Relevant Surgical Anatomy

The hepatobiliary system is most commonly evaluated at the time of celiotomy through a ventral midline approach. This organ system is found in the cranial abdomen sandwiched between the diaphragm and the gastrointestinal tract, and can be thoroughly inspected via palpation and gross visual appearance at the time of surgery.

A large volume of blood continuously flows through the liver at low pressures filtering through the hepatic sinusoids, eventually emptying into the hepatic veins and caudal vena cava. To prevent collapse of the liver lobes and subsequent vascular occlusion, the liver is required to be stiff in its material property. As a result of its stiffness, the liver is friable and easily fractured after trauma. Fortunately, the liver is protected by the caudal aspect of the ribcage in the cranial abdomen and further protected by a cushion of falciform ligament fat ventrally and a dome shaped diaphragm cranially. The liver has seven major lobes or processes: right lateral and medial, left lateral and medial, quadrate and caudate which has a caudate and papillary process. Deep fissures of the liver lobes allow them to collapse on top of each other or slide in a side-to-side fashion depending on movements of the animal. The liver is only partially fixed at its cranial extent where it surrounds the caudal vena cava. Triangular ligaments of the right and left liver lobes are attached to the peritoneal surface of the diaphragm. Histologically, the hepatic lobule is the structural unit of the liver. The lobule consists of hepatocytes arranged in a hexagon surrounding a central hepatic vein. A portal triad is found in each corner of the hexagon that is comprised of a bile duct and terminal branch of the portal vein and hepatic artery. Blood from the portal vein and hepatic artery is delivered to the hepatocytes via the hepatic sinusoids and is cleansed by the reticuloendothelial system.

The biliary system begins as microscopic canaliculi in the hepatic lobule, which eventually coalesce into larger bile ducts that enter the extra-hepatic biliary system. This system consists of hepatic ducts, common bile duct, cystic duct and gall bladder. Upon entering the gall bladder, bile is concentrated and upon stimulation primarily by the hormone cholecystokinin, released into the cystic duct and eventually empties into the duodenum via the common bile duct.

The gall bladder is found centrally in the liver, bordered by the quadrate lobe and right medial liver lobe.

There are key differences in the anatomy of the common bile duct between dogs and cats that explain the pathophysiology of various hepatobiliary diseases. In dogs, the common bile duct enters the dorsal wall of the duodenum and opens into the lumen at the major duodenal papilla alongside the pancreatic duct. The larger accessory pancreatic duct opens at the minor duodenal papilla, which is found a few centimeters aborad from the major duodenal papilla. The pancreas is intimately associated with the common bile duct, and inflammation/swelling can result in extra-hepatic biliary obstruction (EHBO). The feline common bile duct conjoins the only pancreatic duct in this species prior to entering the major duodenal papilla. Due to the fusion of the common bile and pancreatic ducts, the feline is at increased risk of ascending infection of the pancreas.

Extra-Hepatic Biliary Obstruction

Extra-hepatic biliary obstruction leads to severe metabolic derangement in multiple organs, and often requires immediate surgical treatment. EHBO is caused by either intra-luminal common bile duct disease or extra-luminal compression. In dogs, extra-luminal compression is the most common cause of EHBO and diseases that can cause this include gall bladder mucocele and pancreatitis. Diseases leading to intra-luminal pathology include cholelithiasis (gall bladder stones), choledocholithiasis (stones in the common bile duct) and biliary sludge. Inflammatory diseases such as cholangiohepatitis, cholecystitis and pancreatitis are the most commonly implicated diseases leading to EHBO in cats. It has been suggested that the most common cause of feline EHBO is cholangiohepatitis.

Reviewing the pathophysiology of biliary obstruction is pivotal in understanding why patients with EHBO can have severe systemic compromise. One of the major functions of bile salts is to initiate lipid absorption in the small intestine. This includes fat-soluble vitamins A, D, E and K. The coagulation factors II, VII, IX, X are vitamin K dependent, therefore, biliary obstruction leading to deficiency in vitamin K can cause coagulation derangements. This can be evidenced by increases in activated clotting time, prothrombin time and partial thromboplastin time. In health, bile acids are conjugated to bile salts in hepatocytes and secreted continuously into bile canaliculi and eventually into the duodenum.

Approximately 95% of bile salts are reabsorbed in the ileum and then transported to the liver for re-secretion. With EHBO, the liver’s ability to conjugate bile acids is impaired leading to increased levels of unconjugated bile acids in circulation. These substances are cytotoxic and can lead to tissue inflammation in various organs.

