Chapter 150: Cholelithiasis, Cholecystitis, and Cholangitis

There are two major types of gallstones: cholesterol and pigment stones. Cholesterol gallstones contain >50% cholesterol monohydrate. Pigment stones have <20% cholesterol and are composed primarily of calcium bilirubinate. In the United States, 80% of stones are cholesterol and 20% are pigment.

EPIDEMIOLOGY

One million new cases of cholelithiasis per year in the United States. Predisposing factors include demographic/genetics (increased prevalence in North American Indians), obesity, weight loss, female sex hormones, age, ileal disease, pregnancy, type IV hyperlipidemia, and cirrhosis.

SYMPTOMS AND SIGNS

Many gallstones are “silent,” i.e., present in asymptomatic pts. Symptoms occur when stones trigger inflammation or cause obstruction of the cystic or common bile ducts (CBDs). Major symptoms: (1) biliary colic—a severe steady ache in the RUQ or epigastrium that begins suddenly; often occurs 30–90 min after meals, lasts for several hours, and occasionally radiates to the right scapula or back; (2) nausea, vomiting. Physical examination may be normal or show epigastric or RUQ tenderness.

LABORATORY

Occasionally, mild and transient elevations in bilirubin (<85 μmol/L [<5 mg/dL]) accompany biliary colic.

IMAGING

Only 10% of cholesterol gallstones are radiopaque. Ultrasonography is best diagnostic test. The oral cholecystogram has been largely replaced by ultrasound, but may be used to assess the patency of the cystic duct and gallbladder emptying function (Table 150-1).

DIFFERENTIAL DIAGNOSIS

Includes peptic ulcer disease (PUD), gastroesophageal reflux, irritable bowel syndrome, and hepatitis.

COMPLICATIONS

Cholecystitis, pancreatitis, cholangitis.

Acute inflammation of the gallbladder is usually caused by cystic duct obstruction by an impacted stone. Inflammatory response is evoked by (1) mechanical inflammation from increased intraluminal pressure; (2) chemical inflammation from release of lysolecithin; (3) bacterial inflammation, which plays a role in 50–85% of pts with acute cholecystitis.

ETIOLOGY

Approximately 90% calculous; 10% acalculous. Acalculous cholecystitis is associated with higher complication rate and acute illness (i.e., burns, trauma, major surgery), fasting, hyperalimentation leading to gallbladder stasis, vasculitis, carcinoma of gallbladder or CBD, some gallbladder infections (Leptospira, Streptococcus, Salmonella, or Vibrio cholerae), but in >50% of cases an underlying explanation is not found.

SYMPTOMS AND SIGNS

(1) Biliary colic (RUQ or epigastric pain) that progressively worsens; (2) nausea, vomiting, anorexia; and (3) fever. Examination typically reveals RUQ tenderness; palpable RUQ mass found in 20% of pts. Murphy’s sign is present when deep inspiration or cough during palpation of the RUQ produces increased pain or inspiratory arrest.

LABORATORY

Mild leukocytosis; serum bilirubin, alkaline phosphatase, and aspartate aminotransferase (AST) may be mildly elevated.

IMAGING

Ultrasonography is useful for demonstrating gallstones and occasionally a phlegmonous mass surrounding the gallbladder. Radionuclide scans (HIDA, DIDA, DISIDA, etc.) may identify cystic duct obstruction.

DIFFERENTIAL DIAGNOSIS

Includes acute pancreatitis, appendicitis, pyelonephritis, PUD, hepatitis, and hepatic abscess.

COMPLICATIONS

Empyema, hydrops, gangrene, perforation, fistulization, gallstone ileus, porcelain gallbladder.

ETIOLOGY

Chronic inflammation of the gallbladder; almost always associated with gallstones. Results from repeated acute/subacute cholecystitis or prolonged mechanical irritation of gallbladder wall.

SYMPTOMS AND SIGNS

May be asymptomatic for years, may progress to symptomatic gallbladder disease or to acute cholecystitis, or present with complications.

LABORATORY

Tests are usually normal.

IMAGING

Ultrasonography preferred; usually shows gallstones within a contracted gallbladder (Table 150-1).

DIFFERENTIAL DIAGNOSIS

PUD, esophagitis, irritable bowel syndrome.

ETIOLOGY

In pts with cholelithiasis, passage of gallstones into CBD occurs in 10–15%; increases with age. At cholecystectomy, undetected stones are left behind in 1–5% of pts.

SYMPTOMS AND SIGNS

Choledocholithiasis may present as an incidental finding, biliary colic, obstructive jaundice, cholangitis, or pancreatitis. Cholangitis usually presents as fever, RUQ pain, and jaundice (Charcot’s triad).

LABORATORY

Elevations in serum bilirubin, alkaline phosphatase, and aminotransferases. Leukocytosis usually accompanies cholangitis; blood cultures are frequently positive. Amylase is elevated in 15% of cases.

IMAGING

Diagnosis usually made by cholangiography either preoperatively by endoscopic retrograde cholangiopancreatography (ERCP) or intraoperatively at the time of cholecystectomy. Ultrasonography may reveal dilated bile ducts but is not sensitive for detecting CBD stones (Table 150-1).

DIFFERENTIAL DIAGNOSIS

Acute cholecystitis, renal colic, perforated viscus, pancreatitis.

COMPLICATIONS

Cholangitis, obstructive jaundice, gallstone-induced pancreatitis, and secondary biliary cirrhosis.

PSC is a sclerosing, inflammatory, and obliterative process involving the biliary tree.

ETIOLOGY

Associations: inflammatory bowel disease (75% of cases of PSC—especially ulcerative colitis), AIDS, rarely retroperitoneal fibrosis.

SYMPTOMS AND SIGNS

Pruritus, RUQ pain, jaundice, fever, weight loss, and malaise. Approximately 44% may be asymptomatic at diagnosis. May progress to cirrhosis with portal hypertension.

LABORATORY

Evidence of cholestasis (elevated bilirubin and alkaline phosphatase) common.

RADIOLOGY/ENDOSCOPY

Transhepatic or endoscopic cholangiograms reveal stenosis and dilation of the intra- and extrahepatic bile ducts.

DIFFERENTIAL DIAGNOSIS

Cholangiocarcinoma, Caroli disease (cystic dilation of bile ducts), Fasciola hepatica infection, echinococcosis, and ascariasis. IgG4-associated cholangitis.