Etiology
Acute calculous cholecystitis is initially triggered by inflammation caused by direct damage to the gallbladder mucosa at pressure points from gallstones. Bacterial infection typically occurs in the presence of bile stasis. The primary causes include the following:
Cystic Duct Obstruction
Gallstones may obstruct the cystic duct or become impacted at the gallbladder neck. Impacted stones cause direct mucosal damage, leading to impaired bile drainage and bile retention and concentration. High concentrations of bile salts exhibit cytotoxicity, causing cellular damage and exacerbating mucosal inflammation, which may result in edema or even necrosis.
Bacterial Infection
Pathogenic bacteria often enter the gallbladder retrogradely from the bile ducts or via the bloodstream or lymphatic pathways, leading to infection under conditions of impaired bile drainage. Gram-negative bacilli are the most common pathogens, with Escherichia coli being the most frequently encountered, often in conjunction with anaerobic bacteria.
Pathology
Cystic duct obstruction leads to mucosal hyperemia and edema, an increase in exudate within the gallbladder, and gallbladder distention. If obstruction is relieved at this stage, inflammation resolves, and most tissues return to normal without scarring, representing uncomplicated acute cholecystitis. Progression of the condition involving all layers of the gallbladder wall may result in capillary dilation, gallbladder wall thickening, and serosal inflammation accompanied by fibrinous or purulent exudation, indicative of suppurative cholecystitis. In such cases, recovery results in fibrosis and scarring, predisposing to recurrent cholecystitis. Repeated episodes of cholecystitis signify a chronic inflammatory process, leading to complete scarring and atrophy of the gallbladder.
If cystic duct obstruction is not resolved, intragallbladder pressure increases, compressing the gallbladder wall vasculature and causing ischemia and necrosis, resulting in gangrenous cholecystitis. Gallbladder perforation is a common complication of gangrenous cholecystitis, typically occurring in the fundus or neck; widespread gangrene in the gallbladder results in loss of gallbladder function. Acute inflammation may also involve adjacent organs, with perforation creating fistulas to the duodenum, colon, or other structures. These biliary-enteric fistulas may decompress the gallbladder and result in rapid resolution of acute inflammation.
Clinical Manifestations
Incidence is higher among women, with a female-to-male ratio of 3:1 before the age of 50 and 1.5:1 after 50. Acute onset typically presents with upper abdominal pain. Initial symptoms involve vague upper abdominal discomfort and distension, gradually progressing to colicky pain. Nighttime episodes are common, often precipitated by a heavy meal or consumption of fatty foods. Pain may radiate to the right shoulder, scapula, or back and is often accompanied by gastrointestinal symptoms such as nausea, vomiting, anorexia, and constipation.
As the condition progresses, pain may persist with intermittent exacerbations. Mild to moderate fever is common, though chills are usually absent. Severe cases with chills and high fever suggest complications such as gallbladder gangrene, perforation, or empyema, or the presence of concomitant acute cholangitis. Mild jaundice occurs in 10%–20% of cases and may result from bile pigments entering the bloodstream due to mucosal damage or from spasm of the sphincter of Oddi triggered by adjacent inflammation. Approximately 10%–15% of patients may develop jaundice secondary to coexisting common bile duct stones.
On physical examination, tenderness in the right upper quadrant over the gallbladder area is typical, with varying degrees of severity. Signs such as guarding and rebound tenderness may arise if the inflammation extends to the gallbladder serosa. In some patients, an enlarged and tender gallbladder may be palpable, often associated with a positive Murphy’s sign. Encapsulation of the gallbladder by the omentum may result in a poorly defined, fixed, tender mass. In cases of gangrene or perforation, diffuse peritonitis may develop.
Auxiliary Examinations
Hematological changes often include leukocytosis, though elderly patients may not exhibit leukocyte elevation. Serum alanine aminotransferase (ALT) and alkaline phosphatase levels are often elevated. About half of the cases may show elevated serum bilirubin levels, and one-third may demonstrate elevated serum amylase.
Ultrasound is highly accurate for diagnosing acute cholecystitis, with an accuracy rate of 85%–95%. Common findings include an enlarged gallbladder, thickened gallbladder wall (>4 mm), and a "double wall sign" indicative of pronounced edema. Gallstones are typically visible as hyperechoic structures with accompanying acoustic shadows. Further evaluation with CT or MRI may be performed when necessary.
Diagnosis and Differential Diagnosis
Diagnosis is usually straightforward when characteristic clinical presentations are combined with laboratory and imaging findings. Differential diagnoses include perforated peptic ulcer, acute pancreatitis, high retrocecal appendicitis, liver abscess, gallbladder carcinoma, carcinoma of the hepatic flexure of the colon, perforated small bowel diverticulum, as well as right-sided pneumonia, pleurisy, and hepatitis.
Treatment
Acute calculous cholecystitis typically requires surgical intervention, with the general principle favoring elective surgery when feasible.
Non-Surgical Treatment
Non-surgical approaches can also serve as preoperative management strategies. Measures include fasting, intravenous infusion therapy, nutritional support, supplementation of vitamins, and correction of fluid-electrolyte imbalances and acid-base disturbances. Antibiotics effective against Gram-negative bacteria and anaerobic organisms are commonly used, along with antispasmodic, analgesic, anti-inflammatory, and choleretic medications. Among elderly patients, monitoring of blood glucose and the function of critical organs such as the heart, lungs, and kidneys is essential, along with treatment of comorbid conditions. Close monitoring of disease progression is necessary to allow timely adjustments of the treatment plan; surgical intervention is warranted if the condition worsens. For most patients, non-surgical treatment can control disease progression, allowing elective surgery to be performed later.
Surgical Treatment
Surgical intervention during the acute phase should aim to prioritize safety, simplicity, and effectiveness. For elderly or frail patients or those with multiple comorbidities involving vital organs, the selection of surgical methods requires careful consideration.
Indications
Indications for emergency surgery include:
- Onset of disease within 48 to 72 hours.
- Ineffectiveness of non-surgical treatment or clinical deterioration.
- The presence of complications such as gallbladder perforation, diffuse peritonitis, acute suppurative cholangitis, or acute necrotizing pancreatitis.
Surgical Methods
Cholecystectomy
Laparoscopic cholecystectomy is the first-line choice. Conventional open or mini-incision cholecystectomy may also be considered, depending on local medical resources and the patient's clinical condition.
Partial Cholecystectomy
In cases where dissection of the gallbladder bed is challenging or poses a risk of bleeding, part of the gallbladder wall on the gallbladder bed may be preserved. The remaining gallbladder wall mucosa can be destroyed using physical or chemical methods, while the remainder of the gallbladder is removed.
Cholecystostomy
For high-risk patients or those with significant adhesions and unclear anatomical structures, a cholecystostomy can be performed to alleviate pressure and drain the gallbladder. Definitive cholecystectomy can be considered after three months.
Percutaneous Transhepatic Gallbladder Drainage (PTGD)
Ultrasound-guided PTGD can reduce intragallbladder pressure and serve as an interim measure before elective surgery. This method is suitable for critically ill patients with suppurative cholecystitis who are not candidates for immediate surgical intervention.