The intestinal mucosa is highly sensitive to the effects of unconjugated bile acids and increased levels can lead to intestinal mucosal injury and increased permeability. The latter allows bacterial translocation into the systemic circulation resulting in endotoxemia. Furthermore, reduced bile acids within the intestine leads to bacterial over-growth further compounding endotoxemia. In experimental studies performed in mice, EHBO has led to increased sensitivity of the body to endotoxin leading to a severe pro-inflammatory response predisposing the animal to systemic inflammatory response syndrome and multi-organ failure.

Abnormalities in laboratory tests are common in patients with EHBO. These include leukocytosis, hyperbilirubinemia, increased serum alkaline phosphatase, increased serum alanine aminotransferase and increased gamma-glutamyl and prolongation in clotting times. PT and proteins induced by absence of vitamin K test are the most sensitive coagulation tests, however, is not detected until 14 days post-EHBO. The clinician should keep in mind that while increased liver enzyme values are common in cases of EHBO, they are not specific for biliary obstruction.

Abdominal ultrasonography is a valuable imaging modality for evaluating the hepatobiliary system in small animals. Ultrasound can evaluate the gall bladder and the size and tortuosity of the intra-hepatic biliary tree and the common bile duct. Progressive distention of the biliary tract viewed with ultrasound is consistent with EHBO. An enlarged gall bladder with a non-mobile stellate appearance (also termed the “kiwi” gall bladder) is characteristic of gall bladder mucocele. The Cocker Spaniel and Shetland Sheepdog appear to be overrepresented in cases of this disease. Ultrasound is also very useful for evaluating the biliary tract for choleliths and particular attention should be paid to the area surrounding the major duodenal papilla. Finally, ultrasound can also be used to evaluate the regional anatomy of the hepatobiliary system for predisposing causes of EHBO (e.g., pancreatitis).

Exploratory celiotomy is an important diagnostic procedure in cases in which imaging has provided equivocal results yet clinical and laboratory findings are consistent with EHBO. At the time of celiotomy, the gall bladder and the common bile duct can be visually inspected for enlargement/distention and palpated for choleliths/choledocholiths. The gall bladder can also be expressed to determine patency of the extra-hepatic biliary tree. A duodenotomy can be performed for retrograde catheterization of the common bile duct or normograde catheterization can be performed following cholecystotomy. The anatomical structures surrounding the common bile duct can be evaluated for lesions that could be causing EHBO.

As previously discussed, most patients with EHBO present in the later stages of disease and are systemically compromised at the time of presentation. Prior to surgical intervention many patients require aggressive hemodynamic resuscitation. Intravenous (IV) fluid therapy should be initiated following calculation of fluid deficit and administration rate will depend on the clinical assessment of the patients as some patients may present with hypovolemic shock. Depending on the response to initial IV fluid therapy, colloidal therapy may be required for maintaining intravascular volume. Several types of bacteria have been cultured from patients with EHBO including E. coli, Clostridium spp., Enterococcus spp., and Bacteroides spp. An empirically selected antimicrobial with broad-spectrum activity should be administered promptly following diagnosis of EHBO. A second-generation cephalosporin (cefoxitin 20–15 mg/kg IV q 8 h) is preferred by the author and ampicillin (22 mg/kg IV q 8 h) can also be added to increase coverage to include Enterococcus spp. In cases where coagulation deficiencies are present, vitamin K supplementation (0.1–0.2 mg/g SQ q 12 h) should be administered.

Furthermore, fresh frozen plasma transfusion can also be considered for these patients. In anemic patients, packed red blood cells can be considered, however, if concurrent coagulation deficiencies are present, whole blood transfusion should be administered as it contains erythrocytes and clotting factors.

The goal of surgical treatment of patients with EHBO is to re-establish biliary drainage into the intestinal tract as continued obstruction will lead to progressive metabolic derangements and eventually death. The most common surgical interventions include cholecystectomy (gall bladder removal) in cases of gall bladder mucocele or cholecystitis or a biliary re-routing procedure (cholecystoenterostomy—attaching the gall bladder to either the duodenum [cholecystoduodenostomy] or jejunum [cholecystojejunostomy]) for pathology of the common bile duct. The surgeon should keep in mind that these procedures can be technically demanding and are associated with high mortality rates (28–64%) despite improvements in surgical technique and post-operative supportive care. Refractory hypotension in the intra-operative period has been linked to a higher incidence of post-operative mortality.

It has been suggested that the presence of circulating unconjugated bile acids decreases the effect of vasopressors, which leads to the refractory hypotensive state during surgery. Other negative prognostic indicators include azotemia, coagulation deficiencies and septic bile peritonitis.