaundice and ascites with general malaise due to peritonitis is seen.

Diagnosis

The common findings in patients with cholecystitis, such as jaundice, increased AP and GGT activities, and raised bile acids concentration, are not specific for this disease. There is usually leukocytosis. Liver histology reveals a nonspecific re­active hepatitis and is, thus, usually not diagnostic. Ultra­sonography demonstrates possible gall stones, which are often radiolucent. A mucocele has a very specific ultrasonographic appearance. The diagnosis is made by fine-needle aspiration of the gall bladder under ultrasound guidance, for which no an­esthesia is required.

Management

Antibiotic management is the treatment of choice for dogs with cholecystitis. Antibiotics that are effectively excreted in the bile (i.e., ampicillin or chloramphenicol) should be admin­istered for 3-4 weeks. Ampicillin is usually very effective (15 mg/kg IV q 8 h for 4 weeks). In cases of biliary calculi, gallbladder bleeding, biliary mucocele, or gall bladder rupture, a cholecystectomy should be performed.

7.4.3.2 Biliary duct or gall bladder rupture

Pathogenesis

Bile duct rupture is the tearing of the bile duct from the rest of the biliary system. This is usually caused by trauma and leads to leakage of bile from the affected lobe into the peritoneal cavity. Leakage of a large amount of unconcentrated bile (the bile is concentrated more distally, in the gallbladder), causes clinically detectable ascites. The resorption of bilirubin from the peritoneal cavity causes severe icterus. The high concen­tration of bile acids from the leaking bile causes chemical peri­tonitis, resulting in general illness and vomiting. Occasionally, spontaneous rupture of the gallbladder occurs as a result of perforating cholecystitis or a biliary mucocele.⁹⁵

Symptoms

Patients with a rupture of the biliary system develop severe icterus and ascites within a few days.Vomiting is also common and there is general malaise and anorexia.

Diagnosis

A history of recent trauma in a patient with icterus and ascites may be a strong indication of a biliary system rupture. Aspira­tion of the ascitic fluid reveals free bile in the abdominal cavity, which is diagnostic. Due to the resulting bile peritonitis, the fluid is a mixture of bile with erythrocytes and inflammatory cells, resulting in a brown turbid fluid.

Therapy

The therapy of biliary system rupture is surgical and depends on the exact location of the rupture. The prognosis is usually good.

7.4.3.3 Cystic liver disease

There are different types of cysts in the liver that are all usually subclinical.^2,96,97 Such cysts are quite rare and are due to a variety of congenital developmental abnormalities of the in­tra- and/or extrahepatic bile ducts.

is required to further classify the lesion. Severe forms of cystic liver disease can cause hepatic dysfunction. There is no treat­ment for these rare conditions.

7.4.3.4 Extrahepatic bile duct obstruction (EBDO)²-⁹⁸

Extrahepatic bile duct obstruction is an obstruction of the common bile duct due to extraluminal compression or intra­luminal obstructive lesions.⁹⁸ Most frequently, EBDO is caused by tumors arising from the pancreas or the proximal duode­num. Biliary tumors are rare in both dogs and cats. Severe inflammatory conditions of the pancreas, duodenum, or com­mon bile duct may also cause an obstruction. Cholelithiasis can cause EBDO in both dogs and cats. EBDO is more com­mon in dogs than in cats.

ploratory surgery may be necessary for definitive diagnosis. If the obstruction cannot be removed, cholecystojejunostomy may need to be performed to re-establish the bile flow. The importance of supportive care postoperatively cannot be over­emphasized. Attending to fluid, electrolyte, and nutritional needs is critical to a successful outcome. Biochemical abnor­malities associated with EBDO should begin to subside im­mediately after surgery.

Limited information concerning liver fluke infestation in cats suggests that praziquantel may be effective. Several dosage regimens have been used in the reported clinical cases, al­though a regimen of 20 mg/kg praziquantel PO or SQ q 24 h for 3 days is currently recommended. Because the use of prazi­quantel in this situation is an extra-label application, owner consent is recommended.

Clinical features

Clinical signs, clinicopathological findings, and ultrasono­graphic changes in dogs and cats with EBDO, are not distin­guishable from those of lymphocytic cholangitis (i.e., anorexia, depression, vomiting, jaundice, and /or hepatomegaly).

Diagnosis

Dogs and cats with complete EBDO show elevated serum AP and ALT activities. Fasting serum bile acids and bilirubin con­centrations are also highly elevated. An elevated serum GGT activity is also indicative for severe cholestasis. Acholic feces and vitamin K-responsive coagulopathy are rare but important indicators.⁹⁹ Ultrasonography may reveal changes consistent with EBDO and biliary scintigraphy may also provide sup­portive findings.¹⁰⁰ Because bile flow into the intestine is ob­structed, the large bile ducts proximal to the obstruction be­come distended and tortuous. These findings are identical to those of lymphocytic cholangitis. Histological examination of a liver biopsy is thus the only method to discriminate EBDO from chronic cholangitis. Secondary hepatic consequences of an unrelieved EBDO may include bile canalicular plugs, bil­iary epithelial hyperplasia, bile ductule multiplication, peri­portal fibrosis, and variable degrees of neutrophilic inflamma­tion and necrosis.

Treatment

7.4.4