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Alan A Bloom, MD Associate Clinical Professor of Medicine, Albert Einstein College of Medicine; Attending Physician, Department of Gastroenterology, Veterans Affairs Hospital, Bronx
Alan A Bloom, MD is a member of the following medical societies: American College of Physicians, American Gastroenterological Association, American Medical Association, American Society for Gastrointestinal Endoscopy, New York Academy of Medicine, and New York Academy of Sciences
Zahir Amin, MD, MBBS, MRCP, FRCR Consulting Staff, Department of Imaging, University College Hospital, UK
Zahir Amin, MD, MBBS, MRCP, FRCR is a member of the following medical societies: British Institute of Radiology, British Medical Association, and Royal College of Radiologists
BS Anand, MD Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine
BS Anand, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American Gastroenterological Association, and American Society for Gastrointestinal Endoscopy
Cholecystitis is defined as inflammation of the gallbladder that occurs most commonly because of an obstruction of the cystic duct from cholelithiasis. Ninety percent of cases involve stones in the cystic duct (ie, calculous cholecystitis), with the other 10% of cases representing acalculous cholecystitis.
Risk factors for cholecystitis mirror those for cholelithiasis and include increasing age, female sex, certain ethnic groups, obesity or rapid weight loss, drugs, and pregnancy. Although bile cultures are positive for bacteria in 50-75% of cases, bacterial proliferation may be a result of cholecystitis and not the precipitating factor.
Acalculous cholecystitis is related to conditions associated with biliary stasis, including debilitation, major surgery, severe trauma, sepsis, long-term total parenteral nutrition (TPN), and prolonged fasting. Other causes of acalculous cholecystitis include cardiac events; sickle cell disease; Salmonella infections; diabetes mellitus; and cytomegalovirus, cryptosporidiosis, or microsporidiosis infections in patients with AIDS. For more information, see the Medscape Reference article Acalculous Cholecystopathy.
Uncomplicated cholecystitis has an excellent prognosis, with a very low mortality rate. Once complications such as perforation/gangrene develop, the prognosis becomes less favorable. Some 25-30% of patients either require surgery or develop some complication.
The most common presenting symptom of acute cholecystitis is upper abdominal pain. The physical examination may reveal fever, tachycardia, and tenderness in the RUQ or epigastric region, often with guarding or rebound. However, the absence of physical findings does not rule out the diagnosis of cholecystitis.
Delays in making the diagnosis of acute cholecystitis result in a higher incidence of morbidity and mortality. This is especially true for ICU patients who develop acalculous cholecystitis. The diagnosis should be considered and investigated promptly in order to prevent poor outcomes.
Initial treatment of acute cholecystitis includes bowel rest, intravenous hydration, correction of electrolyte abnormalities, analgesia, and intravenous antibiotics. For mild cases of acute cholecystitis, antibiotic therapy with a single broad-spectrum antibiotic is adequate. Outpatient treatment may be appropriate for cases of uncomplicated cholecystitis. If surgical treatment is indicated, laparoscopic cholecystectomy represents the standard of care.
Patients diagnosed with cholecystitis must be educated regarding causes of their disease, complications if left untreated, and medical/surgical options to treat cholecystitis. For patient education information, see the Liver, Gallbladder, and Pancreas Center, as well as Gallstones and Pancreatitis.
Ninety percent of cases of cholecystitis involve stones in the cystic duct (ie, calculous cholecystitis), with the other 10% of cases representing acalculous cholecystitis.
Acute calculous cholecystitis is caused by obstruction of the cystic duct, leading to distention of the gallbladder. As the gallbladder becomes distended, blood flow and lymphatic drainage are compromised, leading to mucosal ischemia and necrosis.
Although the exact mechanism of acalculous cholecystitis is unclear, several theories exist. Injury may be the result of retained concentrated bile, an extremely noxious substance. In the presence of prolonged fasting, the gallbladder never receives a cholecystokinin (CCK) stimulus to empty; thus, the concentrated bile remains stagnant in the lumen.[2, 3]
A study by Cullen et al demonstrated the ability of endotoxin to cause necrosis, hemorrhage, areas of fibrin deposition, and extensive mucosal loss, consistent with an acute ischemic insult. Endotoxin also abolished the contractile response to CCK, leading to gallbladder stasis.
