Gallbladder diseases in dogs and cats (original) (raw)

The biliary system consists of the gallbladder (GB), cystic duct, common bile duct (CBD), hepatic ducts, interlobular ducts, intralobular ducts, bile ductules, and hepatic canaliculi. The GB is a teardrop-shaped organ located in the cranioventral abdomen, attached to the liver to the right of midline within a fossa between the right medial and quadrate liver lobes. The GB acts as a reservoir where bile is stored, modified, and eventually expelled. First, bile is formed in the hepatocytes and is actively secreted into the bile canaliculi. From there, bile flows through the intrahepatic bile duct system (bile ductules-intralobular ducts-interlobular ducts) leaving the liver in the hepatic ducts that finally merge into the CBD after branching off the cystic duct that travels toward the GB. The cystic duct is an important landmark in that it distinguishes the otherwise continuous hepatic ducts from the CBD. At the junction with the intestines, the communication of the CBD and duodenum is anatomically distinct in the dog and cat. After contraction of the GB, bile is released into the CBD and enters the duodenum through the sphincter of Oddi. In the dog, the CBD joins the minor pancreatic duct at the major duodenal papilla. In the cat, the CBD fuses with the major pancreatic duct just before entering the duodenal papilla a few cm caudal to the pylorus. The GB wall of dogs and cats is typically thin-walled (up to 1.5 mm) and the GB volume is approximately 1 mL / kg BW. Its contractions are primarily initiated by cholecystokinin, a peptide hormone secreted in the duodenum in response to fats and proteins entering the small intestine. Bile is primarily composed of cholesterol, lecithin, phospholipids, and bile salts. Bile emulsifies fat and neutralizes acid in partially digested food. The synthesis and secretion of bile acids provides an important method for the excretion of cholesterol. In fact the conversion of cholesterol into bile acids represents the main catabolic escape pathway for cholesterol from the body. This illustrates why hypercholesterolemia is typically seen in cholestatic disease processes. CHOLECYSTITIS The term cholecystitis denotes inflammatory conditions of the GB and encompasses a variety of acute and chronic diseases with or without bacterial infections. Whereas cholecystitis in people is usually seen in the context of cystic duct obstruction, the etiology of cholecystitis has not been well characterized in dogs and cats. Most cases of cholecystitis are associated with conditions leading to prolonged bile stasis with subsequent accumulation of cytotoxic bile acids. The GB epithelium, although normally a robust tissue, is continuously exposed to one of the most noxious agents in the body: a concentrated solution of bile acids detergents. In health, the GB empties the concentrated bile several times a day and is replenished with dilute and less noxious hepatic bile. With prolonged stasis concentrated bile stagnates in the GB lumen. In addition the GB epithelium has relatively high metabolic energy requirements, as it continuously reabsorbs electrolytes and water from the bile. Therefore, in a debilitated, anorectic patient chemical injury to the GB wall may occur. This is why GB mucoceles and cholelithiasis/choledocholithiasis, and rarely biliary neoplasia are known predisposing factors in dogs and cats. Ascending bacterial infection is possible and more commonly found in cases of an advanced extrahepatic biliary stasis. An important and often overlooked factor is GB wall ischemia. Having only a single source of perfusion (i.e. left branch of the hepatic artery) makes the GB also uniquely susceptible to ischemic necrosis following states of splanchnic vasoconstriction (hypovolemic or distributive shock) or blunt abdominal trauma. Studies in humans showed that capillaries barely filled in acalculous cholecystitis, suggesting that altered microcirculation plays an important role in its pathogenesis. A ruptured necrotic GB should be suspected in dogs with a history of (hypovolemic) shock and abdominal effusion with elevated (above serum) bilirubin concentrations. Emphysematous cholecystitis is a rare variant of cholecystitis in dogs and cats and may be seen as a biliary complication in diabetic patients. Prolonged hyperglycemia, lowered resistance to ascending bacterial infections due to hypomotility of the sphincter of Oddi, and delayed GB emptying may contribute to the increased risk of emphysematous cholecystitis in diabetic patients. In addition, infarction and hematogenous spread of bacteria may be involved in septic patients or patients with a distant primary infectious focus. Another well-recognized risk factor for development of acute cholecystitis in humans is the use of total parenteral nutrition (TPN) in critically-ill patients due to complete disuse of gastrointestinal tract and resulting bile stasis. Because cholecystitis is very difficult to diagnose in our patients with multisystemic disease, the relevance of this complication while using TPN has yet to be determined in veterinary medicine. CLINICAL SIGNS Cholecystitis may be either acute or chronic in nature. Mild cases are very likely often asymptomatic. Clinical signs can be vague and unspecific and solely consist of intermittent inappetence and occasional vomiting, which is why the diagnosis usually requires a high index of clinical suspicion. More severe cases of acute cholecystitis present with anorexia, weakness, vomiting, abdominal pain and fever. The presence of icterus is variable. Patients that present with acute cholecystitis as a consequence of splanchnic hypoperfusion may solely exhibit classical shock signs, such as tachycardia, tachypnea, prolonged capillary refill time, and weak pulses. Chronic cholecystitis is much more difficult to diagnose. Clinical signs may include intermittent anorexia, vomiting, and postprandial discomfort (i.e. lip smacking, tachypnea, tense abdomen). Pain is likely present but is not always readily detected on examination.