|Classification and external resources|
Cholecystitis develops when the gallbladder becomes inflamed.
Cholecystitis (Greek, -cholecyst, "gallbladder", combined with the suffix -itis, "inflammation") is inflammation of the gallbladder. Although most people with gallstones do not have symptoms and will not go on to develop cholecystitis, cholecystitis occurs most commonly due to blockage of the cystic duct with gallstones (cholelithiasis). This blockage causes a build up of bile in the gallbladder and increased pressure within the gallbladder, leading to right upper abdominal pain. Concentrated bile, pressure, and sometimes bacterial infection irritate and damage the gallbladder wall, causing inflammation and swelling of the gallbladder. Inflammation and swelling of the gallbladder can reduce normal blood flow to areas of the gallbladder, which can lead to cell death due to inadequate oxygen.
Risk factors for gallstones and cholecystitis are similar and include female sex, increasing age, pregnancy, oral contraceptives, obesity, diabetes mellitus, ethnicity (Native North American), rapid weight loss. Cholecystitis is diagnosed based on the characteristic symptoms of right upper abdominal pain, nausea, vomiting, and fever as well as laboratory testing showing an increased white blood count. Abdominal ultrasound is typically also used in diagnosis. Uncomplicated cholecystitis has an excellent prognosis; however, more than 25% of patients require surgery or develop complications. Delayed diagnosis of acute cholecystitis increases morbidity and mortality. Cholelithiasis and cholecystitis may present as a single episode or may recur on multiple occasions.
- 1 Signs and symptoms
- 2 Causes
- 3 Classification
- 4 Diagnosis
- 5 Management
- 6 Complications
- 7 See also
- 8 References
Signs and symptoms
Most people with gallstones do not have symptoms. When a gallstone becomes intermittently lodged in the cystic duct, they suffer from biliary colic. Biliary colic is abdominal pain in the right upper quadrant or epigastrium that is usually episodic, occurs after eating greasy or fatty foods, and leads to nausea and/or vomiting. People who suffer from cholecystitis most commonly initially have symptoms of biliary colic before developing cholecystitis. The symptoms of cholecystitis are similar to biliary colic but the pain becomes more severe and constant. Nausea is common and vomiting occurs in 75% of people with cholecystitis. In addition to abdominal pain, right shoulder pain can be present.
On physical examination, fever is common. A gallbladder with cholecystitis is almost always tender to touch. Because of the inflammation, its size can be felt from the outside of the body in 25-50% of people with cholecystitis. Pain with deep inspiration leading to termination of the breath while pressing on the right upper quadrant of the abdomen usually causes pain (Murphy's sign). Murphy's sign is sensitive, but not specific for cholecystitis. Jaundice may occur but is usually mild, and if severe, suggests another cause of symptoms such as choledocholithiasis. Elderly patients and those with diabetes, chronic illness, or who are immunocompromised may have vague symptoms that may not include fever or localized tenderness.
Cholecystitis occurs when the gallbladder becomes inflamed. Gallbladder inflammation is most commonly caused by gallstones but can also occur due to blockage from a tumor or scarring of the bile duct. The greatest risk factor for cholecystitis is gallstones. Risk factors for gallstones include female sex, increasing age, pregnancy, oral contraceptives, obesity, diabetes mellitus, ethnicity (Native North American), rapid weight loss.
Acute calculous cholecystitis
Roughly 90% of cases of cholecystitis are caused by gallstones blocking the flow of bile in the biliary tree leading to inflammation of the gallbladder (acute calculous cholecystitis). Blockage of bile flow leads to thickening of bile and bile stasis which lead to an enlarged, red, and tense gallbladder. The gallbladder is initially sterile but often becomes secondarily infected by bacteria, predominantly by E. coli, Klebsiella, Streptococcus, and Clostridium species. Inflammation can spread to the outer covering of the gallbladder, leading to irritation of surrounding structures such as the diaphragm which leads to referred right shoulder pain.
In 5-10% of cases of cholecystitis, the gallbladder may become inflamed in the absence of a gallstone, known as acalculous cholecystitis. Acalculous cholecystitis is more commonly seen in severely-ill people, such as those in intensive care units, or in those who have recently undergone major surgery.