Risk factors for calculous cholecystitis mirror those for cholelithiasis and include the following :
- Female sex
- Certain ethnic groups
- Obesity or rapid weight loss
- Drugs (especially hormonal therapy in women)
- Increasing age
Acalculous Cholecystitis is related to conditions associated with biliary stasis, to include the following :
- Critical illness
- Major surgery or severe trauma/burns
- Long-term total parenteral nutrition (TPN)
- Prolonged fasting
Other causes of acalculous cholecystitis include the following :
- Cardiac events, including myocardial infarction
- Sickle cell disease
- Salmonella infections
- Diabetes mellitus
- Patients with AIDS who have cytomegalovirus, cryptosporidiosis, or microsporidiosis
- Patients who are immunocompromised are at increased risk of developing cholecystitis from a number of different infectious sources. Idiopathic cases exist.
An estimated 10-20% of Americans have gallstones, and as many as one third of these people develop acute cholecystitis. Cholecystectomy for either recurrent biliary colic or acute cholecystitis is the most common major surgical procedure performed by general surgeons, resulting in approximately 500,000 operations annually.
Age distribution for cholecystitis
The incidence of cholecystitis increases with age. The physiologic explanation for the increasing incidence of gallstone disease in the elderly population is unclear. The increased incidence in elderly men has been linked to changing androgen-to-estrogen ratios.
Sex distribution for cholecystitis
Gallstones are 2-3 times more frequent in females than in males, resulting in a higher incidence of calculous cholecystitis in females. Elevated progesterone levels during pregnancy may cause biliary stasis, resulting in higher rates of gallbladder disease in pregnant females. Acalculous cholecystitis is observed more often in elderly men.
Prevalence of cholecystitis by race and ethnicity
Cholelithiasis, the major risk factor for cholecystitis, has an increased prevalence among people of Scandinavian descent, Pima Indians, and Hispanic populations, whereas cholelithiasis is less common among individuals from sub-Saharan Africa and Asia.[6, 7] In the United States, white people have a higher prevalence than black people.
Uncomplicated cholecystitis has an excellent prognosis, with very low mortality. Most patients with acute cholecystitis have a complete remission within 1-4 days. However, 25-30% of patients either require surgery or develop some complication.
Once complications such as perforation/gangrene develop, the prognosis becomes less favorable. Perforation occurs in 10-15% of cases. Patients with acalculous cholecystitis have a mortality ranging from 10-50%, which far exceeds the expected 4% mortality observed in patients with calculous cholecystitis. In patients who are critically ill with acalculous cholecystitis and perforation or gangrene, mortality can be as high as 50-60%.
1. Huffman JL, Schenker S. Acute acalculous cholecystitis - a review. Clin Gastroenterol Hepatol. Sep 9 2009;[Medline].
2. Donovan JM. Physical and metabolic factors in gallstone pathogenesis. Gastroenterol Clin North Am. Mar 1999;28(1):75-97. [Medline].
3. Sitzmann JV, Pitt HA, Steinborn PA, et al. Cholecystokinin prevents parenteral nutrition induced biliary sludge in humans. Surg Gynecol Obstet. Jan 1990;170(1):25-31. [Medline].
4. Cullen JJ, Maes EB, Aggrawal S, et al. Effect of endotoxin on opossum gallbladder motility: a model of acalculous cholecystitis. Ann Surg. Aug 2000;232(2):202-7. [Medline]
5. Forbes LE, Bajaj M, McGinn T, et al. Perihepatic abscess formation in diabetes: a complication of silent gallstones. Am J Gastroenterol. Apr 1996;91(4):786-8. [Medline].
6. Huang J, Chang CH, Wang JL, Kuo HK, Lin JW, Shau WY, et al. Nationwide epidemiological study of severe gallstone disease in Taiwan. BMC Gastroenterol. Aug 22 2009;9:63. [Medline].
7. Lee SW, Yang SS, Chang CS, Yeh HJ. Impact of the Tokyo guidelines on the management of patients with acute calculous cholecystitis. J Gastroenterol Hepatol. Aug 3 2009; [Medline]
Source : http://emedicine.medscape.com