Acute cholecystitis

Most common complication of gallstones.

Associated with gallstones in greater than 90% of cases.

An acute inflammatory disease of the gallbladder that is caused by gallstone obstruction of the cystic duct in approximately 90 to 95% of people diagnosed with this condition.

Occurs when a stone becomes impacted in the cystic duct and inflammation develops behind the obstruction.

Less commonly  acalculus  cholecystitis , an acute inflammation of the gallbladder without gallstones, is present in 5 to 10% of people diagnosed with acute cholecystitis.

Gallbladder disease affects approximately 20 million individuals in the US with a direct annual cost of more than $6.3 billion, with more than 200,000 people diagnosed with acute cholecystitis each year.

People from Central and South America of Hispanic ethnicity and individuals with American Indian ancestry have the highest prevalence of cholelithiasis.

Its prevalence is approximately 27% in Hispanic individuals.

The prevalence of cholelithiasis in sub Saharan Africa is approximately 5% and the prevalence is approximately 3.2 to 15.6% in Asia.

Risk factors for gallbladder disease such as obesity, weight loss, pregnancy, and drinking less than 1 to 2 alcoholic drinks per day do not explain the differences in racial or ethnic prevalence of cholelithiasis.

A diet high in fat or low in fiber may explain a significant fraction of the risk associated with cholelithiasis.

Gall stones are 2 to 3 times more common in women.

The difference between the genders in cholelithiasis diminishes with age and the risk of developing cholelithiasis increases with age.

About 10 to 15% of individuals with gallstones develop acute cholecystitis over their lifetime.

Of the 10 to 15% of adults with cholelithiasis, approximately 80% are asymptomatic.

20% of patients with gallstones will eventually develop gallstone related complications at an incidence rates of 1 to 4% annually, with calculus acute cholecystitis as the first presentation in 10 to 15% of all patients with gallstones.

Congenital hemolytic anemias especially thalassemia and sickle cell disease are common cause of gallstones, particularly in children.

Some medications such as octreotide and cephtriaxone are associated with increased rate of gallstone formation.

Calculous acute cholecystitis is more common with diabetes.

Glucagon like peptide analogs to treat type two diabetes are associated with an increased risk of bile duct and gallbladder disease.


Blocked bile accumulates, and pressure on the gallbladder wall may lead to the release of substances that cause inflammation, such as phospholipase. 


There is a risk of bacterial infection with acute cholecystitis 


An inflamed gallbladder is likely to cause pain, fever, and tenderness in the upper, right corner of the abdomen, and may have a positive Murphy’s sign. 


Cholecystitis is often managed with rest and antibiotics, particularly cephalosporins and, in severe cases, metronidazole.

Acalculus cholecystitis is considered in a patient with fever, right upper quadrant pain in a critically ill patient with no intake for a prolonged period of time, or in a patient with recent major surgery, and in the presence of multiple organ failure.

Acalculous acute cholecystitis risk factors include critical illness, severe trauma, burns, cardiac surgery with cardiopulmonary bypass, total parenteral nutrition and patients undergoing bone marrow transplant.

May occur in patients with AIDS caused by infectious agents.

Commonly associated with fever and sudden appearance of pain in the epigastrium or right upper quadrant.

Abdominal pains may gradually subside over 12-18 hours, and may be associated with vomiting, and that 75% of the patients.

Right upper quadrant abdominal pain may be associated with a Murphy’s sign, guarding and rebound tenderness may be present.

The gallbladder is palpable in about 15% of cases.

25% of patients have jaundice.

Leukocytosis is typical, and bilirubin is generally between one and 4 mg/dL, while AST and output phosphatase are often elevated.

May be associated with moderately elevated amylase level.

Abdominal plain films they demonstrate an radiopaque gallstone in 15% of cases.

Hepatobiliay scanning with technetium or hepatic iminodiacetic acid (HIDA) can demonstrate and obstructive cystic duct, which is the cause of the process in most patients.

HIDA radiotracer is excreted into the bile.

The HIDA scan is reliable if the bilirubin is less than 5 mg/dL and has a 98% sensitivity and an 81% specificity for acute cholecystitis.

