Acute Abdominal Emergencies — Part 2: Acute Cholecystitis, Cholangitis & Acute Pancreatitis

3. Acute Cholecystitis

3.1 Epidemiology and Pathophysiology

Acute cholecystitis accounts for 3% to 10% of all patients presenting with abdominal pain. Approximately 90% to 95% of cases are calculous (gallstone-related), resulting from cystic duct obstruction by a gallstone leading to gallbladder distension, wall inflammation, and secondary bacterial infection. Acalculous cholecystitis (5–10% of cases) occurs predominantly in critically ill patients, the elderly, immunocompromised individuals, and patients on prolonged TPN, and carries a significantly higher morbidity and mortality due to delayed diagnosis and a higher rate of gangrene and perforation.^{1 2}

3.2 Diagnosis — Tokyo Guidelines Diagnostic Criteria (TG18/TG13)

The international hepatobiliary consensus panel established standardized diagnostic criteria that combine local signs of inflammation, systemic signs of inflammation, and imaging findings.¹

Diagnostic Criteria:

Definite diagnosis: One item in A + one item in B + C

Suspected diagnosis: One item in A + one item in B (without imaging confirmation)

3.3 Imaging

Right Upper Quadrant Ultrasound (First-Line)

RUQ ultrasound is the first-line imaging modality for suspected acute cholecystitis.^{1 3}

Ultrasound performance for acute cholecystitis:

HIDA Scan (Hepatobiliary Iminodiacetic Acid Scintigraphy)

HIDA scan is the most accurate imaging study for acute cholecystitis when ultrasound is equivocal.³

Indication: Equivocal ultrasound findings with intermediate clinical suspicion. NOT recommended in critically ill patients or when urgent cholecystectomy is otherwise indicated.

CT Abdomen/Pelvis

CT is less sensitive than ultrasound for uncomplicated cholecystitis but may identify complications (gangrenous cholecystitis, emphysematous cholecystitis, perforation, abscess) and is useful when the diagnosis is unclear or an alternative diagnosis is suspected.³

3.4 Severity Grading — Tokyo Guidelines (TG18)

The international consensus severity classification guides management decisions including timing of cholecystectomy, need for percutaneous drainage, and intensity of support.¹

3.5 Medical Management — Antibiotics

Empiric Antibiotic Regimens for Acute Cholecystitis

Target organisms: E. coli, Klebsiella, Enterococcus, Enterobacter, anaerobes (Bacteroides, Clostridium)

3.6 Surgical Management

Early Laparoscopic Cholecystectomy

Multiple randomized controlled trials and meta-analyses demonstrate that early laparoscopic cholecystectomy (within 72 hours of symptom onset, ideally during the index admission) is superior to delayed cholecystectomy in terms of:^{1 2 4}

• Shorter total hospital stay
• Lower overall complication rate
• No increase in bile duct injury rate
• Lower healthcare costs
• Prevention of recurrent biliary events during the waiting period (up to 20% of patients develop recurrent symptoms while awaiting delayed cholecystectomy)

Critical view of safety (CVS) must be achieved before clipping or dividing any structure — both the cystic duct and cystic artery must be clearly identified with the hepatocystic triangle dissected.

Subtotal (Partial) Cholecystectomy

When the critical view of safety cannot be achieved due to severe inflammation, dense adhesions, or unclear anatomy (particularly in Strasberg Grade II–III inflammation), subtotal cholecystectomy is a safe bailout strategy that reduces the risk of bile duct injury.⁴

Percutaneous Cholecystostomy

Indicated for Grade III (severe) cholecystitis in patients who are too unstable for general anesthesia or have prohibitive surgical risk:¹

• CT or ultrasound-guided percutaneous transhepatic gallbladder drainage
• Clinical improvement expected within 24–72 hours
• Interval cholecystectomy can be considered after recovery (typically 6–8 weeks) in patients who become surgical candidates
• In patients who remain poor surgical candidates, the tube may be removed after a cholangiogram confirms cystic duct patency (typically 2–3 weeks)

4. Choledocholithiasis and Acute Cholangitis

4.1 Choledocholithiasis

Common bile duct (CBD) stones are present in approximately 10% to 15% of patients with symptomatic gallstone disease. Predictors of choledocholithiasis include:^{1 5}

Risk Stratification for Choledocholithiasis:

