Gastrointestinal · PANCE / PANRE

Acute Pancreatitis

Sudden inflammation of the pancreas, most often from gallstones or alcohol; severity-driven management.

Also known as: acute pancreatitis, gallstone pancreatitis, alcoholic pancreatitis

Overview

Acute inflammatory process of the pancreas with potential involvement of peripancreatic tissues or remote organ systems. Diagnosed by ≥2 of: characteristic abdominal pain, lipase or amylase ≥3× upper limit of normal, or characteristic imaging findings.

Epidemiology

Incidence 30-50 per 100,000/yr in the US; rising. Mortality 1-3% overall; up to 20% in severe necrotizing disease. Most common GI cause of hospital admission.

🔒 Free preview limit reached

Keep reading — start your free trial

You've read your 2 free diagnosis previews. Create your free account to unlock the full Acute Pancreatitis outline — plus all 514 diagnoses, 3,500+ board-style questions, flashcards, and an AI tutor. Your 7-day free trial includes everything, and there's no credit card required.

Free to start · No credit card · Cancel anytime

Risk factors

  • Gallstones (most common, ~40%)
  • Alcohol (~30%)
  • Hypertriglyceridemia (>1000 mg/dL; ~5%)
  • Hypercalcemia
  • Post-ERCP (~5% of ERCPs)
  • Medications: azathioprine/6-MP, GLP-1 agonists (debated), DPP-4 inhibitors, valproate, didanosine, pentamidine, estrogens, thiazides, furosemide, sulfa drugs, statins, mesalamine, asparaginase
  • Trauma (especially blunt — pediatric handlebar injury)
  • Autoimmune (IgG4-related — type 1; idiopathic duct-centric — type 2)
  • Hereditary (PRSS1, SPINK1, CFTR mutations)
  • Pancreas divisum, sphincter of Oddi dysfunction
  • Infections: mumps, coxsackievirus, CMV, mycoplasma
  • Smoking
  • Idiopathic (~10-20%)

Pathophysiology

Premature intra-acinar activation of trypsinogen to trypsin initiates auto-digestion of pancreatic tissue. Local inflammatory cascade and release of cytokines drive edema, hemorrhage, fat necrosis, and pancreatic/peripancreatic necrosis. Systemic inflammatory response (SIRS) and multiorgan dysfunction occur in severe disease.

Clinical presentation

Symptoms

  • Sudden, severe epigastric pain radiating to the back, often constant
  • Pain relieved by leaning forward, worse supine
  • Nausea and vomiting (often persistent)
  • Anorexia
  • Fever (mild; high fever suggests cholangitis or necrosis with infection)
  • Symptoms of SIRS/sepsis in severe disease

Signs / physical exam

  • Epigastric tenderness, guarding
  • Diminished bowel sounds (ileus)
  • Tachycardia, hypotension if severe
  • Jaundice if gallstone etiology
  • Cullen sign (periumbilical ecchymosis) — hemorrhagic pancreatitis (rare, late)
  • Grey-Turner sign (flank ecchymosis) — hemorrhagic pancreatitis (rare, late)
  • Fox sign (inguinal ecchymosis)
  • Tetany or trousseau sign if severe hypocalcemia

Classic findings

Sudden epigastric pain radiating to back with markedly elevated lipase (>3× ULN) in a patient with gallstones or alcohol use.

