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  • Complications of the Extrahepatic Biliary Surgery in Companion Animals

    Stephen J. Mehler, DVM


    • Hepatobiliary • Biliary surgery • Extrahepatic biliary tract obstruction • Gallbladder • Hemorrhage

    The earliest documented diagnosis of gall stones dates back to the twenty-first Egyptian Dynasty (1085–945 BC), although cholelithiasis was not recognized as a clinical condition in human subjects until the 5th century AD and the earliest recorded cholecystectomy performed in a living patient did not occur for another 1300 years.1,2

    Physicians continue to struggle with the diagnosis and treatment of extrahepatic biliary disease in human patients today.

    The recognition and treatment of extrahepatic biliary tract (EHBT) disease in small animals has been equally challenging. Although the vague clinical signs associated with extrahepatic biliary disease in small animals often delayed recognition and treatment of the condition in the past, the technological advances in veterinary diagnostic imaging have largely removed this obstacle. However, the recent veterinary literature continues to reflect a poor overall outcome for dogs and cats undergoing surgery of the EHBT. A conservative estimate for survival in dogs undergoing surgery of the extrahepatic biliary tract is (140/220) is 63.6% and for cats is (28/68) 41%.3–16

    The mortality rate in cats that undergo surgical intervention for EHBTO is nearly 100% when neoplasia is involved.5 The high mortality associated with surgery of the EHBT is related not only to technical errors made during surgical procedures but is compounded by the complex pathophysiology of hepatobiliary disease, which has broad effects on wound healing, hemostasis, and sepsis. The recognition and thorough understanding of possible pathophysiologic and surgical complications associated with diseases of the extrahepatic biliary tract is the first step in achieving an improved outcome for small animals undergoing surgery of the EHBT.


    The canine extrahepatic biliary system is composed of the gallbladder, the cystic duct, hepatic ducts, the common bile duct, and the major duodenal papilla. In dogs,

    Veterinary Specialists of Rochester, 825 White Spruce Boulevard, Rochester, NY 14623, USA E-mail address:

    Vet Clin Small Anim 41 (2011) 949–967 doi:10.1016/j.cvsm.2011.05.009

    0195-5616/11/$ – see front matter © 2011 Elsevier Inc. All rights reserved.

  • o a t i a E a r t e

    950 Mehler

    bile flows from the bile canniliculi into the interlobular ducts and into the lobar ducts before leaving the liver. Lobar ducts drain into hepatic ducts, through which bile passes into the common bile duct.17,18 The gallbladder lies within a fossa between the right medial and quadrate lobes of the liver. The gallbladder is drained by the cystic duct which joins with hepatic ducts to form what is often termed the “common bile duct.” It should be noted that although the term “common bile duct” is used frequently in the veterinary literature, this structure is identified simply as the “bile duct” in the standard anatomical text.19 Throughout the following text, common bile duct and bile duct will be used interchangeably. In dogs the common bile duct terminates near the minor pancreatic duct at the major duodenal papilla. In a medium-sized dog the common bile duct is approximately 5 cm long and 2.5 mm in diameter, emptying into the duodenum 1.5 to 6 cm distal to the pylorus at the major duodenal papilla after coursing intramurally for approximately 2 cm. The blood supply to the gallbladder and common bile duct is derived from the left branch of the proper hepatic artery.19

    Bilirubin is a byproduct of the enzymatic cleavage of the heme molecule, a central structural element in the hemoglobin molecule of erythrocytes but also in thousands of ubiquitous cellular enzymes. Unconjugated bilirubin is a hydrophobic molecule but is soluble in plasma due to a strong affinity for albumin. After traveling to the liver, bilirubin is conjugated by the enzyme UDP-GT and is released into the bile caniliculi, eventually draining into the intestine at the major duodenal papilla. Bile salts are a natural detergent for the small intestine, binding endotoxin and bacteria and rendering them ineffective. Bile salts also are important in fat emulsification and absorption, which includes the fat-soluble vitamins. The majority of bilirubin is removed from the body as stercobilinogen in the feces while a smaller portion is removed as urobilino- gen in the urine.


