Acute cholecystitis is defined as an inflammation of the gallbladder wall, which occurs in response to obstruction of the cystic duct. It develops in up to 20% of patients with untreated gallstones.
The disease is related to the following processes: infectious and has an incidence of about 17 / 100.000.
Acute cholecystitis is a pathologic complication of prolonged biliary obstruction. It presents classically with epigastric or right upper quadrant pain which is similar to the pain in gallbladder colic, but it is continuous and more prolonged, lasting for several hours. Low-grade fever, vomiting, anorexia, malaise, and nausea are common symptoms of acute cholecystitis.
Patients with acute cholecystitis are usually more acutely ill-looking than those with biliary colic. Typically, patients with acute cholecystitis tend not to move at all as any movement may exacerbate the peritoneal signs. In elderly patients and diabetics who present with fever, altered mental status, or septic features, acute cholecystitis should be excluded, because in these patients, nonspecific symptoms may be the only presentation of acute cholecystitis.
On abdominal examination, acute cholecystitis and gallstones present with a classic finding of pain in the epigastric or right upper quadrant, with guarding. Murphy's sign is a characteristic finding on abdominal examination in acute cholecystitis and is described as a sudden pause in inspiration on palpation of the right upper quadrant. A study by Singer et al. indicated that Murphy's sign is highly sensitive and diagnostic of acute cholecystitis, with a sensitivity rate of 97% . However, Murphy's sign may not be so sensitive in elderly patients.
In up to 85% of patients with acute cholecystitis, symptoms resolve spontaneously within a week.
Laboratory blood studies, including white blood cell count, and liver function tests, including serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphate (ALP), as well as bilirubin levels are necessary for the diagnosis of acute cholecystitis. These indices may be normal or mildly elevated in uncomplicated cholecystitis, hence, not sensitive for ruling out a diagnosis of acute cholecystitis.
Leukocytosis with a left shift is often present. Total bilirubin and ALP elevation may be absent in uncomplicated cholecystitis. A finding of highly elevated serum bilirubin is highly suggestive of a biliary obstruction or pancreatic duct obstruction. Typically in acute cholecystitis, marked elevation of AST and ALT is suggestive of common bile duct obstruction. However, in all cases where these values are increased, complications of cholecystitis should be excluded.
The preferred imaging studies for the diagnosis of acute cholecystitis and gallstones are ultrasonography and nuclear medicine studies. The initial modality often recommended is ultrasonography while nuclear studies are reserved for cases in which ultrasound scans fail to give conclusive results. Plain radiography, endoscopic retrograde cholangiopancreatography (ERCP), and computed tomography (CT) scans are useful alternatives .
Transabdominal ultrasonography may also be used to elicit Murphy's sign. Typically, the ultrasound images reveal fluid around the gallbladder and thickening of the gallbladder wall, which is indicative of an inflammation of the gallbladder. Abdominal CT scans demonstrate complications of acute cholecystitis such as pancreatitis and perforation.
The diagnostic criteria and treatment guidelines for acute cholecystitis has been established in detail in the "Tokyo guidelines" which was published in 2007 . According to this publication, which was updated in 2013, diagnosis of acute cholecystitis is made when a patient shows at least one sign of local gallbladder inflammation and at least one sign of systemic inflammation. Local signs of inflammation include a positive Murphy's sign and demonstration of mass/tenderness/pain in the right upper quadrant on physical examination, while the systemic features of inflammation include fever, elevated C-reactive protein and leukocytosis . The diagnosis is confirmed by findings on imaging studies .
Upon diagnosis of acute cholecystitis, treatment is commenced and it is usually on an inpatient basis. A few patients may be managed as outpatients. Management of acute cholecystitis consists of IV hydration, antibiotics and analgesia with a strict Nil-per-ora (NPO) protocol. Analgesia may be achieved by NSAIDs or opioids. Nasogastric sanction is recommended if there's concomitant vomiting or ileus. Empiric antimicrobial therapy includes intravenous ceftriaxone 2g daily plus metronidazole 500mg every 8 hours, piperacillin/tazobactam 4g 6 hourly or ticarcillin/clavulanate 4g 6 hourly.