False positive HIDA scans can result from liver disease, chronic cholecystitis, and prolonged fasting.

Abdominal ultrasound may show the presence of gallstones and has a sensitivity of 67%, and a specificity of 82% for the diagnosis of acute cholecystitis by showing gallbladder thickening, pericholecystic fluid, and positive sonographic Murphy’s sign.

HIDA is more sensitive test than ultrasound in diagnosing acute cholecystitis and should be the first diagnostic test in patients with suspected acute cholecystitis., if not confirmed by US.

CT of the abdomen characteristically shows distention of the gallbladder, mural thickening, pericholecystic fat stranding and pericholecystic fluid.

Gallstone detection by CT scan is dependent on the composition of gallstones and the thickness of CT slices: 20% of gallstones have similar attenuation as bile and are not detectable with CT.

Abdominal CT has an estimated sensitivity of 94% and specificity at 59% in the diagnosis of acute cholecystitis.

MRI findings with acute uncomplicated cholecystitis include: gallstones, gallbladder wall thickening, gallbladder wall edema, gallbladder distention, pericholecystic fluid, and fluid around the liver.

The sensitivity of MRI is 88% and specificity 89% for diagnosing acute cholecystitis.

Differential diagnosis: peptic ulcer disease, acute pancreatitis, colonic carcinoma, diverticulitis, liver abscess, hepatitis, pneumonia with pleurisy, perforated viscous, and myocardial infarction.

Complications include gangrene of the gallbladder manifesting by continued or progressive right upper quadrant abdominal pain, tenderness, regarding, fever, leukocytosis from ischemia of the gallbladder.

Gangrene of the gallbladder leads to gallbladder perforation, with abscess formation and rarely peritonitis.

Patients may develop chronic cholecystitis from repeated episodes of acute inflammation, or chronic irritation of the gallbladder by stones.

Chronicle cholecystitis may lead to villi enlargements from cholesterol deposition grossly appearing as a strawberry gallbladder, hyperplasia of the gallbladder wall may give it the appearance of a myoma, and hydrops may occur.

Cholelithiasis with chronic cholecystitis may result in repeated episodes of gallbladder inflammation, bile duct stone formation, pancreatitis, fistulization to the bowel and rarely gallbladder cancer.

Porcelain or calcified gallbladders highly associated with gallbladder cancer and are an indication for cholecystectomy.

Acute cholecystitis can be treated conservatively by withholding feedings, injured venous fluids, analgesics and intravenous antibiotics.

Early cholecystectomy is treatment of choice rather than delaying the process, because of a high risk of recurrent attacks with up to 10% by one month, and over 30% one by one year.

In a study of patients with acute cholecystitis undergoing surgery within 24 hours of admission versus patients treated with antibiotics before undergoing cholecystectomy at significant delay in days: there was a much lower prevalence of postoperative complications within the first 75 days in the group treated with early cholecystectomy at 11.8% for patients treated within 24 hours of admission versus 34.4% of those treated at days seven through 45.

Pther studies have shown that with acute cholecystitis bile duct injury after surgery was lower for patients who underwent cholecystectomy within four days of admission versus those who underwent cholecystectomy after four days: also it has been found that there is a lower death rate with earlier cholecystectomy., and the lower conversion to open procedure.

Cholecystectomy can generally be performed within 2 to 4 days after resolution of the acute process.

Immediate cholecystectomy is required if there is evidence of gangrene or perforation.

Early laparoscopic cholecystectomy compared to initial antibiotic treatment and delayed cholecystectomy associated with a significant reduced hospital stay, no major complications, and no significant difference in open surgical conversion rates (Cassilas).

It is recommended that laparoscopic cholecystectomy be performed for acute cholecystitis during any trimester of pregnancy.

surgical management for acute cholecystitis in pregnancy is preferred over non-operative management.

in the study of nearly 24,000 pregnant women diagnosed with acute cholecystitis early laparoscopic cholecystectomy was associated with lower preterm delivery, preterm labor, or spontaneous abortion when performed within one day of presentation, compared with delayed surgery.

Approximately 2 to 15% of patients undergoing laparoscopic cholecystectomy must be converted to open cholecystectomy.