4.2 Acute Cholangitis — Tokyo Guidelines Diagnostic Criteria (TG18)

Acute cholangitis results from biliary obstruction (most commonly choledocholithiasis) with subsequent bacterial infection of the biliary system. It is a potentially life-threatening condition requiring urgent biliary decompression.⁵

Diagnostic Criteria (Charcot Triad and Reynolds Pentad):

TG18 Diagnostic Criteria:

Suspected diagnosis: A + either B or C

Definite diagnosis: A + B + C

Severity Grading:

4.3 Biliary Drainage — ERCP

Endoscopic retrograde cholangiopancreatography (ERCP) with sphincterotomy and stone extraction is the standard intervention for choledocholithiasis and cholangitis.⁵

• Grade I cholangitis: ERCP within 24–48 hours
• Grade II cholangitis: Urgent ERCP within 24 hours
• Grade III cholangitis: Emergent ERCP (or PTBD if ERCP is not feasible) — biliary decompression is the life-saving intervention; do not delay for hemodynamic optimization alone
• If complete stone clearance is not achieved, a biliary stent should be placed for ongoing drainage

5. Acute Pancreatitis

5.1 Diagnosis

Acute pancreatitis requires at least two of three diagnostic criteria:^{6 7}

1. Abdominal pain consistent with acute pancreatitis (acute onset, severe, persistent epigastric pain often radiating to the back)
2. Serum lipase (or amylase) elevated to ≥3 times the upper limit of normal
3. Characteristic findings on cross-sectional imaging (contrast-enhanced CT, MRI, or transabdominal US)

Important: Imaging is NOT required for diagnosis if criteria 1 and 2 are met. CT should NOT be performed at presentation solely for diagnosis — it is most useful for assessing complications and should be reserved for patients with diagnostic uncertainty, failure to improve within 48–72 hours, or suspected complications.^{7 8}

5.2 Etiology

5.3 Severity Classification — Revised Atlanta Classification (2012)

The revised Atlanta classification, established by international consensus, is the standard system for classifying the severity of acute pancreatitis.⁶

Organ failure is defined using the Modified Marshall Scoring System:

A score of ≥2 in any organ system = organ failure.

5.4 Prognostic Scoring Systems

BISAP Score (Bedside Index for Severity in Acute Pancreatitis)

The BISAP score is calculated within the first 24 hours of admission and is valued for its simplicity and early applicability.⁹

Interpretation:

A BISAP score ≥3 identifies patients at increased risk for organ failure and pancreatic necrosis who warrant ICU-level monitoring.

Ranson Criteria

Ranson criteria remain one of the most widely recognized prognostic systems, though their utility is limited by the requirement for 48-hour reassessment. Separate criteria exist for gallstone vs non-gallstone pancreatitis.¹⁰

Non-Gallstone (Alcoholic) Pancreatitis:

Gallstone Pancreatitis:

Interpretation (Both Types):

CT Severity Index (CTSI) / Balthazar Score

The CTSI is calculated from contrast-enhanced CT and combines morphologic grade with the degree of pancreatic necrosis. CT should generally be performed 72–96 hours after onset (not at initial presentation) to accurately assess necrosis.¹¹

Balthazar CT Grade:

Necrosis Score:

CTSI = Balthazar Grade Points + Necrosis Score (Total: 0–10)

5.5 Management of Acute Pancreatitis

Fluid Resuscitation

Aggressive early fluid resuscitation is a cornerstone of acute pancreatitis management, addressing the significant third-space fluid losses and hypovolemia that characterize the early phase of disease.^{7 8 12}

Key Recommendations:

• Fluid type: Lactated Ringer (LR) solution is preferred over normal saline (NS). LR has demonstrated reduced systemic inflammation (lower CRP, lower SIRS incidence) in randomized trials compared to NS. The anti-inflammatory effect may be related to the buffering capacity of lactate and avoidance of hyperchloremic acidosis
• Rate: Goal-directed fluid resuscitation at 1.5 mL/kg/hour (approximately 200–250 mL/hour for a 70 kg patient) for the first 24 hours, with frequent reassessment
• Initial bolus: 20 mL/kg bolus (approximately 1–1.5 L) over 30–60 minutes for patients with evidence of hypovolemia
• Reassessment: Heart rate, mean arterial pressure, urine output (goal >0.5 mL/kg/hour), BUN trending, hematocrit. Adjust fluid rate based on clinical response
• Caution: Avoid over-resuscitation — excessive fluid administration has been associated with increased rates of abdominal compartment syndrome, respiratory failure, and longer ICU stays. The WATERFALL trial (2022) demonstrated that aggressive fluids (20 mL/kg bolus + 3 mL/kg/hr) did not improve outcomes compared to moderate fluids (1.5 mL/kg/hr with bolus only if hypovolemic) and was associated with higher rates of fluid overload¹²
• Duration: Most patients require aggressive hydration for 24–48 hours; taper as clinical improvement occurs