Chronic cholecystitis occurs after repeated episodes of acute cholecystitis and is almost always due to gallstones. Chronic cholecystitis may be asymptomatic, may present as a more severe case of acute cholecystitis, or may lead to a number of complications such as gangrene, perforation, or fistula formation.
Xanthogranulomatous cholecystitis (XGC) is a rare form of chronic cholecystitis which mimics gallbladder cancer although it is not cancerous. It was first discovered and reported in the medical literature in 1976 by J.J. McCoy, Jr., and colleagues.
The diagnosis of cholecystitis is suggested by the history and physical (abdominal pain, nausea, vomiting, fever) in addition to laboratory and ultrasonographic testing.
In someone suspected of having cholecystitis, blood tests are performed for markers of inflammation (e.g. complete blood count, C-reactive protein), as well as bilirubin levels in order to assess for bile duct blockage. Complete blood count typically shows an increased white blood count (12,000-15,000/mcL). C-reactive protein is usually elevated although not commonly measured in the United States. Bilirubin levels are often mildly elevated (1-4 mg/dL). If bilirubin levels are more significantly elevated, alternate or additional diagnoses should be considered such as gallstone blocking the common bile duct (choledocholethiasis). Less commonly, blood aminotransferases are elevated. The degree of elevation of these laboratory values may depend on the degree of inflammation of the gallbladder.
Right upper quadrant abdominal ultrasound is most commonly used to diagnose cholecystitis. Ultrasound findings suggestive of acute cholecystitis include gallstones, fluid surrounding the gallbladder, gallbladder wall thickening, dilation of the bile duct, and sonographic Murphy's sign. Given its higher sensitivity, hepatic iminodiacetic acid (HIDA) scan can be used if ultrasound is not diagnostic. CT scan may also be used if complications such as perforation or gangrene are suspected.
Many other diagnoses can have similar symptoms as cholecystitis. Additionally the symptoms of chronic cholecystitis are commonly vague and can be mistaken for other diseases. These alternative diagnoses include but are not limited to:
- Perforated peptic ulcer
- Acute pancreatitis
- Liver abscess
- Myocardial ischemia
- Hiatal hernia
- Biliary colic
- Acute peptic ulcer exacerbation
- Amoebic liver abscess
- Acute intestinal obstruction
- Kidney stone
For most patients diagnosed with acute cholecystitis, the definitive treatment is surgical removal of the gallbladder, cholecystectomy. Until the late 1980s surgical removal was usually accomplished by a large incision in the upper right quadrant of the abdomen under the rib cage. Since the advent of laparoscopic surgery in the early 1990s, laparoscopic cholecystectomy has become the treatment of choice for acute cholecystitis. Laparoscopic cholecystectomy is performed using several small incisions located at various points across the abdomen. Several studies have demonstrated the superiority of laparoscopic cholecystectomy when compared to open cholecystectomy. Patient undergoing laparoscopic surgery report less incisional pain postoperatively as well as having fewer long term complications and less disability following the surgery. Additionally, laparoscopic surgery is associated with a lower rate of surgical site infection.
During the days prior to laparoscopic surgery, studies showed that outcomes were better following early removal of the gallbladder, preferably within the first week. Patients receiving early intervention had shorter hospital stays and lower complication rates. In the era of laparoscopic surgery, a similar approach is still advocated. In a 2006 Cochrane review, early laparoscopic cholecystectomy was compared to delayed treatment. The review consisted of 5 trials with 451 patients randomized to either early (223 patients) or delayed (228) surgical management. There was no statistically significant difference in terms of negative outcomes including bile duct injury (OR 0.63, 95% CI 0.15 to 2.70) or conversion to open cholecystectomy (OR 0.84, 95% CI 0.53 to 1.34). However, the early group was found to have shorter hospital stays. For early cholecystectomy, the most common reason for conversion to open surgery is inflammation obscuring Calot's triangle. For delayed surgery, the most common reason was fibrotic adhesions.
