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Cholecystitis

  • Author: Alan A Bloom, MD; Chief Editor: BS Anand, MD  more...
 
Updated: Apr 15, 2016
 

Practice Essentials

Cholecystitis is inflammation of the gallbladder that occurs most commonly because of an obstruction of the cystic duct by gallstones arising from the gallbladder (cholelithiasis). Uncomplicated cholecystitis has an excellent prognosis; the development of complications such as perforation or gangrene renders the prognosis less favorable.

Signs and symptoms

The most common presenting symptom of acute cholecystitis is upper abdominal pain. The following characteristics may be reported:

  • Signs of peritoneal irritation may be present, and the pain may radiate to the right shoulder or scapula
  • Pain frequently begins in the epigastric region and then localizes to the right upper quadrant (RUQ)
  • Pain may initially be colicky but almost always becomes constant
  • Nausea and vomiting are generally present, and fever may be noted

Patients with acalculous cholecystitis may present with fever and sepsis alone, without history or physical examination, findings consistent with acute cholecystitis.

Cholecystitis may present differently in special populations, as follows:

  • Elderly (especially diabetics) – May present with vague symptoms and without many key historical and physical findings (eg, pain and fever), with localized tenderness the only presenting sign; may progress to complicated cholecystitis rapidly and without warning
  • Children – May present without many of the classic findings; those at higher risk for cholecystitis include those who have sickle cell disease, serious illness, a requirement for prolonged total parenteral nutrition (TPN), hemolytic conditions, or congenital and biliary anomalies

The physical examination may reveal the following:

  • Fever, tachycardia, and tenderness in the RUQ or epigastric region, often with guarding or rebound
  • Palpable gallbladder or fullness of the RUQ (30-40% of patients)
  • Jaundice (~15% of patients)

The absence of physical findings does not rule out the diagnosis of cholecystitis.

See Presentation for more detail.

Diagnosis

Laboratory tests are not always reliable, but the following findings may be diagnostically useful:

  • Leukocytosis with a left shift may be observed
  • Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels may be elevated in cholecystitis or with common bile duct (CBD) obstruction
  • Bilirubin and alkaline phosphatase assays may reveal evidence of CBD obstruction
  • Amylase/lipase assays are used to assess for pancreatitis; amylase may also be mildly elevated in cholecystitis
  • Alkaline phosphatase level may be elevated (25% of patients with cholecystitis)
  • Urinalysis is used to rule out pyelonephritis and renal calculi
  • All females of childbearing age should undergo pregnancy testing

Diagnostic imaging modalities that may be considered include the following:

  • Radiography
  • Ultrasonography
  • Computed tomography (CT)
  • Magnetic resonance imaging (MRI)
  • Hepatobiliary scintigraphy (see the image below)
    Cholecystitis. Abnormal finding on hepatoiminodiacCholecystitis. Abnormal finding on hepatoiminodiacetic acid (HIDA) scan.
  • Endoscopic retrograde cholangiopancreatography (ERCP)

The American College of Radiology (ACR) makes the following imaging recommendations:

  • Ultrasonography is the preferred initial imaging test for the diagnosis of acute cholecystitis; scintigraphy is the preferred alternative
  • CT is a secondary imaging test that can identify extrabiliary disorders and complications of acute cholecystitis
  • CT with intravenous (IV) contrast is useful in diagnosing acute cholecystitis in patients with nonspecific abdominal pain
  • MRI, often with IV gadolinium-based contrast medium, is also a possible secondary choice for confirming a diagnosis of acute cholecystitis
  • MRI without contrast is useful for eliminating radiation exposure in pregnant women when ultrasonography has not yielded a clear diagnosis
  • Contrast agents should not be used in patients on dialysis unless absolutely necessary

See Workup for more detail.

Management

Treatment of cholecystitis depends on the severity of the condition and the presence or absence of complications.

