Chapter 147 Extrahepatic Biliary Tract Disease Keith P. Richter, San Diego, California Fred S. Pike, San Diego, California The extrahepatic biliary tract (EHBT) consists of hepatic ducts, the common bile duct (CBD), the gallbladder (GB), cystic duct, and the duodenal papillae. In general the clinical presentations for diseases of the EHBT are the result of alteration in or obstruction of the normal passage of bile. Biliary diseases can be categorized as (1) biliary cystic disease, (2) cholestatic disease, (3) cholangitis, and (4) disorders of the GB. Clinical presentations of patients with extrahepatic biliary obstruction (EHBO) are varied, and the onset of clinical signs can be acute or chronic and insidious. Recent veterinary literature suggests that the prevalence of diseases of the EHBT is increasing. Anatomy In the liver, bile canaliculi unite to form plexiform interlobular ducts. Interlobular ducts congregate to form lobar ducts, which unite to form hepatic ducts. Three or four hepatic ducts terminate in the CBD. The order and location of termination of the hepatic ducts is varied and has been documented. The GB is a vesicle that stores bile. Duplex GB and duplex cystic ducts have been reported in cats. The GB is lined by columnar epithelial cells that reabsorb water and electrolytes, resulting in concentrated bile with increased viscosity. Submucosal mucous glands secrete mucus that acts as a bile lubricant. The GB is nestled in a fossa between the right medial and quadrate liver lobes. The GB has a blind-end, rounded base termed the fundus, a large middle portion termed the body, and a slender tapered region termed the neck. The cystic duct extends from the neck of the GB to the junction with the first hepatic duct. The GB has an end-artery vascularity via the cystic artery. The lack of collateral arterial supply may contribute to vascular compromise during marked distention. The CBD begins at the junction of the last hepatic duct and ends on the major duodenal papilla; its length is approximately 5 cm in the medium-size dog. The normal CBD diameter is 2 to 2.5 mm in the cat and 3 mm in the dog. The canine CBD has a duodenal intramural length of 1.5 to 2 cm and terminates at the sphincter of the major duodenal papilla (commonly called the sphincter of Oddi or sphincter of ampulla). The orifice of the CBD shares the major duodenal papilla with the orifice of the accessory pancreatic duct in approximately 75% of dogs. In the cat the CBD unites with the major pancreatic duct before the duodenal papilla; manipulation and catheterization of the major duodenal papilla in cats may increase the risk of pancreatitis. GB filling is passive; it is the result of retrograde flow into the GB caused by increased intraluminal CBD pressure that occurs when the sphincter of the major duodenal papilla is closed. GB contraction is induced by cholecystokinin synthesized by I cells in the mucosal epithelium of the duodenum. Cholecystokinin also causes increased production of bile and causes relaxation of the sphincter of the major duodenal papilla resulting in excretion of bile into the duodenum. Vagal parasympathetic innervation also contributes to GB contraction. Diagnostic Imaging Radiographic findings generally are insensitive for diseases of the EHBT with the exception of radiodense choleliths and emphysematous cholecystitis. Decreased serosal detail indicative of ascites may be identified radiographically in patients with bile peritonitis. Radiographic contrast studies (percutaneous transhepatic cholangiocystography) have been described for imaging the EHBT but largely have been replaced by ultrasonography. The ultrasonographic findings for EHBT diseases such as cholecystitis, cholelithiasis, and GB mucocele are well documented in the literature with abdominal ultrasound considered the standard imaging modality. A skilled ultrasonographer can evaluate the size and shape of the GB lumen, evaluate the integrity of the GB wall, measure the diameter of the CBD, evaluate the intrahepatic lobar ducts, and evaluate the region of the duodenal papillae. Evaluation for ascitic fluid during sonography is critical and fluid analysis can be a valuable diagnostic tool. (Cytologic evaluation includes evaluation for bile pigment, neutrophilic inflammation, and intracellular bacteria.) Dilation of the EHBT is time dependent after obstruction, and thus lack of dilation does not rule out biliary obstruction. In an experimental model in