Supportive measures are usually instituted prior to surgery. These measures include fluid resuscitation and antibiotics targeting enteric organisms, such as E coli and Bacteroides. Antibiotic regimens usually consist of a broad spectrum antibiotic such as piperacillin-tazobactam (Zosyn), ampicillin-sulbactam (Unasyn), ticarcillin-clavulanate (Timentin), or a cephalosporin (e.g.ceftriaxone) and an antibacterial with good coverage (fluoroquinolone such as ciprofloxacin) and anaerobic bacteria coverage, such as metronidazole. For penicillin allergic patients, aztreonam and clindamycin may be used. Parenteral narcotics can be used for pain control.
In cases of severe inflammation, shock, or if the patient has higher risk for general anesthesia (required for cholecystectomy), the managing physician may elect to have an interventional radiologist insert a percutaneous drainage catheter into the gallbladder ('percutaneous cholecystostomy tube') and treat the patient with antibiotics until the acute inflammation resolves. A cholecystectomy may then be warranted if the patient's condition improves.
Homeopathic approaches to treating cholecystitis have not been validated by evidence and should not be used in place of surgery.
A number of complications may occur from cholecystitis if not detected early or properly treated. Signs of complications include high fever, shock and jaundice. Complications include the following:
- Gallbladder rupture
- Fistula formation and gallstone ileus
- Rokitansky-Aschoff sinuses
Gangrene and gallbladder rupture
Cholecystitis causes the gallbladder to become distended and firm. Distension can lead decreased blood flow to the gallbladder, causing tissue death and eventually gangrene. Once tissue has died, the gallbladder is at greatly increased risk of rupture (perforation). Rupture can also occur in cases of chronic cholecystitis. Rupture is a rare but serious complication that leads to abscess formation or peritonitis. Massive rupture of the gallbladder has a mortality rate of 30%.
Untreated cholecystitis can lead to worsened inflammation and infected bile that can lead to a collection of pus surrounding the gallbladder, also known as empyema. The symptoms of empyema are similar to uncomplicated choleystitis but greater severity: high fever, severe abdominal pain, more severely elevated white blood count.
Fistula formation and gallstone ileus
The inflammation of cholecystitis can lead to adhesions between the gallbladder and other parts of the gastrointestinal tract, most commonly the duodenum. These adhesions can lead to the formation of direct connections between the gallbladder and gastrointestinal tract, callled fistulas. With these direct connections, gallstones can pass from the gallbladder to the intestines. Gallstones can get trapped in the gastrointestinal tract, most commonly at the connection between the small and large intestines (ileocecal valve). When a gallstone gets trapped, it can lead to an intestinal obstruction, called gallstone ileus, leading to abdominal pain, vomiting, constipation, and abdominal distension.
- Strasberg, SM (26 June 2008). "Clinical practice. Acute calculous cholecystitis". The New England journal of medicine 358 (26): 2804–11. doi:10.1056/NEJMcp0800929. PMID 18579815.
- Greenberger N.J., Paumgartner G (2012). Chapter 311. Diseases of the Gallbladder and Bile Ducts. In Longo D.L., Fauci A.S., Kasper D.L., Hauser S.L., Jameson J, Loscalzo J (Eds), 'Harrison's Principles of Internal Medicine, 18e.Retrieved November 08, 2014 fromhttp://accessmedicine.mhmedical.com.ucsf.idm.oclc.org/content.aspx?bookid=331&Sectionid=40727107.
- Friedman L.S. (2015). Liver, Biliary Tract, & Pancreas Disorders. In Papadakis M.A., McPhee S.J., Rabow M.W. (Eds), 'Current Medical Diagnosis & Treatment 2015. Retrieved November 08, 2014 fromhttp://accessmedicine.mhmedical.com.ucsf.idm.oclc.org/content.aspx?bookid=1019&Sectionid=57668608.
- Demehri, FR; Alam, HB (15 October 2014). "Evidence-Based Management of Common Gallstone-Related Emergencies". Journal of intensive care medicine. doi:10.1177/0885066614554192. PMID 25320159.