Most studies show that male sex, older age, higher BMI, the presence of acute cholecystitis, previous up for abdominal surgery, impacted gallstone at the gallbladder neck, and a gallbladder wall thickness greater than 3 mm. are associated with a higher rate of conversion to an open procedure.

Overall mortality rate for cholecystectomy is less than 0.2%.

Acute cholecystitis due to gall stones occurs after a cystic duct obstruction caused by gallstones or sludge or lithogenic bile.

The degree and duration of cystic duct obstruction helps determine the rate of progression of acute cholecystitis and the severity of gallbladder inflammation.

Cystic duct obstruction result in increased intraluminal pressure within the gallbladder and with a supersaturated bile from cholesterol, it initiates an acute inflammatory response.

Secondary bacterial infections with enteric organisms occur in about 20% of patients with acute cholecystitis: E. coli, Klebsiella, and Streptococcus faecalis.

Acute cholecystitis is characterized by inflammation with gallbladder wall congestion and edema followed by hemorrhage and necrosis of the gallbladder wall, which may lead to gallbladder perforation at the site of ischemic gangrene and subsequent biliary peritonitis.

The final phase of acute cholecystitis is a chronic or purulent phase manifested by white blood cell infiltration, necrotic tissue, and development of pus and gross infection.

Subsequently intraluminal purulence is replaced by granulation tissue with a sub acute cholecystitis and eventually chronic cholecystitis.

With acalculous acute cholecystitis ischemia and bile stasis occurs in the gallbladder wall leading to bile insipissation that is is directly toxic to the gallbladder epithelium.

The gallbladder endothelial injury leads to ischemia, hypo perfusion which can occur in critical ill patients.

Acalculous acute cholecystitis could also progress to gangrene, empyema and perforation up to 50% of patients.

Diagnosis: acute cholecystitis is suspected in patients with right upper quadrant pain with the without any association with eating.

Fever, nausea, vomiting with typical presenting symptoms.

The presence of right upper quadrant tenderness, associated with localized peritonitis is present in more than 95% of patients.

Murphy sign is pathopneumonic of acute cause status with a sensitivity of 62% and the specificity of 96% for acute cholecystitis.

Patients typically have leukocytosis with lift shift and immature bands.

With severe acute cholecystitis mild jaundice may be present and it is caused by inflammation around the biliary tract by direct pressure on the biliary tract from a distended gallbladder, which obstructs the biliary tree.

A serum lipase level to rule out acute pancreatitis and chest x-rays and electrocardiography studies help define the diagnosis.

The sensitivity of the above criteria is estimated between 83 and 85% with a specific estimation between 37 and 50% for acute cholecystitis.

Acute, complicating cholecystitis is defined as the presence of your gallbladder necrosis, perforation, pericholecystic abscess, or cholecystoenteric fistula: should be treated initially with antibiotics,  and immediate surgical management with subtotal cholecystectomy.

Operative management of patients with advanced cirrhosis is safer than nonoperative management.

Acute complicated cholecystitis with gallbladder necrosis, perforation, pericholecystic abscess, or cholecystoenteric fistula have higher risk for andverse outcomes after cholecystectomy.

Non-operative management for patients with such complications is inappropriate.

While acute cholecystitis is primarily an inflammatory process, secondary bacterial infection of the gallbladder occurs due to cystic duct obstruction and bile stasis in approximately 20% of patients:combination of anabiotic’s are administered prior to surgery to protect against sepsis and wound infection:postoperative antibiotics are considered only for patients with signs of residual infection or sepsis.

In patients with acute cholecystitis and high perioperative risk, a percutaneous cholecystostomy tube can be an alternative to cholecystectomy.

A percutaneous cholecystostomy tube, decompresses the gallbladder, drains infection, and can improve cholecystitis, allowing greater time to stabilize a patient prior to cholecystectomy.

Controlled studies of acute cholecystitis in high-risk patients showed percutaneous cholecystostomy tube placement had a greater degree of complications, need for reintervention, and recurrent biliary disease than patients underwent laparoscopic cholecystectomy.

A percutaneous cholecystostomy tube may be more beneficial in the setting of acute acalculus cholecystitis in high risk patients with better results, than with laparoscopic or open cholecystectomy.



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