Acute Pancreatitis

📊 Classification

🔍 Pathophysiology

• Acinar cell injury → inappropriate trypsinogen activation → autodigestion.
• Release of pro-inflammatory mediators → SIRS, ↑ vascular permeability, third spacing.
• In severe AP: multiorgan dysfunction, local necrosis, infection.

 Etiologies: “I GET SMASHED”

• Idiopathic
• Gallstones (40–70%)
• Ethanol (25–35%)
• Trauma
• Steroids
• Mumps/malignancy
• Autoimmune
• Scorpion sting
• Hyperlipidemia/hypercalcemia
• ERCP
• Drugs (thiazides, azathioprine, valproate)

🧪 Severity Scoring Systems

• BISAP (Bedside Index of Severity in Acute Pancreatitis): BUN >25, impaired mental status, SIRS, age >60, pleural effusion
• APACHE II
• CT Severity Index (Balthazar)

Persistent organ failure = best single predictor of mortality.

 Management Principles: Logic Behind Each Intervention

 1. Fluid Resuscitation

Why: Prevent/treat third-space losses, reduce hypoperfusion-related necrosis.

Mechanism:

• Pancreatic inflammation → SIRS → ↑ capillary leak → intravascular depletion
• Aggressive fluids = ↓ hypoperfusion = ↓ necrosis & mortality

Preferred Fluid:

• Ringer’s lactate > NS (less hyperchloremic acidosis, anti-inflammatory effect)

Dosing:

• Initial bolus: 20 mL/kg over 1 hour if hypotensive
• Maintenance: 3–5 mL/kg/hr (adjust per response: HR, MAP, UO, Hct, lactate)

Goal-directed monitoring:

• UO > 0.5 mL/kg/h
• Hct target: 35–44%
• Avoid fluid overload → ↑ risk of IAH/ARDS

2. Analgesia

Why: Severe visceral pain worsens stress response, respiratory mechanics.

Drugs:

• IV opioids preferred (e.g., fentanyl, hydromorphone)
  
  • Fentanyl
• Avoid morphine in biliary pancreatitis (sphincter of Oddi spasm concern — theoretical)

Logic: Opioids are effective, safe with renal/hepatic adjustment. Consider PCA or continuous infusion.

3. Antibiotics

When to Use:

• Only if infection is suspected/confirmed (e.g., infected necrosis, cholangitis, sepsis)
• Not for prophylaxis in necrotizing AP (RCTs show no mortality benefit)

Empiric Drugs for Infected Necrosis:

• Imipenem  (good pancreatic penetration)
• Meropenem, Pip-Tazo, or Cefepime + Metronidazole

Fungal coverage only if patient has prolonged antibiotics, central line, or TPN.

4. Nutrition

Why: Reduces gut barrier dysfunction, bacterial translocation.

Mechanism: Early enteral nutrition maintains gut mucosa, reduces systemic inflammation.

Approach:

• Start enteral feeds within 24–72 hrs, even in severe AP.
• NG =NJ unless severe ileus or high aspiration risk.
• If enteral fails: switch to TPN after 5–7 days.

Formulation: Polymeric or elemental feeds; low-fat in chylous ascites.

5. Management of Necrosis & Collections

Types:

• Acute peripancreatic fluid collection (APFC)
• Pseudocyst (matured >4 weeks, no necrosis)
• Acute necrotic collection (ANC)
• Walled-off necrosis (WON): encapsulated necrosis ≥4 weeks

Intervention:

• Only if infected or symptomatic (pain, obstruction)
• Step-up approach:
  
  • 1st: Antibiotics
  • 2nd: Percutaneous drainage / endoscopic transluminal drainage
  • 3rd: Video-assisted retroperitoneal debridement (VARD) or surgical necrosectomy

 6. ERCP in Gallstone Pancreatitis

When:

• Cholangitis present → urgent ERCP
• Biliary obstruction + high bilirubin → early ERCP (<72 hrs)
• No routine ERCP unless confirmed bile duct obstruction

7. Management of Organ Failure / Complications