dogs, complete occlusion of the CBD resulted in GB distention within 24 hours, extrahepatic bile duct distention within 48 to 72 hours, and intrahepatic ductal dilation within 5 to 7 days. Chronic, partial CBD obstructions can provide a diagnostic dilemma because ultrasonographic findings can be subtle; the diagnosis is often presumptive. Other diagnostic modalities infrequently used for the evaluation of the EHBT include cholecystography, hepatobiliary scintigraphy, endoscopic retrograde cholangiopancreatography, computed tomography, and magnetic resonance cholangiopancreatography. Cost, availability, patient size limitations, and the sensitivity of abdominal ultrasound generally preclude the use of these modalities. Diseases Cholecystitis Cholecystitis can be categorized as necrotizing (type I), acute (type II), and chronic (type III) or emphysematous. Ultrasound may identify a thickened GB wall, intraluminal echogenic debris, choleliths, EHBO, and emphysema of the GB wall. Ultrasound is highly sensitive for the identification of GB rupture (85% sensitivity). Loss of the GB wall continuity, hyperechoic fat in the cranial peritoneal cavity, and free abdominal fluid are supportive for GB rupture. Nonsurgical management of cholecystitis may be appropriate in select cases when the GB wall integrity is not compromised. Medical management includes antibiotic and analgesic therapy, choleretics (contraindicated preoperatively in patients with EHBO), and the treatment of any underlying comorbidities. Antibiotic therapy ideally should be guided by culture and sensitivity. In nonsurgical cases this would necessitate cholecystocentesis with the transhepatic method preferred to limit and contain leakage. Without samples for culture, empiric parenteral antibiotic therapy effective against gram-negative bacteria and anaerobic bacteria is advised. Cefoxitin, metronidazole, and/or enrofloxacin are appropriate antibiotic choices. Escherichia coli, Enterococcus spp., Bacteroides spp., and Clostridium spp. are among the most common isolates. In patients with ultrasonographic evidence of severe GB wall compromise or GB rupture, cholecystectomy is advised. Histopathology and culture of the GB wall and luminal contents are imperative, and liver biopsies also are advised. Intraoperative evaluation of the patency of the CBD is mandatory and generally is performed via normograde catheterization of the CBD via the transected cystic duct. A red rubber (Brunswick) catheter generally is used. The surgeon must be certain to advance the catheter into the duodenum to confirm patency of the sphincter of the major duodenal papilla. Patients with cholecystitis can be compromised cardiovascularly with the need for aggressive perioperative crystalloid and colloid therapy. Pressor therapy also is needed frequently. Patients with chronic EHBO may be coagulopathic because of a relative deficiency in vitamin K from altered hepatobiliary excretion of bile acids required for vitamin K absorption. Coagulation profiles are advised perioperatively. Elevations in partial thromboplastin time (PTT) have been associated with a worse short-term outcome in dogs. Vitamin K1 (0.5 mg/kg to 1.5 mg/kg IM or SC) can be administered with or without fresh frozen plasma. Chronic EHBO has been associated with septicemia, endotoxemia, and down-regulation of the reticuloendothelial system in humans and dogs. A theoretic concern regarding perioperative analgesic therapy is the effect of pure mu-agonists, such as morphine, on smooth muscle tone. In humans, pure mu-agonists can increase the tone of the sphincter of the major duodenal papilla, resulting in a functional obstruction and increase in visceral pain. The effect in companion animals is documented poorly. Maropitant (Cerenia), a neurokinin-1 receptor antagonist, should be considered for managing visceral pain management and combating the nausea that can accompany distention of the EHBT.< div class='tao-gold-member'> Only gold members can continue reading. Log In or Register to continue Share this:Click to share on Twitter (Opens in new window)Click to share on Facebook (Opens in new window) Related Related posts: Ventilator Therapy for the Critical Patient Lawn and Garden Product Safety ASPCA Animal Poison Control Center Toxin Exposures for Pets Diabetic Monitoring Stay updated, free articles. Join our Telegram channel Join Tags: Kirks Current Veterinary Therapy XV Jul 18, 2016 | Posted by admin in PHARMACOLOGY, TOXICOLOGY & THERAPEUTICS | Comments Off on Extrahepatic Biliary Tract Disease Full access? Get Clinical Tree
