Gallbladder lies beneath segments IV and V
Cystic artery branches off right hepatic artery
• Is found in the triangle of Calot (cystic duct [lateral], common bile duct [medial], liver [superior])
Right hepatic (lateral) and retroduodenal branches of the gastroduodenal artery (medial) supply the hepatic and common bile duct (9- and 3-o’clock positions when performing endoscopic retrograde cholangiopancreatography [ERCP]); considered longitudinal blood supply
Cystic veins drain into the right branch of the portal vein
Lymphatics are on the right side of the common bile duct
Parasympathetic fibers come from left (anterior) trunk of the vagus
Sympathetic fibers from T7–10 (splanchnic and celiac ganglions)
Gallbladder has no submucosa; mucosa is columnar epithelium
Common bile duct and common hepatic duct do not have peristalsis
Gallbladder normally fills by contraction of sphincter of Oddi at the ampulla of Vater
• Morphine – contracts the sphincter of Oddi
• Glucagon – relaxes the sphincter of Oddi
Normal sizes: common bile duct (CBD) < 8 mm (< 10 mm after cholecystectomy), gallbladder wall < 4 mm, pancreatic duct < 4 mm
After cholecystectomy, total bile salt pools ↓
Highest concentration of CCK and secretin cells are in the duodenum
Rokitansky–Aschoff sinuses – epithelial invaginations in the gallbladder wall; formed from ↑ gallbladder pressure
Ducts of Luschka – biliary ducts that can leak after a cholecystectomy; lie in the gallbladder fossa
Bile excretion regulation
• ↑ bile excretion – CCK, secretin, and vagal input
• ↓ bile excretion – somatostatin, sympathetic stimulation
• Gallbladder contraction – CCK causes constant, steady, tonic contraction
Essential functions of bile:
• Fat-soluble vitamin absorption
• Essential fat absorption
• Bilirubin and cholesterol excretion
Gallbladder – forms concentrated bile by active resorption of NaCl and water
• Active resorption of conjugated bile salts occurs in the terminal ileum (50%)
• Passive resorption of nonconjugated bile salts can occur in the small intestine (45%) and colon (5%)
• Postprandial gallbladder emptying is maximum at 2 hours (80%)
• Bile secreted by hepatocytes (80%) and bile canalicular cells (20%)
• Color of bile is mostly due to conjugated bilirubin
• Stercobilin – breakdown product of conjugated bilirubin in gut; gives stool brown color
• Urobilinogen – conjugated bilirubin is broken down in the gut and reabsorbed; gets converted to urobilinogen and eventually urobilin, which is released in the urine (yellow color)
CHOLESTEROL AND BILE ACID SYNTHESIS
HMG CoA → (HMG CoA reductase) → cholesterol → (7-alpha-hydroxylase) → bile salts (acids)
HMG CoA reductase – rate-limiting step in cholesterol synthesis
GALLSTONES
Occur in 10% of the population; vast majority are asymptomatic
Only 10% of gallstones are radiopaque
Nonpigmented stones
• Cholesterol stones – caused by stasis, calcium nucleation, and ↑ water reabsorption from gallbladder
• Also caused by ↓ lecithin and bile salts
• Found almost exclusively in the gallbladder
• Most common type of stone found in the United States (75%)
Pigmented stones – most common worldwide
• Calcium bilirubinate stones – caused by solubilization of unconjugated bilirubin with precipitation
• Dissolution agents (monooctanoin) do not work on pigmented stones
• Black stones
• Can be caused by hemolytic disorders, cirrhosis, ileal resection (loss of bile salts), chronic TPN
• Factors for development – ↑ bilirubin load, ↓ hepatic function, and bile stasis → get calcium bilirubinate stones
• Almost always form in gallbladder
• Tx: cholecystectomy if symptomatic
• Brown stones (primary CBD stones, formed in ducts, Asians)
• Infection causing deconjugation of bilirubin
• E. coli most common – produces beta-glucuronidase, which deconjugates bilirubin with formation of calcium bilirubinate
• Need to check for ampullary stenosis, duodenal diverticula, abnormal sphincter of Oddi
• Most commonly form in the bile ducts (are primary common bile duct stones)
• Tx: almost all patients with primary stones need a biliary drainage procedure – sphincteroplasty (90% successful)
• Cholesterol stones and black stones found in the CBD are considered secondary common bile duct stones
CHOLECYSTITIS
Caused by obstruction of the cystic duct by a gallstone
Results in gallbladder wall distention and wall inflammation
Symptoms: RUQ pain, referred pain to the right shoulder and scapula, nausea and vomiting, loss of appetite
• Attacks frequently occur after a fatty meal; pain is persistent (unlike biliary colic)
Murphy’s sign – patient resists deep inspiration with deep palpation to the RUQ secondary to pain
Alkaline phosphatase and WBCs are frequently elevated
Suppurative cholecystitis associated with frank purulence in the gallbladder → can be associated with sepsis and shock
Most common organisms in cholecystitis – E. coli (#1), Klebsiella, Enterococcus