In acute cholecystitis, the initial treatment includes bowel rest, IV hydration, correction of electrolyte abnormalities, analgesia, and IV antibiotics. Options include the following:

  • Sanford guide – Piperacillin-tazobactam, ampicillin-sulbactam, or meropenem; in severe life-threatening cases, imipenem-cilastatin
  • Alternative regimens – Third-generation cephalosporin plus metronidazole
  • Emesis can be treated with antiemetics and nasogastric suction
  • Because of the rapid progression of acute acalculous cholecystitis to gangrene and perforation, early recognition and intervention are required.
  • Supportive medical care should include restoration of hemodynamic stability and antibiotic coverage for gram-negative enteric flora and anaerobes if biliary tract infection is suspected.
  • Daily stimulation of gallbladder contraction with IV cholecystokinin (CCK) may help prevent formation of gallbladder sludge in patients receiving TPN

In cases of uncomplicated cholecystitis, outpatient treatment may be appropriate. The following medications may be useful in this setting:

  • Levofloxacin and metronidazole for prophylactic antibiotic coverage against the most common organisms
  • Antiemetics (eg, promethazine or prochlorperazine) to control nausea and prevent fluid and electrolyte disorders
  • Analgesics (eg, oxycodone/acetaminophen)

Surgical and interventional procedures used to treat cholecystitis include the following:

  • Laparoscopic cholecystectomy (standard of care for surgical treatment of cholecystitis)
  • Percutaneous drainage
  • ERCP
  • Endoscopic ultrasound-guided transmural cholecystostomy
  • Endoscopic gallbladder drainage

See Treatment and Medication for more detail.

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Background

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 gallbladder (ie, calculous cholecystitis), with the other 10% of cases representing acalculous cholecystitis.[1]

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. (See Etiology.) 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. (See Prognosis.)

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. (See Clinical Presentation.)

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. (See Diagnosis.)

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 uncomplicated cholecystitis. If surgical treatment is indicated, laparoscopic cholecystectomy represents the standard of care. (See Treatment and Management.)

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.

For further clinical information, see the Medscape Reference topic Cholecystitis and Biliary Colic.

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Pathophysiology

Ninety percent of cases of cholecystitis involve stones in the gallbladder (ie, calculous cholecystitis), with the other 10% of cases representing acalculous cholecystitis.[1]

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.[4] Endotoxin also abolished the contractile response to CCK, leading to gallbladder stasis.

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Etiology

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)
  • Pregnancy
  • Increasing age

Acalculous cholecystitis is related to conditions associated with biliary stasis, and include the following:

  • Critical illness
  • Major surgery or severe trauma/burns
  • Sepsis
  • 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[5]
  • Patients with AIDS who have cytomegalovirus, cryptosporidiosis, or microsporidiosis

Patients who are immunocompromised are at an increased risk of developing cholecystitis from a number of different infectious sources. Idiopathic cases exist.

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Epidemiology

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.

Go to Pediatric Cholecystitis for more complete information on this topic.

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 in 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.

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Prognosis

Uncomplicated cholecystitis has an excellent prognosis, with a 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%.

The severity of acute cholecystitis also has an impact on the risk of iatrogenic bile duct injury during cholecystectomy.[8]  Tornqvist et al reported a doubling of the risk for sustaining a biliary lesion in patients with ongoing acute cholecystitis compared to those without acute cholecystitis. Patients with Tokyo grade II (moderate) acute cholecystitis and those with Tokyo grade III (severe) cholecystitis had, respectively, over double and more than eight times the risk of bile duct injury compared to those without acute cholecystitis. The risk of biliary injury was reduced by 52% with intention to use intraoperative cholangiography.[8]

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Contributor Information and Disclosures
Author

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, New York Academy of Sciences

Disclosure: Nothing to disclose.

Chief Editor

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, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Additional Contributors

Julian Katz, MD Clinical Professor of Medicine, Drexel University College of Medicine

Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law, Medicine & Ethics, American Trauma Society, Association of American Medical Colleges, Physicians for Social Responsibility

Disclosure: Nothing to disclose.