Chapter 147 Extrahepatic Biliary Tract Disease Keith P. Richter, San Diego, California Fred S. Pike, San Diego, California The extrahepatic biliary tract (EHBT) consists of hepatic ducts, the common bile duct (CBD), the gallbladder (GB), cystic duct, and the duodenal papillae. In general the clinical presentations for diseases of the EHBT are the result of alteration in or obstruction of the normal passage of bile. Biliary diseases can be categorized as (1) biliary cystic disease, (2) cholestatic disease, (3) cholangitis, and (4) disorders of the GB. Clinical presentations of patients with extrahepatic biliary obstruction (EHBO) are varied, and the onset of clinical signs can be acute or chronic and insidious. Recent veterinary literature suggests that the prevalence of diseases of the EHBT is increasing. Anatomy In the liver, bile canaliculi unite to form plexiform interlobular ducts. Interlobular ducts congregate to form lobar ducts, which unite to form hepatic ducts. Three or four hepatic ducts terminate in the CBD. The order and location of termination of the hepatic ducts is varied and has been documented. The GB is a vesicle that stores bile. Duplex GB and duplex cystic ducts have been reported in cats. The GB is lined by columnar epithelial cells that reabsorb water and electrolytes, resulting in concentrated bile with increased viscosity. Submucosal mucous glands secrete mucus that acts as a bile lubricant. The GB is nestled in a fossa between the right medial and quadrate liver lobes. The GB has a blind-end, rounded base termed the fundus, a large middle portion termed the body, and a slender tapered region termed the neck. The cystic duct extends from the neck of the GB to the junction with the first hepatic duct. The GB has an end-artery vascularity via the cystic artery. The lack of collateral arterial supply may contribute to vascular compromise during marked distention. The CBD begins at the junction of the last hepatic duct and ends on the major duodenal papilla; its length is approximately 5 cm in the medium-size dog. The normal CBD diameter is 2 to 2.5 mm in the cat and 3 mm in the dog. The canine CBD has a duodenal intramural length of 1.5 to 2 cm and terminates at the sphincter of the major duodenal papilla (commonly called the sphincter of Oddi or sphincter of ampulla). The orifice of the CBD shares the major duodenal papilla with the orifice of the accessory pancreatic duct in approximately 75% of dogs. In the cat the CBD unites with the major pancreatic duct before the duodenal papilla; manipulation and catheterization of the major duodenal papilla in cats may increase the risk of pancreatitis. GB filling is passive; it is the result of retrograde flow into the GB caused by increased intraluminal CBD pressure that occurs when the sphincter of the major duodenal papilla is closed. GB contraction is induced by cholecystokinin synthesized by I cells in the mucosal epithelium of the duodenum. Cholecystokinin also causes increased production of bile and causes relaxation of the sphincter of the major duodenal papilla resulting in excretion of bile into the duodenum. Vagal parasympathetic innervation also contributes to GB contraction. Diagnostic Imaging Radiographic findings generally are insensitive for diseases of the EHBT with the exception of radiodense choleliths and emphysematous cholecystitis. Decreased serosal detail indicative of ascites may be identified radiographically in patients with bile peritonitis. Radiographic contrast studies (percutaneous transhepatic cholangiocystography) have been described for imaging the EHBT but largely have been replaced by ultrasonography. The ultrasonographic findings for EHBT diseases such as cholecystitis, cholelithiasis, and GB mucocele are well documented in the literature with abdominal ultrasound considered the standard imaging modality. A skilled ultrasonographer can evaluate the size and shape of the GB lumen, evaluate the integrity of the GB wall, measure the diameter of the CBD, evaluate the intrahepatic lobar ducts, and evaluate the region of the duodenal papillae. Evaluation for ascitic fluid during sonography is critical and fluid analysis can be a valuable diagnostic tool. (Cytologic evaluation includes evaluation for bile pigment, neutrophilic inflammation, and intracellular bacteria.) Dilation of the EHBT is time dependent after obstruction, and