Acute Pancreatitis: GET SMASHED Causes, Ranson Criteria & Management

Creator: Progress Note
Published: 2026-07-22
Keywords: acute pancreatitis treatment management, acute pancreatitis causes GET SMASHED, Ranson criteria pancreatitis, acute pancreatitis fluid resuscitation, necrotizing pancreatitis treatment, acute pancreatitis ERCP timing

The 60-second version

GET SMASHED: gallstones (#1) and alcohol (#2) cause >80% of cases; lipase >3× ULN is diagnostic
Ranson criteria: ≥3 = severe (40% mortality); CT contrast imaging after 48–72h to assess necrosis
Aggressive LR resuscitation (250–500 mL/hr) is the cornerstone — LR preferred over normal saline
ERCP within 24h only for concurrent cholangitis/biliary obstruction — not routine for gallstone pancreatitis
Cholecystectomy same admission for mild gallstone pancreatitis; no prophylactic antibiotics for sterile necrosis

Causes and Diagnosis: GET SMASHED

**GET SMASHED** mnemonic: **G**allstones (#1 cause, 40%), **E**thanol/alcohol (#2, 35%), **T**rauma, **S**teroids, **M**umps (and other viruses: Coxsackie B, EBV, CMV), **A**utoimmune (IgG4-related pancreatitis), **S**corpion sting (rare, causes hyperstimulation), **H**yperlipidemia (triglycerides >1000 mg/dL) / Hypercalcemia, **E**RCP (iatrogenic), **D**rugs (thiazides, furosemide, azathioprine, valproate, tetracyclines, sulfonamides, DDI). **Diagnosis**: clinical + lipase >3× ULN (more specific than amylase, stays elevated longer). Two of three criteria: (1) typical epigastric pain radiating to back, (2) lipase/amylase ≥3× ULN, (3) imaging (CT with IV contrast) — CT only needed if diagnosis uncertain or to assess complications (necrosis) after 48–72h when contrast best shows non-enhancing pancreatic parenchyma. Ultrasound is first imaging for gallstone evaluation.

Severity Assessment: Ranson Criteria

**Ranson criteria** predict mortality. On admission: Age >55, WBC >16,000, glucose >200 (not diabetic), LDH >350, AST >250. At 48 hours: Hematocrit drop >10%, BUN rise >5, Ca²⁺ <8, PO₂ <60, Base deficit >4, Fluid sequestration >6L. Score: 0–2 = mild (1% mortality), 3–4 = moderate (15%), 5–6 = severe (40%), >6 = ~100%. **CT severity index** (CTSI): Balthazar grade (A–E based on inflammation/fluid) + necrosis score → 0–10. CTSI ≥7 = severe disease. **Atlanta Classification (2012)**: Mild (no organ failure, no local complications), Moderately severe (transient organ failure <48h or local complications), Severe (persistent organ failure >48h). **Complications**: Pancreatic necrosis (non-enhancing parenchyma on CT with contrast); infected necrosis (air in necrotic collection, fever, + FNA cultures) → requires drainage ± necrosectomy (step-up approach: percutaneous drainage → endoscopic → surgical). Pseudocyst (fluid collection >4 weeks, no necrosis debris); pancreatic abscess; splenic vein thrombosis → gastric varices.

Management: Fluids, NPO, and Timing of Interventions

**Aggressive fluid resuscitation** is the cornerstone: **Lactated Ringer's** preferred over normal saline (LR reduces SIRS response in multiple RCTs; normal saline causes non-anion gap hyperchloremic acidosis with large volumes). Goal-directed: 250–500 mL/hr LR initially, adjust to UO >0.5 mL/kg/hr, HR <120, hematocrit 35–44%. **NPO initially**, but early enteral nutrition (within 24–48h if possible) via nasojejunal tube is preferred for severe pancreatitis — maintains gut barrier, reduces infectious complications. TPN only if enteral not tolerated. **Pain management**: IV opioids (hydromorphone); ketorolac adjunct. **ERCP timing**: indicated within 24h for gallstone pancreatitis with concurrent cholangitis or biliary obstruction (rising bilirubin, dilated CBD). NOT indicated for uncomplicated gallstone pancreatitis. **Antibiotics**: NOT prophylactic for pancreatitis or sterile necrosis — only for proven infected necrosis (imipenem or meropenem penetrate pancreatic tissue). **Cholecystectomy**: for gallstone pancreatitis, same-admission cholecystectomy for mild pancreatitis (before discharge) reduces recurrence from 30% to <3%. Defer for severe/necrotizing pancreatitis until resolved (≥6 weeks).

Test yourself

Quick check — 3 questions

1. A 45-year-old man with epigastric pain radiating to the back is found to have lipase 1,200 U/L (ULN 60) and a CBD stone on ultrasound. His bilirubin is 4.2 mg/dL and rising. What is the most appropriate next step?

2. Which fluid is preferred for aggressive resuscitation in acute pancreatitis?

3. A patient with severe acute pancreatitis (CTSI 8) develops fever, WBC 22,000, and CT shows air bubbles within the pancreatic necrotic collection. What is the most appropriate management?

Frequently asked questions

Why is lactated Ringer's preferred over normal saline for acute pancreatitis resuscitation?

Large volumes of normal saline cause hyperchloremic non-anion gap metabolic acidosis (dilutional acidosis + excess chloride inhibits renal acid secretion). Lactated Ringer's is more physiologically balanced and multiple RCTs (including the WATERFALL trial) have shown LR reduces SIRS response and clinical outcomes in acute pancreatitis. LR is also contraindicated in hypercalcemia-induced pancreatitis (LR contains calcium) — use NS in that case.

When should antibiotics be given in acute pancreatitis?

Prophylactic antibiotics are NOT indicated for acute pancreatitis or sterile pancreatic necrosis — multiple RCTs have failed to show benefit and increase antibiotic resistance risk. Antibiotics are indicated only when infected pancreatic necrosis is confirmed (CT showing air bubbles in necrotic collection, positive FNA cultures, or clinical deterioration with fever/leukocytosis). Use carbapenems (imipenem/meropenem) or fluoroquinolones — they penetrate pancreatic tissue.

Practice makes permanent

Lock this into long-term memory

Progress Note's adaptive engine spaces your reviews automatically — so this stays with you through boards and onto the wards.

Start practicing free

Share Post LinkedIn Reddit

Continue the curriculum

Liver Function Tests: Hepatocellular vs Cholestatic Patterns

GI Bleeding: Upper vs Lower GIB Approach

Acute Kidney Injury: Prerenal, Intrinsic, and Postrenal