Differential diagnosis

  • Peptic ulcer (perforated) — Sudden severe epigastric pain, peritonitis, free air on imaging
  • Acute cholecystitis / cholangitis — RUQ pain, fever, jaundice; lipase may be mildly elevated
  • Mesenteric ischemia — Pain out of proportion, lactic acidosis, atrial fibrillation; CT angio
  • Ruptured AAA — Hypotension, pulsatile abdominal mass, severe back pain; emergent CT
  • Inferior MI — Atypical epigastric pain; ECG and troponin in older patients
  • Diabetic ketoacidosis — Hyperglycemia, anion gap acidosis, ketones; lipase mildly elevated (false positive)
  • Bowel obstruction — Distension, constipation/obstipation, vomiting; imaging
  • Renal colic — Flank pain, hematuria; CT

Diagnostic workup

Diagnostic criteria

Revised Atlanta Classification (2012): diagnosis requires 2 of 3: (1) typical abdominal pain; (2) lipase/amylase ≥3× ULN; (3) characteristic imaging. Severity: Mild (no organ failure, no local/systemic complications), Moderate (transient organ failure <48 h or local/systemic complications), Severe (persistent organ failure ≥48 h).

Labs

  • LIPASE (preferred) or amylase — elevation ≥3× ULN supports diagnosis; lipase more specific and remains elevated longer
  • CBC — hematocrit (hemoconcentration from third-spacing); WBC
  • BMP — BUN/creatinine (volume status, prognostic); glucose; calcium
  • LFTs — ALT >150 strongly suggests gallstone etiology (NPV high if normal)
  • Triglycerides — exclude hypertriglyceridemic pancreatitis (>500-1000)
  • Calcium — hyper- (cause) or hypocalcemia (complication)
  • Lactate if severe
  • ABG, lactate dehydrogenase for severity scoring (Ranson, APACHE)
  • CRP at 48 h — >150 predicts severe disease

Imaging

  • Abdominal ultrasound — FIRST imaging in all patients to exclude gallstones (etiology), not for severity
  • CT abdomen with IV contrast — NOT required at presentation if diagnosis is clinical; obtain at 72 h or later to stratify severity and identify necrosis, peripancreatic collections; earlier CT if diagnosis unclear or rapid deterioration
  • MRI/MRCP — if CT contraindicated or CBD stone suspected
  • EUS — recurrent idiopathic pancreatitis evaluation

Diagnostic algorithm

BISAP Criterion (0-5)Threshold
B — BUN>25 mg/dL
I — Impaired mental statusGCS <15
S — SIRS≥2 criteria
A — Age>60 yr
P — Pleural effusionPresent on imaging
Score interpretation≥3 = high risk for severe pancreatitis and mortality
BISAP score — bedside index for severity in acute pancreatitis (Wu et al., Gut 2008).

Treatment

First-line

  • Aggressive IV fluid resuscitation — lactated Ringer's at 5-10 mL/kg/h titrated to urine output >0.5 mL/kg/h and clinical response; avoid over-resuscitation (worsens outcomes)
  • Pain control — IV opioids (hydromorphone, fentanyl)
  • Antiemetics, NPO initially but early oral feeding (low-fat soft diet) within 24-48 h as tolerated improves outcomes
  • Identify and treat etiology
  • Monitor in step-down or ICU based on severity

Gallstone pancreatitis

  • Same-admission cholecystectomy for mild disease (PONCHO trial) to prevent recurrence
  • Delay cholecystectomy 4-6 weeks for severe disease until inflammation resolves
  • ERCP only if concurrent cholangitis or persistent obstruction

Alcohol-induced pancreatitis

  • Alcohol cessation counseling; treat withdrawal
  • Nutritional support (thiamine, folate, multivitamin)
  • Smoking cessation (synergistic risk for chronic pancreatitis)

Hypertriglyceridemic pancreatitis

  • IV insulin infusion (lowers TG) ± plasmapheresis if TG >1000 with end-organ damage
  • Long-term fibrate ± omega-3 fatty acids; dietary fat restriction
  • Control underlying diabetes, alcohol, OCP, estrogens, beta-blockers

