Benign Gallbladder and Biliary Tree

I

Anatomy

A

Gallbladder

1.
Pear-shaped sac lying in gallbladder fossa on inferior surface of liver with 30–50-mL capacity, greater than 300-mL capacity when obstructed
2.
Divided into four anatomic portions: fundus, corpus, infundibulum, and neck
3.
Demarcates anatomic division between left and right hepatic lobes (Cantlie line runs between gallbladder and inferior vena cava [IVC] and divides liver in two lobes)
4.
Supplied by the cystic artery
- a.
  Originates from the right hepatic artery in 90%; can arise from left hepatic, common hepatic, gastroduodenal, or superior mesenteric arteries
- b.
  Courses superiorly and posteriorly to the cystic duct until it reaches the peritoneal surface of the gallbladder and divides
5.
Venous drainage
- a.
  Rarely a cystic vein drains to right portal vein.
- b.
  Primarily through small veins, these drain directly into liver
6.
Cystic duct
- a.
  Connects the gallbladder to the common duct system
- b.
  Sits just anterior to the right hepatic artery
- c.
  Valves of Heister—mucosal folds at the gallbladder/cystic duct junction
- d.
  Highly variable in length and anatomic course
7.
Calot triangle
- a.
  Common hepatic duct, liver, cystic duct define the boundaries (modern definition)
- b.
  Cystic artery, right hepatic artery, and the cystic duct lymph node (Calot node) lie within this triangle.

B

Bile Ducts

1.
Left and right hepatic ducts join to form a common hepatic duct.
- a.
  Left is longer than right and is at increased risk for dilatation from distal obstruction.
- b.
  They are joined by the cystic duct to form the common bile duct (CBD).
2.
CBD is approximately 8–11.5 cm in length and 2–10 mm in diameter.
3.
There are three portions to the CBD: suprapancreatic, intrapancreatic, and intraduodenal.
4.
CBD empties into the duodenum in one of two patterns:
- a.
  Unites with the pancreatic duct outside the duodenum and enters the duodenum as a single duct (75%)
- b.
  Exits into the duodenum via a separate orifice (25%)
5.
Blood supply of CBD is from gastroduodenal artery and right hepatic artery.

C

Anomalies

Awareness of the highly variable nature of the gallbladder and associated structures is critical in the approach to the patient undergoing gallbladder or biliary surgery.

1.
Gallbladder—duplication, intrahepatic, left-sided, or bilobed
2.
Cystic duct—short or absent, long with alternative course, double cystic duct, accessory cystic duct, ducts of Luschka (drain directly from liver into gallbladder and may require clipping to prevent postoperative biloma)
3.
Cystic artery and hepatic arteries—double cystic artery, accessory left hepatic artery, replaced right hepatic artery

II

Cholelithiasis

A

Incidence

1.
Found in 12% of general population
2.
Majority (80%) are asymptomatic.
3.
Predisposing conditions
- a.
  Sex distribution—twice as common in women
- b.
  Age—found in 20% of adults older than 40 years and 30% of adults older than 50
- c.
  Medical—obesity, pregnancy, rapid weight loss, total parenteral nutrition, diabetes, pancreatitis, chronic hemolytic states, malabsorption, Crohn disease, spinal cord injuries, increased triglycerides, decreased high-density lipoprotein
- d.
  Drugs—exogenous estrogens, clofibrate, octreotide, ceftriaxone
- e.
  Ethnic factors—Pima Indians, other Native Americans, Scandinavians, persons living in Chile

B

Causative Factors

Three principal defects contribute to gallstone formation.

