Acalculous cholecystitis: Clinical manifestations, diagnosis, and management
- Nezam H Afdhal, MD, FRCPI
Nezam H Afdhal, MD, FRCPI
- Senior Physician in Hepatology
- Beth Israel Deaconess Medical Center
- Section Editors
- Stanley W Ashley, MD
Stanley W Ashley, MD
- Section Editor — Pancreatic and Hepatobiliary Surgery
- Chief Medical Officer and Senior Vice President for Clinical Affairs
- Brigham and Women’s Hospital
- Frank Sawyer Professor of Surgery
- Harvard Medical School
- Keith D Lindor, MD
Keith D Lindor, MD
- Section Editor — Alcoholic and Metabolic Liver Disease
- Professor of Medicine, Mayo Clinic College of Medicine
- Dean, College of Health Solutions
- Arizona State University
Acalculous cholecystitis is an acute necroinflammatory disease of the gallbladder with a multifactorial pathogenesis. It accounts for approximately 10 percent of all cases of acute cholecystitis and is associated with high morbidity and mortality rates.
This topic will review the pathophysiology, diagnosis, and management of acalculous cholecystitis. Clinical issues related to acute calculous cholecystitis and chronic cholecystitis are discussed separately. (See "Acute cholecystitis: Pathogenesis, clinical features, and diagnosis" and "Treatment of acute calculous cholecystitis".)
Acalculous cholecystitis results from gallbladder stasis and ischemia, which then cause a local inflammatory response in the gallbladder wall. The majority of patients with acalculous cholecystitis have multiple risk factors (table 1) [1-7]. In some cases, specific primary infections predispose to acalculous cholecystitis (table 2). As an example, acalculous cholecystitis occurring in patients with acquired immunodeficiency syndrome (AIDS) and other immunosuppressed patients may be due to opportunistic infections such as microsporidia, Cryptosporidium, or cytomegalovirus . More often, however, these infections cause a cholangiopathy without cholecystitis. (See "AIDS cholangiopathy".)
Pathologically in patients with acalculous cholecystitis, endothelial injury, gallbladder ischemia, and stasis, lead to concentration of bile salts, gallbladder distension, and eventually necrosis of the gallbladder tissue. Once acalculous cholecystitis is established, secondary infection with enteric pathogens, including Escherichia coli, Enterococcus faecalis, Klebsiella spp, Pseudomonas spp, Proteus spp, and Bacteroides fragilis and related strains, is common . Perforation occurs in severe cases [10,11]. (See 'Complications' below.)
Acalculous cholecystitis is typically seen in patients who are hospitalized and critically ill, though it may also be seen in the outpatient setting in patients with risk factors for acalculous cholecystitis (table 1). Acalculous cholecystitis has been reported in 0.7 to 0.9 percent of patients following open abdominal aortic reconstruction, in 0.5 percent of patients following cardiac surgery, and in as many as 4 percent of patients who have undergone bone marrow transplantation [4,12-15]. There is a male preponderance among patients with acute acalculous cholecystitis ranging from 40 to 80 percent [12,16].To continue reading this article, you must log in with your personal, hospital, or group practice subscription. For more information on subscription options, click below on the option that best describes you:
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- CLINICAL MANIFESTATIONS
- Clinical presentation
- Laboratory tests
- DIAGNOSTIC APPROACH
- Clinical suspicion and evaluation
- - Ultrasonography
- - Computed tomography
- - Cholescintigraphy
- DIFFERENTIAL DIAGNOSIS
- Overall approach
- General measures for all patients
- - Supportive care
- - Antibiotics
- Gallbladder drainage
- - Percutaneous cholecystostomy
- - Endoscopic drainage
- - Management following gallbladder drainage
- SUMMARY AND RECOMMENDATIONS