Acute cholecystitis is a sudden inflammation of the gallbladder that requires prompt medical attention. This condition typically develops when a gallstone blocks the pathway through which bile flows, causing pain, swelling, and potentially serious complications if left untreated.

Understanding Acute Cholecystitis

Acute cholecystitis represents inflammation of the gallbladder, a small pear-shaped organ located beneath the liver on the right side of the abdomen. The gallbladder’s primary function is to store bile, a digestive fluid produced by the liver that helps break down fats during digestion. When the gallbladder becomes inflamed and swollen, it can no longer function properly, leading to a range of uncomfortable and potentially dangerous symptoms.^[1]

The condition develops rapidly, typically over a matter of hours rather than days or weeks. What makes acute cholecystitis particularly concerning is that without appropriate treatment, the inflammation can worsen and lead to serious complications. The swollen gallbladder may become infected by bacteria, or in severe cases, the tissue can die or the gallbladder can rupture, creating a life-threatening emergency.^[2]

Epidemiology

Gallstones affect more than one in ten adults in the United Kingdom, making them extremely common throughout the population. However, most people with gallstones never experience any symptoms or problems. Only about twenty percent of individuals with gallstones will develop complications such as acute cholecystitis.^[3]

Worldwide, approximately fifteen percent of the population has gallstones. Among those who develop gallstones, gallstones are responsible for ninety-five percent of all cases of cholecystitis. This makes acute cholecystitis one of the most frequent complications arising from gallstone disease.^[6]

The condition affects both men and women, though women tend to have a higher susceptibility to developing gallstones and subsequently cholecystitis. The risk increases with age, and certain demographic groups, including Native American and Hispanic populations, face higher rates of gallstone formation.^[4]

Causes

The overwhelming majority of acute cholecystitis cases—approximately ninety to ninety-five percent—result from gallstones blocking the cystic duct, which is the main opening of the gallbladder. This type is known as calculous cholecystitis. Gallstones are small, hardened pieces of material, usually made of cholesterol, that form inside the gallbladder. While they often remain harmless at the bottom of the gallbladder, they can travel and become lodged in narrow passages.^[3]

When a gallstone blocks the cystic duct, it prevents bile from flowing normally out of the gallbladder. This obstruction causes bile to accumulate inside the organ, increasing pressure and triggering an inflammatory response. The trapped bile and rising pressure damage the gallbladder’s inner lining, which begins secreting even more fluid. This creates a vicious cycle where the gallbladder becomes increasingly distended and inflamed.^[7]

In some cases, a thick mixture called biliary sludge can cause the same blockage. Biliary sludge consists of bile mixed with tiny cholesterol and salt crystals. Like a gallstone, it can obstruct the cystic duct and initiate inflammation.^[3]

A less common form called acalculous cholecystitis occurs without any gallstones present. This type accounts for five to ten percent of cases and is typically more serious. Acalculous cholecystitis usually develops as a complication of severe illness, critical injury, or major surgery. The exact mechanism isn’t fully understood, but it likely involves inflammatory mediators released due to reduced blood flow to the gallbladder, infection, or bile remaining stagnant for prolonged periods.^[7]

Risk Factors

Several factors increase the likelihood of developing gallstones, which in turn raises the risk of acute cholecystitis. Being female is a significant risk factor, as women develop gallstones more frequently than men. Pregnancy and hormone therapy also increase risk, likely due to hormonal changes that affect bile composition and gallbladder emptying.^[4]

Age plays an important role, with older adults facing higher risk. Certain ethnic backgrounds, particularly Native American and Hispanic heritage, are associated with increased gallstone formation. Body weight matters considerably—obesity significantly raises risk, but so does rapid weight loss or rapid weight gain. Both extremes can alter the balance of substances in bile, promoting stone formation.^[4]

People with diabetes face elevated risk for both gallstones and acalculous cholecystitis. Physical inactivity and diets low in fiber may contribute to gallstone development. Specific medications, including certain antibiotics like ceftriaxone and immunosuppressive drugs like ciclosporin, have been linked to increased risk.^[5]

