Acute pancreatitis management

Initial Assessment - Spotting the Fire

• Clinical Picture: Sudden, severe epigastric pain radiating to the back, often relieved by leaning forward. Nausea/vomiting are common.
• Key Exam Signs: Epigastric tenderness, guarding. In severe cases, look for retroperitoneal hemorrhage signs: Cullen's (periumbilical) & Grey Turner's (flank) ecchymosis.
• Diagnostic Criteria (Need ≥2 of 3):
  • 1. Characteristic acute epigastric pain.
  • 2. Lipase (preferred) or amylase ≥ 3x ULN.
  • 3. Findings on imaging (CT/MRI/US).

⭐ Lipase is more specific and has a longer half-life than amylase, making it the superior diagnostic marker.

Severity Scoring - How Big's the Blaze?

• Ranson's Criteria: Assesses severity at admission & 48h. Score ≥3 → severe pancreatitis, increased mortality.

  • 📌 On Admission (GA LAW): Glucose >200, Age >55, LDH >350, AST >250, WBC >16,000.
  • 📌 At 48h (C HOBBS): Ca²⁺ <8.0, Hct drop >10%, pO₂ <60, BUN ↑ >5, Base deficit >4, Fluid Sequestration >6L.

• BISAP Score: Simpler bedside index within 24h. Score ≥3 correlates with significantly increased mortality.

  • BUN >25
  • Impaired mental status
  • SIRS criteria met
  • Age >60
  • Pleural effusion

⭐ A BUN >25 mg/dL on admission is one of the most reliable single predictors of severe acute pancreatitis.

Core Management - Putting Out the Fire

• Aggressive IV Hydration (Priority #1)

  • Goal: Prevent pancreatic necrosis & organ failure.
  • Fluid: Lactated Ringer's (LR) is preferred over Normal Saline.
  • Rate: Start with a bolus of 5-10 mL/kg, then maintain at 250-500 mL/hr.
  • Titrate to: Urine output >0.5-1 mL/kg/hr, ↓BUN, and ↓Hematocrit.

• Pain Control

  • IV opioids (e.g., Hydromorphone, Fentanyl) are the mainstay.

• Nutritional Support

  • Decision depends on severity. Early enteral feeding is key in severe cases.

⭐ The single most crucial intervention in early management is aggressive IV fluid resuscitation. It directly combats hypovolemia and reduces the risk of progression to necrotizing pancreatitis.

Complications - The Afterburn

• Local Complications: Progression of fluid collections is key.

  • Pancreatic Pseudocyst: Encapsulated fluid collection developing >4 weeks after acute pancreatitis. Lacks a true epithelial lining.
  • Pancreatic Abscess/Infected Necrosis: Necrotic tissue becomes infected, often with gas-forming organisms. High mortality.
  • Splenic vein thrombosis, pseudoaneurysm.

• Systemic Complications: Widespread inflammatory response.

  • ARDS, pleural effusion
  • Hypocalcemia (from fat saponification)
  • Acute kidney injury (AKI)
  • Disseminated intravascular coagulation (DIC)

⭐ Drain pancreatic pseudocysts only if they are symptomatic, >6 cm in diameter, or persist for >6 weeks.

High‑Yield Points - ⚡ Biggest Takeaways

• Aggressive IV fluid resuscitation is the cornerstone of management to prevent pancreatic necrosis.
• Diagnosis requires 2 of 3 criteria: characteristic pain, lipase >3x normal, or imaging findings.
• Gallstones and alcohol are the leading causes; always perform a RUQ ultrasound.
• Systemic Inflammatory Response Syndrome (SIRS) on admission is a key predictor of severity.
• Early enteral feeding is superior to TPN to maintain gut integrity.
• Prophylactic antibiotics are not recommended; use only for confirmed infected necrosis.