Stone risk factors – age > 40, female, obesity, pregnancy, rapid weight loss, vagotomy, TPN (pigmented stones), ileal resection (pigmented stones)
Ultrasound – 95% sensitive for picking up stones → hyperechoic focus, posterior shadowing, movement of focus with changes in position
• Best initial evaluation test for jaundice or RUQ pain
• Findings suggestive of acute cholecystitis – gallstones, gallbladder wall thickening (> 4 mm), pericholecystic fluid
• Dilated CBD (> 8 mm) suggests CBD stone and obstruction
HIDA scan – technetium taken up by liver and excreted in the biliary tract
CCK-CS test (cholecystokinin cholescintigraphy)
• Most sensitive test for cholecystitis (also uses HIDA above)
• Indications for cholecystectomy after CCK-CS test:
• If gallbladder not seen (the cystic duct likely has a stone in it)
• Takes > 60 minutes to empty (chronic cholecystitis)
• Ejection fraction < 40% (biliary dyskinesia)
Indications for immediate ERCP (signs that a common bile duct stone is present) – jaundice, cholangitis, U/S shows stone in CBD
Indications for pre-op ERCP (any of following needs to be persistently high for > 24 hours to justify pre-op ERCP) – AST or ALT (> 200), bilirubin (> 4), or amylase or lipase (> 1,000)
• < 5% of patients undergoing cholecystectomy will have a retained CBD stone → 95% of these are cleared with ERCP
Tx for cholecystitis – cholecystectomy; cholecystostomy tube can be placed in patients who are very ill and cannot tolerate surgery
ERCP – best treatment for late common bile duct stone
• Sphincterotomy allows for removal of stone
• Risks: bleeding, pancreatitis, perforation
Biliary colic – transient cystic duct obstruction caused by passage of a gallstone
• Resolves within 4–6 hours
Air in the biliary system most commonly occurs with previous ERCP and sphincterotomy
• Can also occur with cholangitis or erosion of the biliary system into the duodenum (ie gallstone ileus)
Bacterial infection of bile – dissemination from portal system is the most common route (not retrograde through sphincter of Oddi)
Highest incidence of positive bile cultures occurs with postoperative strictures (usually E. coli, often polymicrobial)
ACALCULOUS CHOLECYSTITIS
Thickened wall, RUQ pain, ↑ WBCs, no stones
Occurs most commonly after severe burns, prolonged TPN, trauma, or major surgery
Primary pathology is bile stasis (narcotics, fasting), leading to distention and ischemia
Also have ↑ viscosity secondary to dehydration, ileus, transfusions
Ultrasound shows sludge, gallbladder wall thickening, and pericholecystic fluid
HIDA scan is positive
Tx: cholecystectomy; percutaneous drainage if patient too unstable
EMPHYSEMATOUS GALLBLADDER DISEASE
Gas in the gallbladder wall – can see on plain film
↑ in diabetics; usually secondary to Clostridium perfringens
Symptoms: severe, rapid-onset abdominal pain, nausea, vomiting, and sepsis
Perforation more common in these patients
Tx: emergent cholecystectomy; percutaneous drainage if patient is too unstable
GALLSTONE ILEUS
Fistula between gallbladder and duodenum that releases stone, causing small bowel obstruction; elderly
• Can see pneumobilia (air in the biliary system) on plain film
Terminal ileum – most common site of obstruction
Tx: remove stone through enterotomy proximal to obstruction
• Perform cholecystectomy and fistula resection if patient can tolerate it (if old and frail, just leave the fistula)
COMMON BILE DUCT INJURIES
Most commonly occur after laparoscopic cholecystectomy
Intraoperative CBD injury – if < 50% the circumference of the common bile duct, can probably perform primary repair; in all other cases, will likely need hepaticojejunostomy (or choledochojejunostomy)
Persistent nausea and vomiting or jaundice following laparoscopic cholecystectomy → get U/S to look for fluid collection
• If fluid collection is present, may be bile leak → percutaneous drain into the collection
• If fluid is bilious, get ERCP → sphincterotomy and stent if due to cystic duct remnant leak, small injuries to the hepatic or common bile duct, or a leak from a duct of Luschka
• Larger lesions (ie complete duct transection) will require hepaticojejunostomy or choledochojejunostomy (see below for timing)
• If fluid collection not present and the hepatic ducts are dilated, likely have a completely transected common bile duct (PTC tube initially, then hepaticojejunostomy or choledochojejunostomy)
• For lesions that cause early symptoms (≤ 7 days) – hepaticojejunostomy
• For lesions that cause late symptoms (> 7 days) – hepaticojejunostomy 6–8 weeks after injury (tissue too friable for surgery after 7 days)
Sepsis following laparoscopic cholecystectomy → fluid resuscitation and stabilize
• May be due to complete transection of the CBD and cholangitis → get U/S to look for dilated intrahepatic ducts or fluid collections (pathway same as above)
Anastomotic leaks following transplantation or hepaticojejunostomy → usually handled with percutaneous drainage of fluid collection followed by ERCP with temporary stent (leak will heal)