INTRODUCTION

Biliary disease includes diseases of the gallbladder and biliary tract (both intrahepatic and extrahepatic). Clinically, diseases of the biliary system are considered either obstructive or nonobstructive. Obstructive diseases, with or without biliary tract rupture, are classically managed with surgery in animals, but laparoscopy, interventional radiology, or interventional endoscopy are usually considered primarily in humans.^1,2 Nonobstructive diseases are often managed medically, interventionally, or surgically. Biliary obstructive disease is most commonly due to pancreatitis in dogs and to neoplasia or inflammatory disease (pancreatitis, cholangitis, and inflammatory bowel disease, also know as triaditis) in cats.^3-5 In comparison with human medicine, biliary stone disease is relatively uncommon in small animal patients. The prognosis for dogs with extrahepatic biliary duct obstruction (EHBDO) is often better than that for cats, because pancreatitis is often self-limiting. Nonobstructive biliary disease occurs most commonly as a result of biliary sludge, cholecystitis, cholangitis (bacterial or immune mediated), and/or nonobstructive cholelithiasis. Less common causes include viral, fungal, parasitic, congenital diseases, or gallbladder infarction.^3-8 Biliary rupture can occur with either obstructive or nonobstructive diseases, as well as with trauma or secondary to diagnostic testing. Rupture of the biliary system causes bile peritonitis (bile is extremely irritating to extrabiliary or extraintestinal structures) and requires immediate surgical intervention. This chapter will discuss the physiology of the biliary system, clinical presentation of animals with biliary tract disease, diagnostic testing, specific disease entities, therapeutic approaches to these patients, and, finally, the prognosis and potential future interventions for animals with biliary tract disease.

PHYSIOLOGY

Bile is the product of the combination of water, conjugated bile acids, bile pigments, cholesterol, and inorganic salts.³ It is transported from the bile ductules and ducts in the hepatic parenchyma to the cystic duct, common bile duct, and gallbladder. The common bile duct runs through the lesser omentum and enters the mesenteric wall of the duodenum. The canine common bile duct terminates in the duodenum near the minor pancreatic duct at the major duodenal papilla of the proximal duodenum. The feline common bile duct usually joins the major pancreatic duct before entering the duodenum at the papilla, similar to humans.³ Once bile exits the extrahepatic biliary system into the duodenum, over 90% of bile salts are reabsorbed from the intestinal tract, transported back to the liver via the portal system, and recirculated. Bilirubin and biliverdin contribute to the yellow-green color of bile. Bile is deposited continuously into the biliary ducts and stored and modified in the gallbladder. Gallbladder emptying is controlled by both humoral (cholecystokinin, amino acids, fats, etc) and neural stimulation (vagal [parasympathetic] innervation). Along the tract from the bile ductules to the bile ducts and cystic duct, gallbladder, and common bile duct, different disease processes can occur, and often present in similar ways but require different interventions.

PRESENTATION OF BILIARY TRACT DISEASE

Icterus, vomiting, diarrhea, abdominal discomfort, lethargy, fever, and ascites are all common clinical findings in an animal with biliary tract disease. The patient’s clinical signs may be slow and progressive (chronic pancreatitis, cholangitis, cholangiohepatitis, biliary mucocele, neoplasia, cholelithiasis) or acute and severe (biliary tract rupture, acute pancreatitis, necrotizing cholecystitis, emphysematous cholecystitis, EHBDO). An acute condition of the abdomen (see Chapter 123, Acute Abdominal Pain) may be caused by biliary leakage into the peritoneum, particularly if the fluid is septic.

DIAGNOSIS OF BILIARY TRACT DISEASE

History and physical examination findings are usually vague and rarely diagnostic for a specific cause of biliary tract disease. An icteric animal should be considered to have either prehepatic, hepatic, or posthepatic disease, although not all animals with biliary tract disease present with icterus. Further diagnostic testing can help to differentiate among the conditions that cause icterus. A complete blood count, serum biochemical profile, and urinalysis are indicated as part of a minimum database in dogs with such clinical signs. Icterus in the face of a normal or near-normal hematocrit (particularly those lacking a severe regenerative response) is usually suggestive of either hepatic or posthepatic icterus. Elevations in white blood cell parameters can be suggestive of an inflammatory condition (hepatitis, cholangiohepatitis, cholecystitis, bile peritonitis), whether the etiology is infectious, neoplastic, or immune mediated (see Chapter 126, Hepatitis and Cholangiohepatitis). The serum biochemical profile is usually more diagnostic. An increase in the alanine aminotransferase (ALT) is common if inflammation has ascended from the biliary tract to the liver, causing cholangiohepatitis (see Chapter 126, Hepatitis and Cholangiohepatitis). Increases in serum alkaline phosphatase (ALP), with or without hyperbilirubinemia, can be seen with obstructive or nonobstructive biliary diseases. Typically cats tend to have lower ALP elevations than dogs.³ Gamma-glutamyltransferase (GGT) typically is elevated with cholestatic liver disease, although there are exceptions (feline hepatic lipidosis, biliary mucoceles). Hyperbilirubinemia is common, although bilirubinuria occurs before hyperbilirubinemia and should be assessed with routine urinalysis. Hypercholesterolemia may occur secondary to EHBDO, pancreatitis, or biliary tract rupture. If bile peritonitis is suspected, the abdominal fluid bilirubin level will be greater than the serum bilirubin.³