1.
Cholesterol supersaturation—most critical to stone formation
- a.
  Three major constituents in bile:
  - (1)
    Bile salts—primary: cholic and chenodeoxycholic acids; secondary: deoxycholic and lithocholic
  - (2)
    Phospholipids—90% lecithin
  - (3)
    Cholesterol—Bile containing excess cholesterol relative to bile salts and lecithin is predisposed to gallstone formation.
2.
Accelerated nucleation
- a.
  Mucin and bilirubin are pronucleators associated with increased stone formation.
3.
Gallbladder hypomotility/stasis

C

Types of Gallstones

1.
Mixed (75%)
- a.
  Most common, relatively small in size, usually multiple
- b.
  Predominantly cholesterol (at least 50% of content)
2.
Pure cholesterol (10%)
- a.
  Often solitary with large, round configuration
- b.
  Usually not calcified
3.
Pigment (15%)
- a.
  Result from bilirubin precipitation
- b.
  More common in women and Asian individuals
- c.
  Black pigment—associated with cirrhosis and chronic hemolytic states
- d.
  Brown pigment—usually associated with biliary infection and more common in biliary tree than in gallbladder
- e.
  Approximately 50% are radiopaque.

D

Treatment of Asymptomatic Cholelithiasis

1.
Prophylactic cholecystectomy is not indicated in most patients (only approximately 20% become symptomatic).
2.
Certain subgroups may benefit from prophylactic cholecystectomy.
- a.
  American Indians with gallstones who have a greater rate of gallbladder cancer
- b.
  Heart and lung transplant patients because the morbidity of acute cholecystitis is severe in this subgroup (kidney transplant candidates do not appear to benefit)
- c.
  Diabetes is no longer considered an indication for prophylactic cholecystectomy.
- d.
  Gastric bypass with prophylactic cholecystectomy is controversial; it does not appear to improve outcome.

III

Symptomatic Cholelithiasis

A

Biliary Colic

Defined as pain arising from the gallbladder without established inflammation or infection

1.
Pathology—results from intermittent obstruction of the cystic duct by stone
2.
Natural history
- a.
  Rate of recurrence is between 50% and 70% after first episode.
- b.
  Risk for development of biliary complications is 1%–2% per year.
3.
Clinical manifestations
- a.
  Severe pain, often visceral in nature, involving right upper quadrant (RUQ) or midepigastrium
- b.
  May radiate to back or below right scapula
- c.
  Often follows a fatty meal
- d.
  Pain lasts between 1 and 6 hours (if >6 hours, think cholecystitis).
- e.
  Steady pain, not undulating like that of renal colic
- f.
  Can be associated with nausea and vomiting
4.
Physical examination—usually normal, only mild-to-moderate tenderness during an attack or mild residual tenderness lasting for a few days after an attack; usually negative Murphy sign
5.
Diagnosis
- a.
  Reference laboratory values
- b.
  Ultrasound is 95% sensitive and 90% specific for diagnosis of cholelithiasis and is diagnostic procedure of choice.
- c.
  Plain radiography detects only 10%–15% of cholesterol stones (50% of pigment stones).
6.
Complications
- a.
  Prolonged obstruction can lead to acute cholecystitis.
- b.
  Stones may pass into the CBD, resulting in choledocholithiasis, cholangitis, or pancreatitis.
7.
Treatment: patients with biliary colic and documented gallstones generally treated with an elective laparoscopic cholecystectomy (lap chole)