- Singer, AJ; McCracken, G; Henry, MC; Thode HC, Jr; Cabahug, CJ (September 1996). "Correlation among clinical, laboratory, and hepatobiliary scanning findings in patients with suspected acute cholecystitis.". Annals of emergency medicine 28 (3): 267–72. PMID 8780468.
- "Cholecystitis". Mayo Clinic. Mayo Clinic. 28 August 2014. Retrieved 13 November 2014.
- Makino I, Yamaguchi T, Sato N, Yasui T, Kita I; Yamaguchi; Sato; Yasui; Kita (August 2009). "Xanthogranulomatous cholecystitis mimicking gallbladder carcinoma with a false-positive result on fluorodeoxyglucose PET". World J. Gastroenterol. 15 (29): 3691–3. doi:10.3748/wjg.15.3691. PMC 2721248. PMID 19653352.
- Rao RV, Kumar A, Sikora SS, Saxena R, Kapoor VK; Kumar; Sikora; Saxena; Kapoor (2005). "Xanthogranulomatous cholecystitis: differentiation from associated gall bladder carcinoma". Trop Gastroenterol 26 (1): 31–3. PMID 15974235.
- McCoy JJ, Vila R, Petrossian G, McCall RA, Reddy KS; Vila; Petrossian; McCall; Reddy (March 1976). "Xanthogranulomatous cholecystitis. Report of two cases". J S C Med Assoc 72 (3): 78–9. PMID 1063276.
- Shea JA, Berlin JA, Escarce JJ, Clarke JR, Kinosian BP, Cabana MD, Tsai WW, Horangic N, Malet PF, Schwartz JS; Berlin; Escarce; Clarke; Kinosian; Cabana; Tsai; Horangic; Malet; Schwartz (November 1994). "Revised estimates of diagnostic test sensitivity and specificity in suspected biliary tract disease". Arch. Intern. Med. 154 (22): 2573–81. doi:10.1001/archinte.154.22.2573. PMID 7979854.
- Fink-Bennett D, Freitas JE, Ripley SD, Bree RL; Freitas; Ripley; Bree (August 1985). "The sensitivity of hepatobiliary imaging and real-time ultrasonography in the detection of acute cholecystitis". Arch Surg 120 (8): 904–6. doi:10.1001/archsurg.1985.01390320028004. PMID 3893388.
- Strasberg SM (2008). "Acute Calculous Cholecystitis". New England Journal of Medicine 358 (26): 2804–2811. doi:10.1056/NEJMcp0800929. PMID 18579815.
- Velanovich V (2000). "Laparoscopic vs open surgery: A preliminary comparison of quality-of-life outcomes". Surgical endoscopy 14 (1): 16–21. doi:10.1007/s004649900003. PMID 10653229.
- Chen L, Tao SF, Xu Y, Fang F, Peng SY; Tao; Xu; Fang; Peng (2005). "Patients' quality of life after laparoscopic or open cholecystectomy". Journal of Zhejiang University SCIENCE 6B (7): 678–681. doi:10.1631/jzus.2005.B0678. PMC 1389804. PMID 15973772.
- Richards C, Edwards J, Culver D, Emori TG, Tolson J, Gaynes R; Edwards; Culver; Emori; Tolson; Gaynes; National Nosocomial Infections Surveillance (Nnis) System (2003). "Does Using a Laparoscopic Approach to Cholecystectomy Decrease the Risk of Surgical Site Infection?". Annals of Surgery 237 (3): 358–362. doi:10.1097/01.SLA.0000055221.50062.7A. PMC 1514308. PMID 12616119.
- Banz V, Gsponer T, Candinas D, Güller U; Gsponer; Candinas; Güller (2011). "Population-Based Analysis of 4113 Patients with Acute Cholecystitis". Annals of Surgery 254 (6): 964–970. doi:10.1097/SLA.0b013e318228d31c. PMID 21817893.
- Gurusamy KS, Samraj K; Samraj (2006). Gurusamy, Kurinchi Selvan, ed. "Cochrane Database of Systematic Reviews". Cochrane database of systematic reviews (Online) (4): CD005440. doi:10.1002/14651858.CD005440.pub2. PMID 17054258.