Causes
Acute: gallstones (most common), alcohol (second), hypertriglyceridemia, ERCP. Auto-digestion by activated enzymes causes inflammation, necrosis, SIRS. Chronic: recurrent inflammation leading to fibrosis.
Acute Management
NPO. Aggressive IV fluids (LR, 250-500 mL/hr initially). Pain: IV opioids (hydromorphone). Antiemetics. Monitor: lipase (more specific), CBC, electrolytes (calcium), glucose. ICU for severe cases.
Complications
Local: pseudocyst, abscess, necrosis. Systemic: ARDS, AKI, DIC, hypocalcemia, hyperglycemia. Severe can progress to SIRS and multiorgan failure. Chronic: malabsorption (steatorrhea), diabetes, chronic pain.
Important Notes
- Hypocalcemia caused by saponification of fats — monitor for tetany, Chvostek/Trousseau signs.
- Severe acute pancreatitis can progress to SIRS and multiorgan failure — ICU monitoring required.
Clinical Tips
- Lipase more specific than amylase — amylase normalizes within 3-5 days.
- Cullen sign (periumbilical bruising) and Grey Turner sign (flank bruising) indicate hemorrhagic pancreatitis.
Summary
Pancreatitis management requires aggressive IV fluids, pain control, NPO status, and monitoring for systemic complications.
