OBJECTIVES: The aim of the study was to investigate the etiology, clinical presentation, and risk factors for poor prognosis of acute acalculous cholecystitis (AAC) in children. PATIENTS AND METHODS: Children younger than 18 years diagnosed as having AAC were analyzed retrospectively from 2000 to 2009. The demographic and clinical characteristics, etiology, and outcomes were recorded. AAC was defined as a gallbladder wall thickness of >3.5 mm in sonogram with a duration of symptoms <1 month. The severity of sonographic findings was scored, with 1 point each given for wall thickness >3.5 mm, gallbladder distention, sludge, and pericholecystic fluid. RESULTS: A total of 109 children (boys:girls 1:2, median age 4.9 years) were diagnosed. The most common clinical presentation was fever (88%), followed by hepatomegaly (72%). The rates of elevated alanine aminotransferase and thrombocytopenia were 72% and 65%, respectively. The most common causative etiology was infectious diseases (74%). All of the patients were treated nonoperatively. Sixteen (15%) patients died. Children with mortality had a significantly higher rate of septic shock (P < 0.001), anemia (P = 0.01), thrombocytopenia (P = 0.04), hypofibrinogenemia (P = 0.002), the presence of pericholecystic fluid (P = 0.04), and higher sonographic scores (P = 0.04) than those with survival. Multiple logistic regression analysis confirmed that the presence of septic shock (P = 0.004) and hypofibrinogenemia (P = 0.014) were independent risk factors that predict mortality. CONCLUSIONS: Childhood AAC is usually secondary to a variety of etiologies, especially during the course of infectious diseases. The presence of septic shock and a low value of fibrinogen determine a fatal outcome in childhood AAC.
OBJECTIVES: The aim of the study was to investigate the etiology, clinical presentation, and risk factors for poor prognosis of acute acalculous cholecystitis (AAC) in children. PATIENTS AND METHODS: Children younger than 18 years diagnosed as having AAC were analyzed retrospectively from 2000 to 2009. The demographic and clinical characteristics, etiology, and outcomes were recorded. AAC was defined as a gallbladder wall thickness of >3.5 mm in sonogram with a duration of symptoms <1 month. The severity of sonographic findings was scored, with 1 point each given for wall thickness >3.5 mm, gallbladder distention, sludge, and pericholecystic fluid. RESULTS: A total of 109 children (boys:girls 1:2, median age 4.9 years) were diagnosed. The most common clinical presentation was fever (88%), followed by hepatomegaly (72%). The rates of elevated alanine aminotransferase and thrombocytopenia were 72% and 65%, respectively. The most common causative etiology was infectious diseases (74%). All of the patients were treated nonoperatively. Sixteen (15%) patients died. Children with mortality had a significantly higher rate of septic shock (P < 0.001), anemia (P = 0.01), thrombocytopenia (P = 0.04), hypofibrinogenemia (P = 0.002), the presence of pericholecystic fluid (P = 0.04), and higher sonographic scores (P = 0.04) than those with survival. Multiple logistic regression analysis confirmed that the presence of septic shock (P = 0.004) and hypofibrinogenemia (P = 0.014) were independent risk factors that predict mortality. CONCLUSIONS: Childhood AAC is usually secondary to a variety of etiologies, especially during the course of infectious diseases. The presence of septic shock and a low value of fibrinogen determine a fatal outcome in childhood AAC.