    The effects of EHBT obstruction are widespread and devastating. When bile is retained due to EHBT obstruction, an accumulation of bilirubin in the blood occurs and down-regulation of the reticuloendothelial system (RES) soon follows.20,21 Lack

    f bile in the intestinal tract leads to diminished absorption of vitamin K in the ileum nd, with time, vitamin K deficiency can lead to coagulopathies. Since factor VII has he shortest half-life of the routinely measured coagulation factors in dogs and cats, t would be expected that prothrombin time (PT) would commonly be elevated in nimals with extrahepatic biliary tract obstruction; however, in many chronic cases of HBT obstruction partial thromboplastin time (PTT) is also elevated and this finding is ssociated with a worse short-term outcome in dogs.4 Prolongation in PTT may be elated to the binding of coagulation factors XI and XII by endotoxin. Endotoxemia in he obstructive jaundice patient has been documented in humans and has been xperimentally produced in multiple animal models.21–29 Development of sepsis is

    believed to be related to the lack of a detergent effect on bacteria and endotoxin within the lumen of the small intestine, allowing delivery of unbound bacteria and endotoxin to the liver and the already failing RES. Thus, through direct and indirect effects, EHBT obstruction can produce a variety of sequelae including acute tubular necrosis, hypotension, coagulopathy, decreased wound healing, gastrointestinal hemorrhage, systemic and portal endotoxemia and bacteremia, continued gastroin- testinal bacterial translocation, SIRS, sepsis, disseminated intravascular coagulation

    (DIC), and myocardial damage.23–27

  • c f s v t o

    951Extrahepatic Biliary Surgery in Companion Animals


    Clinical signs in dogs and cats with extrahepatic biliary tract obstruction include decreased appetite and lethargy in up to 100% of patients, icterus in up to 100%, vomiting in up to 92%, weight loss in up to 82%, abdominal pain on palpation in up to 50%, and fever in 38%.5,9,30,31 The duration of clinical signs before presentation for surgery in dogs ranges from 2 hours to 210 days8,31 and 14 to 150 days in cats5,8,9

    and signs may wax and wane for several weeks before presentation or may be acute and life threatening. Clinical signs associated with surgical complications of the biliary tree are nonspecific and mimic other abdominal disorders. Following surgery, development of abdominal pain, vomiting, anorexia, diarrhea, lethargy, icteric mucous membranes and serum, and signs of shock are all potential indicators of surgical complications that warrant further diagnostic investigations. Careful attention to daily physical examination findings in the perioperative period is an essential step in detecting complications.


    Delays in initiating definitive therapy for EHBT disease have been shown to signifi- cantly affect outcome in human patients. In the past, cholelithiasis in human beings was treated medically until the patient suffered from severe abdominal pain or when obstructive jaundice developed. Morbidity and mortality rates in human EHBT surgery were approximately 30% when surgical intervention was used as a last resort.22,32–34

    Due to these poor success rates, the current surgical trend for patients with potential surgical EHBT disease is to provide an interventional, and often definitive, surgical therapy as soon as possible, and preferentially before the patient is systemically ill. The early use of cholecystectomy to treat human patients with nonobstructive cholelithiasis has significantly lowered the morbidity and mortality rates in humans undergoing EHBT surgery.23 Due to the influence of economics on provision of veterinary care, delays in providing definitive surgical care are also quite common in small animals with EHBT disease. Interestingly, use of surgery as a last resort has produced relatively high mortality rates in small animals, paralleling the historical results for this failed approach in human beings. Although there is no data to directly support the effects of early intervention in animals in EHBT disease, it would appear logical that adoption of this approach may show similar benefits in outcomes for animals.

    Several recent publications have described the use of percutaneous biliary diversion in dogs with EHBT obstruction until the cause of the obstruction has resolved or until the patient is more stable for surgery.35–37 Although this strategy can be effective in lowering serum bilirubin concentrations and avoiding its sequelae, it does not address the physiologic consequences that are due to the absence of bile within the small intestine. Availability of interventional and laparoscopic techniques in human medicine produced a similar use of preoperative biliary drainage and decom- pression or definitive extracorporeal drainage.38 Unfortunately, most investigators