Second-line / adjunct

  • Enteral nutrition (nasogastric or nasojejunal) preferred over TPN in severe disease unable to eat by day 5-7
  • Antibiotics — NOT routine; reserve for confirmed infected necrosis (positive FNA culture or gas in necrosis) or concurrent extra-pancreatic infection (cholangitis, pneumonia, line sepsis); carbapenem or piperacillin-tazobactam
  • ERCP within 24-48 h ONLY if concurrent ascending cholangitis or persistent CBD obstruction; not for uncomplicated gallstone pancreatitis
  • Plasmapheresis or insulin/heparin infusion for hypertriglyceridemic pancreatitis (TG >1000)
  • Step-up approach for necrotizing pancreatitis: percutaneous drainage → minimally invasive necrosectomy (video-assisted retroperitoneal debridement or endoscopic transluminal) → open necrosectomy as last resort (PANTER trial)

Complications

  • Acute peripancreatic fluid collection (early; resolves spontaneously)
  • Pancreatic pseudocyst (after 4 weeks; intervene only if symptomatic or infected)
  • Acute necrotic collection (early necrosis)
  • Walled-off pancreatic necrosis (after 4 weeks)
  • Infected pancreatic necrosis — high mortality; FNA + culture; step-up drainage
  • ARDS, AKI, DIC, shock (severe disease)
  • Hypocalcemia (saponification), hypomagnesemia, hyperglycemia
  • Pancreatic abscess
  • Splenic vein thrombosis with isolated gastric varices
  • Pseudoaneurysm (especially splenic artery)
  • Progression to chronic pancreatitis (especially alcohol etiology)
  • Diabetes mellitus, exocrine insufficiency

PANCE pearls

  • Lipase >3× ULN is more specific than amylase and remains elevated longer.
  • Magnitude of lipase does NOT correlate with severity.
  • ALT >150 strongly suggests gallstone etiology — pursue RUQ ultrasound.
  • DO NOT routinely give prophylactic antibiotics for sterile necrosis — only for infected necrosis or extra-pancreatic infection.
  • Aggressive IV fluids in the first 24 h reduce mortality; lactated Ringer's reduces SIRS compared with normal saline (Wu, Clin Gastroenterol Hepatol 2011).
  • AVOID over-resuscitation — increases mortality, ARDS, abdominal compartment syndrome.
  • Same-admission cholecystectomy for mild gallstone pancreatitis (PONCHO trial).
  • Early enteral feeding within 24-48 h improves outcomes vs prolonged NPO.
  • Step-up approach (drainage first, surgery last) reduces morbidity in necrotizing pancreatitis (PANTER trial).
  • Revised Atlanta Classification: mild, moderate, severe — severity determined by organ failure (Marshall score) and complications.
  • BISAP score (BUN >25, impaired mental status, SIRS ≥2, age >60, pleural effusion) — practical early severity score.
  • ERCP urgent only for concurrent cholangitis or persistent obstruction — not for uncomplicated gallstone pancreatitis.

References

  • ACG 2013 — Tenner S et al. American College of Gastroenterology Guideline: Management of Acute Pancreatitis. Am J Gastroenterol 2013;108:1400-1415
  • Revised Atlanta — Banks PA et al. Classification of acute pancreatitis—2012: revision of the Atlanta classification and definitions. Gut 2013;62:102-111
  • PANTER Trial — van Santvoort HC et al. A Step-up Approach or Open Necrosectomy for Necrotizing Pancreatitis. NEJM 2010;362:1491-1502
  • PONCHO Trial — da Costa DW et al. Same-admission versus interval cholecystectomy for mild gallstone pancreatitis. Lancet 2015;386:1261-1268

Practice Gastrointestinal questions on FirstPassPA

Turn this outline into retention. 3,500+ board-style questions with an AI tutor that explains every answer — free to start, no card required.

Start studying free → Browse all 514 diagnoses

Educational use only. This outline is a study aid for PA students and is not medical advice or a substitute for clinical judgment. FirstPassPA is an independent study tool and is not affiliated with, endorsed by, or sponsored by NCCPA. PANCE® and PANRE® are registered trademarks of the National Commission on Certification of Physician Assistants.