Acute cholecystitis is secondary to gallstones in 90 to 95% of cases. Acute acalculous cholecystitis is a condition that typically occurs in patients with other acute systemic diseases (see Acalculous Cholecystitis section below). In <1% of acute cholecystitis, the cause is a tumor obstructing the cystic duct. Obstruction of the cystic duct by a gallstone is the initiating event that leads to gallbladder distention, inflammation, and edema of the gallbladder wall. Why inflammation develops only occasionally with cystic duct obstruction is unknown. It is probably related to the duration of obstruction of the cystic duct. Initially, acute cholecystitis is an inflammatory process, probably mediated by the mucosal toxin lysolecithin, a product of lecithin, as well as bile salts and platelet-activating factor. Increase in prostaglandin synthesis amplifies the inflammatory response. Secondary bacterial contamination is documented in 15 to 30% of patients undergoing cholecystectomy for acute uncomplicated cholecystitis. In acute cholecystitis, the gallbladder wall becomes grossly thickened and reddish with subserosal hemorrhages. Pericholecystic fluid often is present. The mucosa may show hyperemia and patchy necrosis. In severe cases, about 5 to 10%, the inflammatory process progresses and leads to ischemia and necrosis of the gallbladder wall. More frequently, the gallstone is dislodged and the inflammation resolves.35
When the gallbladder remains obstructed and secondary bacterial infection supervenes, an acute gangrenous cholecystitis develops, and an abscess or empyema forms within the gallbladder. Rarely, perforation of ischemic areas occurs. The perforation is usually contained in the subhepatic space by the omentum and adjacent organs. However, free perforation with peritonitis, intrahepatic perforation with intrahepatic abscesses, and perforation into adjacent organs (duodenum or colon) with cholecystoenteric fistula occur. When gas-forming organisms are part of the secondary bacterial infection, gas may be seen in the gallbladder lumen and in the wall of the gallbladder on abdominal radiographs and CT scans, an entity called an emphysematous gallbladder.
About 80% of patients with acute cholecystitis give a history compatible with chronic cholecystitis. Acute cholecystitis begins as an attack of biliary colic, but in contrast to biliary colic, the pain does not subside; it is unremitting and may persist for several days. The pain is typically in the right upper quadrant or epigastrium, and may radiate to the right upper part of the back or the interscapular area. It is usually more severe than the pain associated with uncomplicated biliary colic. The patient is often febrile, complains of anorexia, nausea, and vomiting, and is reluctant to move, as the inflammatory process affects the parietal peritoneum. On physical examination, focal tenderness and guarding are usually present in the right upper quadrant. A mass, the gallbladder and adherent omentum, is occasionally palpable; however, guarding may prevent this. A Murphy’s sign, an inspiratory arrest with deep palpation in the right subcostal area, is characteristic of acute cholecystitis.
A mild to moderate leukocytosis (12,000 to 15,000 cells/mm3) is usually present. However, some patients may have a normal WBC. A high WBC (above 20,000) is suggestive of a complicated form of cholecystitis such as gangrenous cholecystitis, perforation, or associated cholangitis. Serum liver chemistries are usually normal, but a mild elevation of serum bilirubin, <4 mg/mL, may be present along with mild elevation of alkaline phosphatase, transaminases, and amylase.31 Severe jaundice is suggestive of common bile duct stones or obstruction of the bile ducts by severe pericholecystic inflammation secondary to impaction of a stone in the infundibulum of the gallbladder that mechanically obstructs the bile duct (Mirizzi’s syndrome). In elderly patients and in those with diabetes mellitus, acute cholecystitis may have a subtle presentation resulting in a delay in diagnosis. The incidence of complications is higher in these patients, who also have approximately 10-fold the mortality rate compared to that of younger and healthier patients.
The differential diagnosis for acute cholecystitis includes a peptic ulcer with or without perforation, pancreatitis, appendicitis, hepatitis, perihepatitis (Fitz-Hugh–Curtis syndrome), myocardial ischemia, pneumonia, pleuritis, and herpes zoster involving the intercostal nerve.
Ultrasonography is the most useful radiologic test for diagnosing acute cholecystitis. It has a sensitivity and specificity of 95%. In addition to being a sensitive test for documenting the presence or absence of stones, it will show the thickening of the gallbladder wall and the pericholecystic fluid (Fig. 32-14). Focal tenderness over the gallbladder when compressed by the sonographic probe (sonographic Murphy’s sign) also is suggestive of acute cholecystitis. Biliary radionuclide scanning (HIDA scan) may be of help in the atypical case. Lack of filling of the gallbladder after 4 hours indicates an obstructed cystic duct and, in the clinical setting of acute cholecystitis, is highly sensitive and specific for acute cholecystitis. A normal HIDA scan excludes acute cholecystitis. CT scan is frequently performed on patients with acute abdominal pain. It demonstrates thickening of the gallbladder wall, pericholecystic fluid, and the presence of gallstones as well as air in the gallbladder wall, but is less sensitive than ultrasonography.
Patients who present with acute cholecystitis will need IV fluids, antibiotics, and analgesia. The antibiotics should cover gram-negative aerobes as well as anaerobes. A third-generation cephalosporin with good anaerobic coverage or a second-generation cephalosporin combined with metronidazole is a typical regimen. For patients with allergies to cephalosporins, an aminoglycoside with metronidazole is appropriate. Although the inflammation in acute cholecystitis may be sterile in some patients, more than one half will have positive cultures from the gallbladder bile. It is difficult to know who is secondarily infected; therefore, antibiotics have become a part of the management in most medical centers.
Cholecystectomy is the definitive treatment for acute cholecystitis.36 In the past, the timing of cholecystectomy has been a matter of debate. Early cholecystectomy performed within 2 to 3 days of the illness is preferred over interval or delayed cholecystectomy that is performed 6 to 10 weeks after initial medical treatment and recuperation. Several studies have shown that unless the patient is unfit for surgery, early cholecystectomy should be recommended, as it offers the patient a definitive solution in one hospital admission, quicker recovery times, and an earlier return to work.37
Laparoscopic cholecystectomy is the procedure of choice for acute cholecystitis. The conversion rate to an open cholecystectomy is higher (10 to 15%) in the setting of acute cholecystitis than with chronic cholecystitis. The procedure is more tedious and takes longer than in the elective setting. However, when compared to the delayed operation, early operation carries a similar complication rate.
When patients present late, after 3 to 4 days of illness, or if they are unfit for surgery, they can be treated with antibiotics with laparoscopic cholecystectomy scheduled for approximately 2 months later. Approximately 20% of patients will fail to respond to initial medical therapy and require an intervention. Laparoscopic cholecystectomy could be attempted, but the conversion rate is high and some prefer to go directly for an open cholecystectomy. For those unfit for surgery, a percutaneous cholecystostomy or an open cholecystostomy under local analgesia can be performed. Failure to improve after cholecystostomy usually is due to gangrene of the gallbladder or perforation. For these patients, surgery is unavoidable. For those who respond after cholecystostomy, the tube can be removed once cholangiography through it shows a patent ductus cysticus. Laparoscopic cholecystectomy may then be scheduled in the near future.38 For the rare patients who can’t tolerate surgery, the stones can be extracted via the cholecystostomy tube before its removal.39