Acknowledgements

Clinton S Beverly, MD Clinical Assistant Professor, Department of Surgery, Mercer University School of Medicine

Clinton S Beverly, MD is a member of the following medical societies: American College of Surgeons and Society of American Gastrointestinal and Endoscopic Surgeons

Disclosure: Nothing to disclose.

Barry E Brenner, MD, PhD, FACEP Professor of Emergency Medicine, Professor of Internal Medicine, Program Director for Emergency Medicine, Case Medical Center, University Hospitals, Case Western Reserve University School of Medicine

Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Jack A Di Palma, MD Director, Division of Gastroenterology, Professor, Department of Internal Medicine, University of South Alabama College of Medicine

Jack A Di Palma, MD is a member of the following medical societies: American College of Gastroenterology and American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Don Gladden, DO Staff Physician, Department of Emergency Medicine, Seton Medical Center Williamson

Don Gladden, DO is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

Eugene Hardin, MD, FAAEM, FACEP Former Chair and Associate Professor, Department of Emergency Medicine, Charles Drew University of Medicine and Science; Former Chair, Department of Emergency Medicine, Martin Luther King Jr/Drew Medical Center

Disclosure: Nothing to disclose.

Samuel M Keim, MD Associate Professor, Department of Emergency Medicine, University of Arizona College of Medicine

Samuel M Keim, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Public Health Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Alexandre F Migala, DO Staff Physician, Department of Emergency Medicine, Denton Regional Medical Center

Alexandre F Migala, DO is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Osteopathic Association, Association of Military Osteopathic Physicians and Surgeons, and Texas Medical Association

Disclosure: Nothing to disclose.

Anil Minocha, MD, FACP, FACG, AGAF, CPNSS Professor of Medicine, Director of Digestive Diseases, Medical Director of Nutrition Support, Medical Director of Gastrointestinal Endoscopy, Internal Medicine Department, University of Mississippi Medical Center; Clinical Professor, University of Mississippi School of Pharmacy

Anil Minocha, MD, FACP, FACG, AGAF, CPNSS is a member of the following medical societies: American Academy of Clinical Toxicology, American Association for the Study of Liver Diseases, American College of Forensic Examiners, American College of Gastroenterology, American College of Physicians, American Federation for Clinical Research, American Gastroenterological Association, and American Society of Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Tushar Patel, MB, ChB Professor of Medicine, Ohio State University Medical Center

Tushar Patel, MB, ChB is a member of the following medical societies: American Association for the Study of Liver Diseases and American Gastroenterological Association

Disclosure: Nothing to disclose.

Rahul Sharma, MD, MBA, FACEP Medical Director and Associate Chief of Service, NYU Langone Medical Center, Tisch Hospital Emergency Department; Assistant Professor of Emergency Medicine, New York University School of Medicine

Rahul Sharma, MD, MBA, FACEP is a member of the following medical societies: American College of Emergency Physicians, American College of Physician Executives, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Peter A D Steel, MA, MBBS Attending Physician, Department of Emergency Medicine, Joan and Sanford I Weill Cornell Medical Center, New York Presbyterian Hospital

Peter A D Steel, MA, MBBS is a member of the following medical societies: American College of Emergency Physicians, British Medical Association, Emergency Medicine Residents Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Alan BR Thomson, MD Professor of Medicine, Division of Gastroenterology, University of Alberta, Canada

Alan BR Thomson, MD is a member of the following medical societies: Alberta Medical Association, American College of Gastroenterology, American Gastroenterological Association, Canadian Association of Gastroenterology, Canadian Medical Association, College of Physicians and Surgeons of Alberta, and Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Jeffery Wolff, DO Consulting Staff, Department of Gastroenterology, Brooke Army Medical Center; Staff Gastroenterologist, Landstuhl Regional Medical Center

Jeffery Wolff, DO, is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, and American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

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Cholecystitis. Normal finding on hepatoiminodiacetic acid (HIDA) scan.
Cholecystitis. Abnormal finding on hepatoiminodiacetic acid (HIDA) scan.
 
 
 
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