Acute Cholecystitis
Acute inflammation of the gallbladder, mostly due to gallstone obstruction of the cystic duct, causing severe right upper quadrant pain.
Emergency Management: Sepsis secondary to gallbladder perforation requires immediate aggressive fluid resuscitation, broad-spectrum IV antibiotics, and emergent surgical exploration/cholecystectomy.
Acute cholecystitis is an inflammatory condition of the gallbladder, typically resulting from obstruction of the cystic duct by gallstones. This obstruction leads to bile stasis, mucosal ischemia, and secondary bacterial infection. It represents a common surgical emergency in patients presenting with right upper quadrant abdominal pain.
Detailed Overview
Approximately 90% of cases are calculous, meaning they are caused by a gallstone impacting the gallbladder neck or cystic duct. The remaining 10% are acalculous, typically occurring in critically ill patients due to gallbladder stasis and ischemia. The continuous obstruction leads to an increase in intraluminal pressure, compromising venous return and potentially causing necrosis and perforation if left untreated. Early surgical intervention is standard to prevent complications such as gangrenous cholecystitis, gallbladder perforation, or cholecystoenteric fistulas.
Epidemiology & Demographics
Occurs in approximately 10-20% of patients with symptomatic gallstones. More common in women than men (ratio 2:1) up to age 50, after which the incidence becomes more equal. Peak incidence is in the 5th and 6th decades of life.
Etiological Mechanism
Primary cause is cholelithiasis (gallstones) obstructing the cystic duct (90%). Secondary causes (acalculous) include prolonged fasting, total parenteral nutrition, critical illness (trauma, burns, sepsis), and infections (e.g., Salmonella, CMV in immunocompromised).
Primary Causes
Cholelithiasis (Gallstones)
Biliary sludge
Gallbladder dysmotility/stasis
A gallstone becomes impacted in the cystic duct. Biliary stasis leads to concentrated bile, which is toxic to the gallbladder mucosa (chemical cystitis). Increased intraluminal pressure compromises venous and lymphatic drainage, leading to ischemia. Prostaglandin release exacerbates inflammation. Secondary bacterial colonization (typically E. coli, Klebsiella, Enterococcus) occurs in 50-75% of cases. Without treatment, full-thickness wall ischemia leads to gangrene or perforation.
Diagnostic Criteria & Guidelines
Tokyo Guidelines (2018): Suspected diagnosis requires one local sign of inflammation (Murphy's sign, RUQ pain) AND one systemic sign of inflammation (Fever, CRP > 3 mg/dL, WBC > 10,000/mcL). Definite diagnosis requires both plus imaging findings of acute cholecystitis.
1. NPO, IV fluids (Lactated Ringer's 100-150 mL/hr). 2. Analgesia: Ketorolac 30 mg IV or Morphine 2-4 mg IV. 3. Antibiotics: Piperacillin-tazobactam 3.375 g IV q6h OR Ceftriaxone 1g IV daily + Metronidazole 500mg IV q8h. 4. Early Laparoscopic Cholecystectomy (within 72 hours).
Second-Line & Adjunctive Therapy
Percutaneous cholecystostomy tube placement under ultrasound or CT guidance to decompress the gallbladder for very high-risk surgical candidates.
Surgical & Procedural Management
Laparoscopic cholecystectomy is the definitive treatment. Open cholecystectomy if severe inflammation obscures anatomy.
Patient Counseling & Advice
Explain that surgery cures the condition. Discuss the possibility of post-cholecystectomy syndrome (mild persistent symptoms or diarrhea in 5-10% of patients).
Follow-Up & Monitoring Schedule
Post-operative follow-up at 1-2 weeks for wound check and review of surgical pathology.
Preventive Strategies
Prophylactic cholecystectomy for asymptomatic gallstones is generally NOT recommended.
Excellent with timely surgical intervention. Mortality rate for uncomplicated laparoscopic cholecystectomy is < 0.5%.