Cholecystectomy is the definitive treatment for acute cholecystitis providing significant pain relief. Cholecystectomy is best done early: within the first 48 hours of presentation especially in diabetic or elderly patients, in cases where investigations reveal inconclusive results, and in complicated cholecystitis. However, delayed cholecystectomy may be recommended in patients with severe coexisting chronic disease such as cardiac or pulmonary disease, in which case stabilization of the comorbid disease must be achieved preoperatively. If symptoms resolve, interval cholecystectomy (done after 6 weeks of onset of symptoms) may be performed. Recurrence of biliary complications is common when surgery is delayed. High-risk patients such as elderly patients, patients with acalculous cholecystitis, and those managed in the ICU for acute severe illnesses such as trauma, may need percutaneous cholecystectomy.
Acute cholecystitis develops more frequently as a complication of gallstones in diabetic patients than in non-diabetics. Complications of acute cholecystitis are also more common in diabetics than non-diabetics .
Generally, uncomplicated cholecystitis is not associated with significant mortality, however, in the immunocompromised patient, mortality may be up to 15%. Complicated cholecystitis, on the other hand, is associated with a mortality rate of 25%. Such complications include perforation and gangrenous transformation of the gallbladder, and emphysematous infection by gas-forming organisms such as the clostridium species. Gallbladder perforation occurs in 3-15% of cases and may cause death in 60% of cases. While localized perforation of the gallbladder is seen in 10% of the cases, peritonitis is seen in 1% of patients. Findings of abdominal pain increasing in intensity, very high fever, and rebound tenderness are suggestive of gangrene, perforation, and empyema of the gallbladder.
If acute cholecystitis presents with jaundice, it suggests a common bile duct obstruction.
Mirizzi syndrome is a rare complication of acute cholecystitis which is characterized by the impaction of stones in the cystic duct, obstructing the common bile duct and causing cholestasis. Stones may also move from the gallbladder through the biliary tract into the pancreatic duct causing acute pancreatitis.
Cholecystoenteric fistula is another rare complication of acute cholecystitis in which a large stone damages and erodes the gallbladder wall, leading to the formation of a fistula into the adjacent viscera particularly the small intestine. In some cases, the stone may pass through the bowel without causing complications, however, if large enough, it may obstruct the bowel, causing gallstone ileus.
Generally, prompt treatment is recommended if any of these complications sets in.
The risk factors for acute cholecystitis as well as gallstones include obesity, advanced age, pregnancy, Northern European and Hispanic ethnicity and history of liver transplant . The risk factors for acute cholecystitis and gallstones are highlighted as persons who are "fair, female, fat, and fertile". Although acute cholecystitis is more common in women than in men, men present with severer symptoms and are more likely to develop cholecystitis from gallstones .
Certain medications are associated with an increased risk of gallstones and acute cholecystitis, and these include estrogen replacements, oral contraceptives, ceftriaxone and octreotide  .
Cholecystitis occurring in the absence of gallstones (acalculous cholecystitis) develops in the setting of many risk factors including diabetes, HIV infection, prolonged fasting, vascular diseases, total parenteral nutrition and ICU care. Acalculous cholecystitis is most commonly seen in children. Additionally, gallstones in children most likely result from hemolytic diseases, burns, trauma, and total parenteral nutrition.
Inflammatory changes to the gallbladder wall are triggered when continuous obstruction of the gallbladder by the stone occurs, causing bile stasis. The release of inflammatory enzymes such as phospholipase A is triggered by bile stasis. Phospholipase A converts lecithin to lysolecithin , which is a pro-inflammatory agent. With the inflammation, mucosal fluid secretion occurs which eventually overwhelms the absorptive capacity of the gallbladder, thus resulting in its distension. The distension of the gallbladder, in turn, triggers the release of other pro-inflammatory agents which aggravate the inflammatory processes in the gallbladder mucosa. There may be a superimposed bacterial infection which further worsens the inflammation. These inflammatory changes, if uncontrolled, lead to necrotic changes and perforation of the gallbladder walls. Over time, chronic inflammation sets in with the gallbladder becoming fibrotic and shrunken.
