Acalculous Cholecystitis: Background, Pathophysiology, Etiology (original) (raw)
Overview
Background
Acalculous cholecystitis is an inflammatory disease of the gallbladder without evidence of gallstones or cystic duct obstruction [1, 2] ; it is a severe illness that is a complication of various other medical or surgical conditions. Duncan first recognized it in 1844 when a fatal case of acalculous cholecystitis complicating an incarcerated hernia was reported. The condition causes approximately 5%-10% of all cases of acute cholecystitis and is usually associated with more serious morbidity and higher mortality rates than calculous cholecystitis. It is most commonly observed in the setting of very ill patients (eg, on mechanical ventilation, with sepsis or severe burn injuries, [3] after severe trauma [4] ). In addition, acalculous cholecystitis is associated with a higher incidence of gangrene and perforation compared to calculous disease.
The usual finding on imaging studies is a distended acalculous gallbladder with thickened walls (>3-4 mm) with or without pericholecystic fluid. Acalculous cholecystitis can be observed in patients with human immunodeficiency virus (HIV) infection, although it is a late manifestation of this disease. Acalculous cholecystitis can also be found in patients on total parenteral nutrition (TPN), typically those on TPN for more than three months.
Pathophysiology
The main cause of this illness is thought to be bile stasis and increased lithogenicity of bile. Critically ill patients are more predisposed because of increased bile viscosity due to fever and dehydration and because of prolonged absence of oral feeding resulting in a decrease or absence of cholecystokinin-induced gallbladder contraction. Gallbladder wall ischemia that occurs because of a low-flow state due to fever, dehydration, or heart failure may also play a role in the pathogenesis of acalculous cholecystitis.
Etiology
The main cause of acalculous cholecystitis is gallbladder stasis with resulting stagnant bile. This is observed most commonly in patients with sepsis, patients in intensive care units, patients on long-term total parenteral nutrition (TPN), those with cardiovascular disease, [2] patients with diabetes (occasionally), or other patients with gallbladder dysmotility. The condition has been reported during pregnancy, as a complication of hepatitis A. [5] It has been rarely reported in children, also as a complication of hepatitis A, [6] with a favorable course with conservative treatment. This disease has also been reported as associated with aortic dissection. [7]
Epidemiology
United States statistics
Acalculous cholecystitis comprises approximately 5-10% of all cases of acute cholecystitis.
Race-, sex-, age-related demographics
It can occur in all races.
Acalculous cholecystitis has a slight male predominance, unlike calculous cholecystitis, which has a female predominance.
The condition can occur in persons of any age, although a higher frequency is reported in persons in their fourth and eighth decades of life.
Prognosis
The prognosis of patients with acalculous cholecystitis is guarded.
Mortality/Morbidity
The mortality and morbidity rates associated with acalculous cholecystitis can be high; the illness is frequently observed in patients with sepsis or other serious conditions. The reported mortality range is 10%-50% for acalculous cholecystitis as compared to 1% for calculous cholecystitis.
A study by Gu et al found a significantly higher frequency of cerebrovascular accidents in patients with acute acalculous cholecystitis (AAC) than those with acute calculous cholecystitis (ACC), the respective rates being 15.9% and 6.7%. The incidence of gangrenous cholecystitis was also greater in the AAC than in ACC (31.2% vs 5.6%, respectively). [8]
Complications
Perforation or gangrene of the gallbladder and extrabiliary abscess formation may occur. [9]
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- Wood BE, Trautman J, Smith N, Putnis S. Rare case report of acalculous cholecystitis: Gallbladder torsion resulting in rupture. SAGE Open Med Case Rep. 2019. 7:2050313X18823385. [QxMD MEDLINE Link]. [Full Text].
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Author
Coauthor(s)
Specialty Editor Board
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Chief Editor
John Geibel, MD, MSc, DSc, AGAF Vice Chair and Professor, Department of Surgery, Section of Gastrointestinal Medicine, Professor, Department of Cellular and Molecular Physiology, Yale University School of Medicine; Director of Surgical Research, Department of Surgery, Yale-New Haven Hospital; American Gastroenterological Association Fellow; Fellow of the Royal Society of Medicine
John Geibel, MD, MSc, DSc, AGAF is a member of the following medical societies: American Gastroenterological Association, American Physiological Society, American Society of Nephrology, Association for Academic Surgery, International Society of Nephrology, New York Academy of Sciences, Society for Surgery of the Alimentary Tract
Disclosure: Nothing to disclose.
Additional Contributors
Marco G Patti, MD Surgeon, UNC Hospitals Multispecialty Surgery Clinic
Marco G Patti, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Surgeons, American Gastroenterological Association, American Medical Association, American Surgical Association, Association for Academic Surgery, Pan-Pacific Surgical Association, Society for Surgery of the Alimentary Tract, Society of American Gastrointestinal and Endoscopic Surgeons, Southwestern Surgical Congress, Western Surgical Association
Disclosure: Nothing to disclose.
Acknowledgements
Michael A Grosso, MD Consulting Staff, Department of Cardiothoracic Surgery, St Francis Hospital
Michael A Grosso, MD is a member of the following medical societies: American College of Surgeons, Society of Thoracic Surgeons, and Society of University Surgeons
Disclosure: Nothing to disclose.