Biliary imaging is often necessary to differentiate hepatic from posthepatic icterus. Abdominal radiographs may reveal radiodense choleliths or air within the gallbladder (emphysematous cholecystitis). Animals with pancreatitis could have a loss of serosal detail in their right cranial abdomen (see Chapter 124, Acute Pancreatitis). Contrast radiographs of the biliary system (percutaneous cholecystography) have been described, but alternative safer imaging modalities often yield comparable information (abdominal ultrasound, computed tomography, and endoscopic retrograde cholangiopancreatography [ERCP]).^1,2,9

Ultrasonography is the most useful and available noninvasive technique to differentiate intrahepatic from extrahepatic disease. It can identify lesions within the gallbladder and biliary tract (biliary mucocele, choleliths, biliary debris or “sludge,” gas associated with emphysematous cholecystitis, tumors), most biliary tract obstructions (secondary to tumors, choleliths, pancreatitis, debris), and peritoneal effusion due to biliary tract rupture (secondary to a biliary mucocele, trauma, cholecystocentesis, obstruction). Echogenic contents within the gallbladder, or biliary sludge, are often considered an incidental finding by most radiologists, although they can also occur secondary to stagnant biliary flow and may be suggestive of biliary or nonbiliary disease.^10,11 During states of biliary stasis, water is absorbed from the bile and it becomes thicker, resulting in sludge which can be obstructive as it passes.

Biliary sludge should be differentiated from a biliary mucocele, which can be a life-threatening condition and should be considered a significant finding and followed carefully.^4,6,7 Mucoceles cause distention of the gallbladder resulting from an inappropriate accumulation of mucus and inspissated bile. Ultrasound examination reveals an immobile bile pattern with a finely striated and stellate appearance, often referred to as a kiwi gallbladder.¹¹ A significant number of cases (15%) with biliary mucoceles who do not have ultrasonographic evidence of biliary rupture are found to be ruptured during surgical exploration, making clinical impression of patient progression the most important parameter for therapeutic decision making.^6,7,11 Animals that have been fasted or are anorexic may also have a distended gallbladder, which can be misdiagnosed as a biliary obstruction. The progression of ultrasound changes with biliary tract obstructions have been documented.^3,8 Dilation of the gallbladder and a loss of the gallbladder neck tapering typically occurs within 24 hours of duct ligation; after 48 hours dilation of the common bile duct is seen; after 72 hours dilation of the extrahepatic biliary ducts are present; and after approximately 7 days diffuse dilation of the intrahepatic biliary tree are observed.^3,8 Gallstones are often hyperechoic foci and display acoustic shadowing from within the gallbladder or biliary tree. Cholecystitis may cause gallbladder wall thickening or edema, and a double-wall appearance has been described.^3,8

Cholecystocentesis can be performed diagnostically to obtain bile for cytology and aerobic and anaerobic culture, as well as therapeutically for decompression in the case of obstructive disease, although therapeutic intervention needs further investigation before it is recommended for clinical use.^3,12 To prevent bile leakage into the abdomen, reports have recommended performing this procedure through the liver parenchyma.¹³

A diagnostic peritoneal lavage (see Chapter 156, Diagnostic Peritoneal Lavage), laparoscopy, and/or surgical exploration should be performed when a ruptured biliary tract is suspected, or there is evidence of EHBDO, neoplasia, cholelithiasis, biliary mucoceles, trauma, necrotizing cholecystitis, or emphysematous cholecystitis.^3,4,6,7 Patency of the biliary tract can be evaluated carefully during surgical exploration. Nuclear scintigraphy is rarely used to define canine or feline biliary tract diseases, although this technique has been performed in humans.^3,14