B

Acute Calculous Cholecystitis

Defined as pain arising from inflammation of the gallbladder wall

1.
Pathology
- a.
  Impacted stone in the cystic duct results in prolonged obstruction.
- b.
  Stasis of bile damages gallbladder mucosa, resulting in the release of enzymes and inflammatory mediators.
- c.
  Histology ranges from mild acute inflammation to edema to necrosis and perforation of the gallbladder wall.
- d.
  Forty percent of bile cultures are positive for bacteria in this setting.
  - (1)
    Usually single-organism growth
  - (2)
    Most likely organisms include Escherichia coli, Klebsiella, Enterococcus, Enterobacter.
2.
Natural history
- a.
  Seventy-five percent of cases report previous attack of biliary pain.
- b.
  If untreated, 80% resolve within 7–10 days.
- c.
  Complications develop in approximately 17%.
3.
Clinical manifestations
- a.
  As inflammation progresses, visceral pain gives way to parietal pain localized to RUQ.
- b.
  Duration of pain is beyond 6 hours.
- c.
  Nausea and vomiting are more common than in biliary colic.
4.
Physical examination
- a.
  Fevers are common.
- b.
  Murphy sign—During palpation of the RUQ and deep inspiration, the inflamed gallbladder comes in contact with the examiner’s hand, resulting in pain and inspiratory arrest (patient stops breathing momentarily).
- c.
  The gallbladder is palpable in one-third of the patients.
5.
Diagnosis
- a.
  Laboratory tests—Leukocytosis is common; there are increases in alkaline phosphatase and serum aminotransferase, and serum bilirubin level between 2 and 4 mg/dL can also occur.
- b.
  Ultrasound is useful in diagnosing acute cholecystitis and is diagnostic procedure of choice.
  - (1)
    Sonographic Murphy sign in the presence of stones predicts acute cholecystitis 90% of the time.
  - (2)
    Gallbladder wall is thickened and there is pericholecystic fluid in up to 50% of patients with acute cholecystitis.
  - (3)
    Ultrasound shows echoic shadowing from stones.
- c.
  Computed tomography (CT) scan is useful in diagnosing complications of acute cholecystitis (empyema, perforation, or emphysematous cholecystitis).
- d.
  Cholescintigraphy (i.e., hepatobiliary iminodiacetic acid [HIDA] scan)
  - (1)
    Intravenously administer gamma-emitting technetium 99m ( ^99m Tc)-labeled hydroxyl iminodiacetic acid, which is rapidly taken up by the liver and secreted into bile.
  - (2)
    Nonfilling of the gallbladder within 4 hours with preserved excretion into the CBD and small bowel indicates an obstructed cystic duct.
  - (3)
    Accuracy in diagnosing acute cholecystitis is 95%, which is superior to ultrasound.
6.
Complications
- a.
  If left untreated and the cystic duct remains obstructed, the gallbladder can fill with a clear mucoid fluid— hydrops of the gallbladder.
  - (1)
    This can lead to ischemia/necrosis/perforation of gallbladder wall.
- b.
  Results are gangrenous cholecystitis 7% of the time, gallbladder empyema (6%), perforation (3%), and emphysematous cholecystitis (<1%).
7.
Treatment
- a.
  Intravenous hydration and correction of electrolyte imbalance may be necessary.
- b.
  Antibiotics
  - (1)
    They are not necessary in mild acute cholecystitis.
  - (2)
    Coverage for gram-negative organisms can be initiated if severe or complicated cholecystitis is suspected (first-generation or second-generation cephalosporin is first choice).
  - (3)
    Patients who have more severe complications or are toxic in appearance should be given broad-spectrum antibiotics, including anaerobic coverage.
- c.
  Cholecystectomy is the definitive treatment for acute cholecystitis and its complications.
  - (1)
    This can usually be performed laparoscopically.
  - (2)
    Cholecystectomy within 72 hours of symptom onset is optimal, but Cochrane review suggests no difference in outcomes if inter val cholecystectomy is delayed and performed 6–12 weeks after initial cool-down period.
  - (3)
    Patients who are immunosuppressed (steroid use, diabetes) should have immediate cholecystectomy.
  - (4)
    Delayed cholecystectomy (initial conservative management with intravenous fluids and antibiotics followed by cholecystectomy on an elective basis) is justified in some patients who are at high surgical risk.
  - (5)
    In patients who are not stable enough to undergo anesthesia, ultrasound or CT-guided percutaneous cholecystostomy with external drainage can be performed to decompress the gallbladder; this is followed by delayed cholecystectomy when the patient is more stable.
- d.
  Intraoperative cholangiogram (IOC) can be helpful to define ductal anatomy when dissection is difficult due to inflammation or biliary tract variation.

IV

Choledocholithiasis

Choledocholithiasis is the occurrence of stones in the bile ducts.

A

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