Kolesistitis Akut

01Pathophysiology

Acute cholecystitis begins, in the vast majority of cases, with a gallstone becoming impacted in the cystic duct. This obstruction prevents the gallbladder from draining bile. The retained bile concentrates and causes chemical irritation of the gallbladder mucosa. Intraluminal pressure rises, compressing the mucosal blood supply, which leads to ischemia and inflammation of the gallbladder wall. Secondary bacterial infection occurs in roughly 50% of cases, most commonly with enteric organisms such as Escherichia coli, Klebsiella, and Enterococcus.

This mechanism directly explains the clinical picture. The sustained cystic duct obstruction is why the pain persists beyond 6 hours, a critical distinction from biliary colic, where the stone transiently impacts but then dislodges, causing pain that typically resolves within 4 to 6 hours. The inflammatory response in the gallbladder wall explains the fever, leukocytosis, and localized peritoneal signs (Murphy sign). As the inflamed gallbladder comes into contact with the parietal peritoneum, patients experience well-localized RUQ pain rather than the vague, visceral discomfort seen in uncomplicated biliary colic.

Acalculous cholecystitis follows a different pathway. In critically ill patients, gallbladder stasis from prolonged fasting, opioid use, and diminished enteric stimulation leads to bile concentration and inspissation. Combined with microvascular ischemia from hypotension, sepsis, or vasopressor use, the gallbladder wall undergoes inflammation and necrosis without a stone ever being present. This form carries a higher morbidity and mortality because the patients are already debilitated and because the diagnosis is often delayed due to the absence of classic risk factors.

Complications arise when the process is left unchecked. Gangrenous cholecystitis develops when transmural ischemia causes necrosis of the wall, increasing the risk of perforation. Emphysematous cholecystitis occurs when gas-forming organisms (especially Clostridium species) infect the gallbladder wall, a variant more common in diabetic men and associated with high mortality. Gallbladder perforation can result in a localized abscess, a cholecystoenteric fistula, or, if a large gallstone erodes into the small bowel, gallstone ileus (mechanical bowel obstruction, classically at the ileocecal valve, with pneumobilia on imaging).

02Classification and Clinical Manifestation

03Diagnostic Workup

The first test you should order in any patient with RUQ pain, fever, and a positive Murphy sign is a right upper quadrant ultrasound. This is the best initial test because it is noninvasive, widely available, highly sensitive for detecting gallstones (over 95%), and can be performed at the bedside. The hallmark findings on ultrasound are gallstones combined with secondary signs of inflammation: gallbladder wall thickening greater than 3 mm, pericholecystic fluid, and a positive sonographic Murphy sign (maximal tenderness when the ultrasound probe is pressed directly over the gallbladder). The sonographic Murphy sign is more reliable than the bedside Murphy sign because it confirms that the point of maximal tenderness anatomically overlies the gallbladder.

If the ultrasound is equivocal or if clinical suspicion remains high despite a negative ultrasound, the next step is a HIDA scan (hepatobiliary iminodiacetic acid scan, also called cholescintigraphy). This is the most accurate test for acute cholecystitis. The principle is straightforward: a radiolabeled tracer is injected intravenously, taken up by hepatocytes, and excreted into the biliary system. In a normal study, the tracer fills the gallbladder within 30 to 60 minutes. In acute cholecystitis, the cystic duct is obstructed, so the gallbladder fails to visualize (non-filling). If the gallbladder does not fill after 60 minutes, morphine can be administered to contract the sphincter of Oddi, forcing tracer toward the cystic duct. Persistent non-visualization after morphine augmentation is considered a positive study, confirming the diagnosis. The HIDA scan has a sensitivity and specificity approaching 95 to 97%.

Laboratory studies play a supporting role. A CBC will typically show leukocytosis. The hepatic panel helps differentiate cholecystitis from other biliary pathology: in uncomplicated cholecystitis, liver enzymes may be mildly elevated, but a significantly elevated direct bilirubin (greater than 4 mg/dL) with a dilated common bile duct on ultrasound should prompt concern for choledocholithiasis or cholangitis rather than isolated cholecystitis. Ordering a lipase is important to rule out concurrent gallstone pancreatitis, which would change your management approach.

A CT scan is not the first-line test for acute cholecystitis but becomes important when you suspect complications such as gangrenous cholecystitis, perforation, abscess, emphysematous cholecystitis (gas in the gallbladder wall), or gallstone ileus. CT is also useful in obese patients or when the ultrasound is technically limited.