Symptoms

The hallmark symptom of acute cholecystitis is sudden, sharp pain in the upper right portion of the abdomen. This pain typically develops quickly, building to a peak within minutes to an hour. Unlike brief episodes of digestive discomfort, the pain of acute cholecystitis is persistent and does not subside after a few hours. The pain often radiates toward the right shoulder blade or into the back.^[3]

The affected area of the abdomen becomes very tender to touch. Taking a deep breath can intensify the pain significantly. This occurs because during deep breathing, the gallbladder moves downward and presses against inflamed surrounding tissues. Healthcare providers test for this characteristic response, known as Murphy’s sign, by placing a hand below the rib cage and asking the patient to breathe in deeply. If acute cholecystitis is present, the pain becomes so severe during inhalation that the patient cannot complete the breath.^[3]

Nausea and vomiting commonly accompany the pain. Many people develop a fever, usually exceeding 38 degrees Celsius (100 degrees Fahrenheit), which may indicate that infection has developed alongside the inflammation. Loss of appetite is typical. Some people experience sweating and a general sense of being unwell.^[2]

In approximately ten percent of cases, jaundice—a yellowing of the skin and the whites of the eyes—may develop. This suggests that bile flow is being obstructed beyond the gallbladder, possibly in the common bile duct. Clay-colored stools can occur when bile isn’t reaching the intestines properly.^[4]

Older adults may experience milder or different symptoms. Rather than intense pain, they might only feel vague discomfort, loss of appetite, or general malaise and weakness. Fever may not develop in elderly patients even when infection is present, making diagnosis more challenging in this age group.^[7]

Prevention

Since most cases of acute cholecystitis stem from gallstones, preventing gallstone formation represents the primary approach to reducing risk. Maintaining a healthy body weight through balanced eating and regular physical activity helps prevent gallstones. However, if weight loss is necessary, it should be gradual rather than rapid, as sudden weight reduction can actually trigger gallstone formation.^[4]

A diet rich in fiber and healthy fats, while moderate in cholesterol, may help reduce gallstone risk. Staying physically active rather than leading a sedentary lifestyle appears protective. For people already known to have gallstones who experience symptoms, surgical removal of the gallbladder prevents future attacks and complications, including acute cholecystitis.^[4]

In hospitalized patients receiving nutrition through intravenous feeding for extended periods, stimulation of gallbladder contraction using certain medications has shown promise in preventing sludge buildup and acalculous cholecystitis, though this approach requires medical supervision.^[10]

Pathophysiology

The disease process of acute cholecystitis begins with obstruction of the cystic duct. When bile cannot exit the gallbladder normally, it accumulates and creates increased pressure within the organ. This rising pressure damages the gallbladder’s inner lining, the mucosa.^[7]

The stagnant bile triggers release of inflammatory enzymes. One particularly important enzyme, phospholipase A, converts a substance called lecithin into lysolecithin, which promotes further inflammation. As the mucosa becomes damaged, it secretes more fluid into the gallbladder than it can absorb, causing additional distention.^[7]

The expanding gallbladder releases inflammatory mediators such as prostaglandins. These chemical signals worsen the damage to the gallbladder wall and can reduce blood flow to the tissue, causing ischemia—a dangerous lack of oxygen. All these processes create a self-perpetuating cycle: inflammation leads to more fluid secretion, which increases pressure, which causes more inflammation.^[7]

Bacteria can invade the inflamed gallbladder, adding infection to the existing inflammation. If the inflammation and pressure continue unchecked, the gallbladder tissue can die—a condition called gangrene. In the worst cases, the gallbladder wall can rupture, spilling infected bile into the abdominal cavity and causing peritonitis, a life-threatening infection.^[7]

If acute inflammation resolves but episodes keep recurring, the gallbladder becomes scarred and contracted, developing thick, fibrotic walls. It loses its ability to concentrate bile or empty properly. This represents chronic cholecystitis, a long-term condition that develops from repeated acute episodes.^[7]