Preventive measures for gallstones and cholecystitis include maintaining a healthy weight and gradual weight loss for overweight individuals. Sudden weight loss may increase one's risk of cholelithiasis. A diet rich in fat, as well as a diet low in fiber may increase the risk of cholelithiasis and cholecystitis, while vegetables, fruits, and whole grains tend to reduce the risk.
Acute cholecystitis is the inflammation of the gallbladder. It often develops secondary to obstruction of the gallbladder and cystic duct by gallstones . Risk factors for cholelithiasis and acute cholecystitis are similar and include obesity, pregnancy, diabetes mellitus, and old age. It is, however, more common among women than men.
Acute cholecystitis presents with sudden severe epigastric or right upper quadrant pain which is continuous and prolonged. Nonspecific symptoms, including nausea, vomiting, malaise, and anorexia, are also common in acute cholecystitis.
Diagnosis of acute cholecystitis may be made on physical examination of the patient with a characteristic finding of a momentary halt in inspiration on palpation of the epigastrium or right upper quadrant of the abdomen; this finding is referred to as "Murphy's sign". However, diagnosis is confirmed by findings of imaging studies, preferably ultrasonography. Liver function tests and other blood tests are necessary but not sensitive enough to confirm or exclude acute cholecystitis.
Treatment of acute cholecystitis is mainly conservative with IV fluids, empirical antibiotics and analgesia. Surgery may be immediate or delayed depending on the presence of complications.
Acute cholecystitis is defined as a sudden onset of symptoms caused by inflammation of the gallbladder. The gallbladder is an organ located in the upper abdomen, which stores bile. The gallbladder delivers bile through the cystic duct which becomes the common bile duct after joining a duct from the liver. Finally, the common bile duct joins the duct from the pancreas before entering the small bowel, where bile serves to emulsify fats. These ducts are small passageways. Acute cholecystitis presents with a sudden sharp abdominal pain which is severe and lasts for several hours.
Acute cholecystitis is most commonly caused by gallstones, a condition in which tiny to large-sized particles accumulate in the gallbladder and block the ducts. There are a number of risk factors for both gallstones and acute cholecystitis and these can be highlighted in a phrase "fair, fertile, fat female" indicating a few of the risk factors including obesity, pregnancy and the female gender. However, other risk factors include advanced age, a history of liver transplant, Northern European descent, and use of birth control pills or hormone replacement drugs. Acute cholecystitis may occur without gallstones and is common in patients who have HIV, diabetes, and those who have been receiving treatment in an ICU for a long time.
Although cholecystitis which does not progress to severe complications rarely causes death; if it progresses to complications such as perforation and death of the gallbladder tissue, or obstruction of the bile duct or pancreatic duct, death may occur. Complications are more commonly seen amongst diabetics and patients with severe underlying diseases.
The condition presents with a sudden sharp pain at the center of the upper part of the abdomen called the epigastrium or the right upper part of the abdomen. This pain is often very severe and continuous, occurring for several hours. Low-grade fever, vomiting, nausea, loss of appetite and weakness are other common symptoms of this disease.
Laboratory investigations necessary in the diagnosis of acute cholecystitis include a white blood cell count and liver function tests, which show the level of certain critical chemicals which change with diseases of the liver and gallbladder. However, imaging studies are used to confirm a diagnosis of acute cholecystitis. An ultrasound scan is the preferred modality, while cholescintigraphy, an imaging study which employs nuclear medicine, is the second choice. These imaging studies reveal features in the gallbladder which indicate inflammation.
The initial treatment of acute cholecystitis basically involves antibiotics and pain relief medications. In patients who are hospitalized, fluids and antibiotics would be administered intravenously and the patient is prohibited from taking anything by mouth for a given period of time. Surgery is the standard treatment for acute cholecystitis. Surgery may be done early, that is within 2 days of onset of symptoms or of presentation of the patient especially in those who have developed serious complications. However, it may be delayed by up to 6 weeks in those with no complications after the symptoms have subsided.