04Management and Treatment

The initial management of acute cholecystitis follows a stepwise approach. Upon diagnosis, the patient should be made NPO (nothing by mouth) to reduce gallbladder stimulation, started on IV fluid resuscitation, and given analgesia. For pain, NSAIDs (such as ketorolac 30 mg IV or diclofenac 75 mg IM) are preferred because they reduce inflammation and do not affect smooth muscle tone in the biliary tract. Opioids can be used for severe pain, though there is a frequently tested teaching point that morphine may cause sphincter of Oddi contraction, theoretically worsening biliary obstruction. While the clinical relevance of this effect is debated, exam questions often test whether you know to consider it.

Empiric IV antibiotics should be initiated promptly to cover the common enteric pathogens. A reasonable regimen is piperacillin-tazobactam (3.375 g IV every 6 hours) as monotherapy, or a combination of ceftriaxone (2 g IV once daily) plus metronidazole (500 mg IV every 8 hours). The choice depends on local resistance patterns and patient factors. Antibiotics are continued perioperatively and can typically be discontinued 24 hours after cholecystectomy if the case is uncomplicated.

The definitive treatment is early laparoscopic cholecystectomy, ideally performed within 72 hours of symptom onset. Multiple randomized trials and meta-analyses have shown that early surgery (within 72 hours) is superior to delayed surgery (performed 6 to 8 weeks later after initial conservative management) in terms of shorter hospital stays, fewer complications, and lower overall costs. The key teaching point for exams: do not delay surgery hoping for the inflammation to "cool down." Early cholecystectomy is the standard of care.

For patients who are not candidates for surgery due to prohibitive operative risk (severe sepsis, hemodynamic instability, advanced comorbidities), a percutaneous cholecystostomy tube is placed under imaging guidance to decompress the gallbladder. This serves as a bridge, and interval cholecystectomy can be considered once the patient has stabilized.

In the setting of gangrenous or emphysematous cholecystitis, the urgency of surgery increases. These patients require emergent rather than early cholecystectomy, along with broad-spectrum antibiotics covering anaerobes and, in the emphysematous variant, Clostridium species.

A frequently tested clinical scenario involves a patient found to have choledocholithiasis (common bile duct stone) in addition to cholecystitis. The management sequence here is important: perform ERCP (endoscopic retrograde cholangiopancreatography) to clear the CBD stone first, followed by laparoscopic cholecystectomy. Alternatively, intraoperative cholangiography with laparoscopic CBD exploration can be performed. The principle is that you must address both the gallbladder disease and the CBD stone.

05Differential Diagnosis and Distractors

06Traps and High-Yield Pearls

The most common way students miss questions about acute cholecystitis is by confusing it with biliary colic. Both involve RUQ pain after fatty meals in similar patient populations, and both show gallstones on ultrasound. The discriminating factor is duration and systemic signs: biliary colic resolves within 4 to 6 hours and produces no fever, no leukocytosis, and no peritoneal signs. The moment a vignette describes pain lasting longer than 6 hours with fever and a positive Murphy sign, the answer shifts from biliary colic to acute cholecystitis, and the management shifts from elective cholecystectomy to early (within 72 hours) cholecystectomy with IV antibiotics.

Another common trap involves the HIDA scan. Students sometimes order a HIDA scan as the first test. Remember: ultrasound is always the best initial test for RUQ pain. The HIDA scan is reserved for when ultrasound is inconclusive but clinical suspicion remains high.

A third testing point is the "next best step" when cholecystitis is accompanied by a dilated CBD or significantly elevated bilirubin. Students may jump straight to cholecystectomy, but the correct sequence is to obtain MRCP (or endoscopic ultrasound) to confirm choledocholithiasis, then ERCP to clear the stone, and only then proceed with cholecystectomy. Failing to address the CBD stone before surgery is a common error.

Finally, watch for the acalculous cholecystitis vignette: a critically ill ICU patient on TPN with new-onset fever, RUQ tenderness, and leukocytosis, but no gallstones on ultrasound. The absence of stones does not rule out cholecystitis. A HIDA scan showing non-visualization of the gallbladder confirms the diagnosis, and the treatment in these patients is typically percutaneous cholecystostomy rather than surgery, given their overall condition.

The core competency being tested is your ability to recognize the clinical pattern (RUQ pain plus systemic inflammation), sequence the diagnostic workup correctly (ultrasound first, HIDA if needed), and select the appropriate definitive management (early cholecystectomy versus percutaneous drainage based on surgical candidacy).