Pain Control

• First-line: IV opioids (morphine, hydromorphone, fentanyl). The historical concern that morphine causes sphincter of Oddi spasm and worsens pancreatitis is NOT supported by clinical evidence
• Adjuncts: IV acetaminophen (1g q6h), NSAIDs (ketorolac 15–30mg IV q6h — avoid in renal insufficiency)
• PCA (patient-controlled analgesia): Consider for severe pain requiring frequent dosing
• Epidural analgesia: May be beneficial in severe pancreatitis refractory to IV opioids; improves splanchnic perfusion

Nutrition

The approach to nutrition in acute pancreatitis has shifted dramatically from prolonged bowel rest to early oral/enteral feeding.^{7 8}

Key Recommendations:

• Mild pancreatitis: Initiate oral feeding as soon as tolerated — do not wait for complete normalization of lipase or resolution of pain. Start with a low-fat solid diet (not clear liquids — early solid feeding has been shown to be safe and may reduce hospital stay)
• Moderately severe/severe pancreatitis: If oral feeding is not tolerated within 72 hours, initiate enteral nutrition via nasogastric (NG) or nasojejunal (NJ) tube. NG feeding has been shown to be equivalent to NJ feeding in randomized trials and is easier to place
• TPN (total parenteral nutrition): Reserved for patients who do not tolerate enteral nutrition after a reasonable trial (5–7 days). TPN is associated with increased infectious complications and should be avoided when enteral feeding is feasible
• Rationale: Enteral nutrition maintains gut mucosal integrity, reduces bacterial translocation, lowers infectious complications, and may reduce mortality in severe pancreatitis

Antibiotics

• Prophylactic antibiotics are NOT recommended in acute pancreatitis, even in predicted severe disease or sterile necrosis. Multiple randomized controlled trials and meta-analyses have failed to demonstrate benefit, and prophylactic antibiotics increase the risk of fungal superinfection^{7 8}
• Antibiotics ARE indicated for:
  • Documented infected necrosis (gas in necrotic collection on CT, positive culture from FNA or drainage)
  • Concurrent cholangitis
  • Other documented infections (UTI, pneumonia, bacteremia)
  • Clinical sepsis with a high suspicion for infected necrosis (persistent fever, rising WBC, clinical deterioration after initial improvement)

Empiric regimen for infected necrosis: Meropenem 1g IV q8h or imipenem-cilastatin 500mg IV q6h (carbapenems have the best penetration into pancreatic and peripancreatic tissue). Alternatives: piperacillin-tazobactam 4.5g IV q6h or ciprofloxacin 400mg IV q12h + metronidazole 500mg IV q8h.

5.6 Necrotizing Pancreatitis

Pancreatic necrosis develops in approximately 5% to 10% of patients with acute pancreatitis and is a major determinant of morbidity and mortality.^{6 13}

Local Complications — Revised Atlanta Classification

Infected Necrosis — Step-Up Approach

The management of infected pancreatic necrosis has been revolutionized by the “step-up” approach, which was validated by the landmark PANTER trial and subsequently confirmed by multiple studies. This approach is superior to primary open necrosectomy.^{13 14}

Step-Up Protocol:

Timing: Intervention for necrotizing pancreatitis should be delayed as long as possible (ideally ≥4 weeks from onset) to allow demarcation and walling-off of necrosis, unless the patient is clinically deteriorating. Earlier intervention is associated with higher morbidity and mortality due to poorly demarcated tissue planes.

Indications for intervention in necrotizing pancreatitis:

1. Documented or strongly suspected infected necrosis with clinical deterioration
2. Ongoing organ failure for weeks without clinical improvement
3. Disconnected duct syndrome with ongoing symptoms
4. Symptomatic organized necrosis (WON) causing gastric outlet obstruction, biliary obstruction, or persistent pain

5.7 Biliary Pancreatitis — Specific Considerations

References