thus lack of dilation does not rule out biliary obstruction. In an experimental model in dogs, complete occlusion of the CBD resulted in GB distention within 24 hours, extrahepatic bile duct distention within 48 to 72 hours, and intrahepatic ductal dilation within 5 to 7 days. Chronic, partial CBD obstructions can provide a diagnostic dilemma because ultrasonographic findings can be subtle; the diagnosis is often presumptive. Other diagnostic modalities infrequently used for the evaluation of the EHBT include cholecystography, hepatobiliary scintigraphy, endoscopic retrograde cholangiopancreatography, computed tomography, and magnetic resonance cholangiopancreatography. Cost, availability, patient size limitations, and the sensitivity of abdominal ultrasound generally preclude the use of these modalities. Diseases Cholecystitis Cholecystitis can be categorized as necrotizing (type I), acute (type II), and chronic (type III) or emphysematous. Ultrasound may identify a thickened GB wall, intraluminal echogenic debris, choleliths, EHBO, and emphysema of the GB wall. Ultrasound is highly sensitive for the identification of GB rupture (85% sensitivity). Loss of the GB wall continuity, hyperechoic fat in the cranial peritoneal cavity, and free abdominal fluid are supportive for GB rupture. Nonsurgical management of cholecystitis may be appropriate in select cases when the GB wall integrity is not compromised. Medical management includes antibiotic and analgesic therapy, choleretics (contraindicated preoperatively in patients with EHBO), and the treatment of any underlying comorbidities. Antibiotic therapy ideally should be guided by culture and sensitivity. In nonsurgical cases this would necessitate cholecystocentesis with the transhepatic method preferred to limit and contain leakage. Without samples for culture, empiric parenteral antibiotic therapy effective against gram-negative bacteria and anaerobic bacteria is advised. Cefoxitin, metronidazole, and/or enrofloxacin are appropriate antibiotic choices. Escherichia coli, Enterococcus spp., Bacteroides spp., and Clostridium spp. are among the most common isolates. In patients with ultrasonographic evidence of severe GB wall compromise or GB rupture, cholecystectomy is advised. Histopathology and culture of the GB wall and luminal contents are imperative, and liver biopsies also are advised. Intraoperative evaluation of the patency of the CBD is mandatory and generally is performed via normograde catheterization of the CBD via the transected cystic duct. A red rubber (Brunswick) catheter generally is used. The surgeon must be certain to advance the catheter into the duodenum to confirm patency of the sphincter of the major duodenal papilla. Patients with cholecystitis can be compromised cardiovascularly with the need for aggressive perioperative crystalloid and colloid therapy. Pressor therapy also is needed frequently. Patients with chronic EHBO may be coagulopathic because of a relative deficiency in vitamin K from altered hepatobiliary excretion of bile acids required for vitamin K absorption. Coagulation profiles are advised perioperatively. Elevations in partial thromboplastin time (PTT) have been associated with a worse short-term outcome in dogs. Vitamin K1 (0.5 mg/kg to 1.5 mg/kg IM or SC) can be administered with or without fresh frozen plasma. Chronic EHBO has been associated with septicemia, endotoxemia, and down-regulation of the reticuloendothelial system in humans and dogs. A theoretic concern regarding perioperative analgesic therapy is the effect of pure mu-agonists, such as morphine, on smooth muscle tone. In humans, pure mu-agonists can increase the tone of the sphincter of the major duodenal papilla, resulting in a functional obstruction and increase in visceral pain. The effect in companion animals is documented poorly. Maropitant (Cerenia), a neurokinin-1 receptor antagonist, should be considered for managing visceral pain management and combating the nausea that can accompany distention of the EHBT.< div class='tao-gold-member'> Only gold members can continue reading. Log In or Register to continue Share this:Click to share on Twitter (Opens in new window)Click to share on Facebook (Opens in new window) Related Related posts: Ventilator Therapy for the Critical Patient Lawn and Garden Product Safety ASPCA Animal Poison Control Center Toxin Exposures for Pets Diabetic Monitoring Stay updated, free articles. Join our Telegram channel Join
