Acute cholecystitis may result from any of three primary events in the gallbladder: bile stasis, an inflammatory response, or ischemia. Stasis usually results from obstruction of the cystic duct due to gallstones but may occur secondary to the edema produced by stones, hyperplastic lymph nodes, or a neoplasm. Starvation, dehydration, and immobilization are associated with stasis due to interruption of gallbladder contraction and
emptying. Bile salts, lysolecithin, pancreatic juice, and bacteria have been implicated as agents responsible for inciting the inflammatory response. Torsion of the gallbladder or systemic vascular disease may lead to ischemic changes of the biliary tract. Empyema or gangrene may lead to perforation. After the initial attack subsides, the mucosal surface of the biliary tract heals, and the wall becomes scarred. If the inflammation subsides but the cystic duct remains obstructed, the gallbladder may become distended (i.e., hydrops). Recurrent attacks of obstruction and inflammation lead to progressive scarring of the gallbladder with loss of function and additional gallstone formation. Rarely, adenomatous hyperplasia with polyp formation may portend cholecystitis.

The pathologic features of acute cholecystitis include an enlarged gallbladder that is filled with turbid bile, fine sandy gravel, or gallstones. The gallbladder wall is thickened and may be ulcerated or perforated. The inflammatory response is characterized by edema, polymorphonuclear cell infiltration, vascular congestion, and necrosis.

The pathologic features of chronic cholecystitis vary. The gallbladder may be contracted or enlarged. The gallbladder wall is thickened, and the mucosal folds may be flattened. The lumen contains clear, mucoid bile; formed stones usually are present. Ninety percent of all gallstones are made of calcium bilirubinate and calcium carbonate. Rarely, gallstones consist primarily of cholesterol. Microscopic features of chronic cholecystitis include increased subepithelial fibrosis and an infiltrate of lymphocytes, plasma cells, macrophages, and mononuclear cells. Cholesterolosis occurs when crystals of cholesterol are deposited in the submucosal macrophages of the gallbladder.

The incidence of cholecystitis in children ranges from less than 1% to 4%. Although this disorder is less common in children than in adults, its frequency in childhood appears to be increasing. Girls are affected more commonly than are boys after adolescence. Both sexes are affected equally before this age. The occurrence of cholecystitis in the white population is almost twice that in the black population. Acute and chronic cholecystitis, with or without gallstones, has been reported in all age ranges and may even occur in the fetus. Approximately 40% of all pediatric cases occur in children less than 11 years of age and 60% occur in children 11 to 20 years of age. Acalculous cholecystitis affects younger children more commonly, and calculous cholecystitis occurs more frequently in adolescents.

Several entities have been implicated as predisposing factors for cholecystitis in children (Table 369.2). Hemolytic disease, including congenital spherocytosis, sickle cell anemia, and thalassemia, has been found in more than one-third of children with cholecystitis and gallstones. Children who receive cyclosporine in conjunction with heart transplantation are known to be at risk for cholecystitis, possibly because of hepatotoxicity and bile stasis. Children who are maintained on total parenteral nutrition for more than 4 weeks are at risk of developing biliary tract disease due to bile stasis. Ileal abnormalities, particularly ileal resection and the loss of the ileocecal valve associated with necrotizing enterocolitis, intestinal atresia, short gut syndrome, cystic fibrosis, cirrhosis, or Crohn disease, potentiate the development of biliary tract disease and gallstone formation. Pregnancy, with its attendant hormonal alterations, and obesity each are associated with approximately 30% of the cases of cholecystitis and cholelithiasis.

Bacterial (e.g., Salmonella, Shigella, Yersinia, Aerobacter, Brucella, Pseudomonas, Staphylococcus, group B streptococci, Leptospira, Listeria, Escherichia coli, Clostridium, Vibrio cholerae), fungal (Candida albicans), parasitic (Giardia, Ascaris, Leishmania donovani), and protozoan (Cryptosporidium, Plasmodium falciparum) infections, viral gastroenteritis, infectious hepatitis (type A), urinary tract infections, sepsis, Kawasaki disease, measles, scarlet fever, endocarditis, and pneumonia have been implicated as causes of acalculous cholecystitis.