Last reviewed: March 2026
Contents
MDM Templates
Mild Acute Pancreatitis
Patient presents with epigastric pain radiating to the back with nausea and vomiting. Labs confirm acute pancreatitis with lipase elevated at ***. Well appearing without signs of organ failure or systemic toxicity. No Cullen or Grey Turner signs.
History, exam, and workup not consistent with AAA, SBO, mesenteric ischemia, peptic ulcer perforation, or other surgical abdomen.
Plan: IV fluid resuscitation with lactated Ringer’s. Analgesia and antiemetic. Diet advanced as tolerated — low-fat, soft diet when patient reports hunger.
Disposition: Admit for continued hydration and monitoring. If tolerating PO within 24 hours with pain controlled and no organ failure, candidate for early discharge.
If mild case, tolerating PO, and pain controlled in the ED:
Mild acute pancreatitis by clinical criteria — no organ failure, no systemic complications, lipase elevated, pain improving. Patient tolerating clear liquids and advancing diet in the ED. No biliary etiology on RUQ ultrasound.
Disposition: Discharge with return precautions for worsening pain, inability to tolerate PO, fever, or persistent vomiting. PPI and antiemetic prescribed. Follow up with PCP within 48 hours for repeat assessment.
Severe / Necrotizing Pancreatitis
Patient presents with severe epigastric pain, vomiting, and hemodynamic instability consistent with severe acute pancreatitis. Signs of organ failure present — ***. No Grey Turner or Cullen signs on exam, though these are late findings.
Plan: Aggressive IV fluid resuscitation with lactated Ringer’s. Analgesia (IV hydromorphone or fentanyl preferred, avoid morphine if concern for sphincter of Oddi spasm). No role for prophylactic antibiotics at this time. CT for severity assessment if concern for necrotizing pancreatitis and patient not improving within 48–72 hours.
Disposition: Admit to ICU for monitoring and aggressive supportive care.
Gallstone Pancreatitis
Patient presents with acute pancreatitis and RUQ ultrasound demonstrating cholelithiasis, consistent with gallstone pancreatitis. LFTs elevated with obstructive pattern.
If cholangitis or persistent biliary obstruction:
Concurrent cholangitis / persistent common bile duct obstruction suspected (persistent elevation of bilirubin and transaminases, fever). GI consulted for urgent ERCP within 24 hours. Surgery consulted for cholecystectomy during same admission once pancreatitis resolves.
If uncomplicated gallstone pancreatitis:
No cholangitis. Bilirubin and transaminases trending down. Plan for same-admission cholecystectomy once pancreatitis resolves to prevent recurrence. Surgery consulted.
Disposition: Admit.
Chronic Pancreatitis Flare
Patient with known chronic pancreatitis presents with acute exacerbation of epigastric pain. Lipase may be mildly elevated or normal (burned-out pancreas with insufficient acinar tissue to produce significant enzyme elevation). No signs of organ failure.
Presentation consistent with chronic pancreatitis flare without evidence of complications (pseudocyst, pancreatic duct obstruction, new-onset diabetes, pancreatic malignancy).
Plan: Analgesia, antiemetic, IV fluids. Diet as tolerated. Alcohol cessation counseled if applicable.
Disposition: If pain controlled and tolerating PO, discharge with PCP and GI follow-up. If not improving, admit for further workup including CT to evaluate for complications.
Clinical Education
Diagnosis Pearls
Acute pancreatitis requires 2 of 3 criteria: (1) Characteristic epigastric pain (acute onset, severe, radiating to the back), (2) Lipase ≥3x the upper limit of normal, (3) Characteristic findings on imaging. Most patients are diagnosed on clinical and lab criteria alone — imaging is not required to make the diagnosis.[1]
Lipase is the preferred enzyme — more specific and stays elevated longer than amylase. A lipase ≥3x ULN has >95% sensitivity and specificity for acute pancreatitis. The degree of lipase elevation does not correlate with disease severity.[2]
Don’t order amylase. Lipase is superior in every respect — more sensitive, more specific, and stays elevated longer. Amylase adds nothing and can be misleadingly elevated in other conditions (parotitis, macroamylasemia, renal failure).
In chronic pancreatitis, lipase may be normal during a flare. The pancreas is “burned out” with insufficient acinar tissue to produce enzyme elevation. Diagnosis relies on clinical history and imaging.
Severity Assessment
Early aggressive IV fluid resuscitation is the most impactful intervention in acute pancreatitis. Lactated Ringer’s is preferred over normal saline (lower rate of SIRS in one RCT). Goal-directed resuscitation targeting urine output 0.5 mL/kg/hr and normalizing BUN/Hct. However, avoid over-resuscitation — recent data (WATERFALL trial, 2022) suggests moderate resuscitation (1.5 mL/kg/hr) may be safer than aggressive (3 mL/kg/hr) in some patients.[3]
The BISAP Score is the most practical bedside severity tool. Five criteria: BUN > 25, impaired mental status, SIRS, age > 60, pleural effusion. Score ≥3 predicts severe pancreatitis and increased mortality. Calculate it in the ED — it uses only information available at admission.[4]
CT is not needed early. CT in the first 48–72 hours underestimates necrosis because it has not yet fully developed. CT is indicated when: the diagnosis is uncertain, the patient fails to improve after 48–72 hours of treatment, or there is concern for a complication (abscess, pseudocyst, hemorrhage).[1]
| Severity | Definition | Mortality |
| Mild | No organ failure, no local complications | <1% |
| Moderately severe | Transient organ failure (<48 hrs) or local complications | ~5% |
| Severe | Persistent organ failure (>48 hrs) | 30–50% |
Etiology Workup
Gallstones and alcohol account for ~80% of acute pancreatitis. RUQ ultrasound should be obtained on all patients with acute pancreatitis to evaluate for gallstone etiology — if present, cholecystectomy during the same admission prevents recurrence (recurrence rate ~30–50% without cholecystectomy within 6 months).[5]
In the ED, check: LFTs (obstructive pattern suggests gallstone pancreatitis), triglycerides (hypertriglyceridemic pancreatitis if TG > 1000 mg/dL), calcium (hypercalcemia), and a thorough medication review. Common drug causes: valproic acid, azathioprine, GLP-1 agonists, and didanosine.
ALT > 150 U/L has a positive predictive value of 95% for gallstone pancreatitis. This is a useful early clue before ultrasound results are available.[6]
Treatment Pearls
Early oral feeding is the standard. NPO is no longer recommended. Feed the patient when they report hunger — a low-fat solid diet is safe and reduces hospital length of stay compared to clear-liquid-first protocols. “Feed the gut” is the current approach.[7]
Prophylactic antibiotics are NOT indicated in acute pancreatitis, even in necrotizing disease. They do not reduce infected necrosis, mortality, or need for surgery. Reserve antibiotics for documented infection (infected necrosis with gas on CT, positive cultures).[1]
Pain management: IV opioids are the mainstay (fentanyl, hydromorphone). The old teaching that morphine causes sphincter of Oddi spasm is based on poor evidence and should not limit its use if it’s the best available analgesic. Ketorolac is a useful adjunct if not contraindicated. PCA may be needed for severe cases.[8]
For hypertriglyceridemic pancreatitis (TG > 1000): Insulin drip (regular insulin 0.1–0.3 units/kg/hr) to rapidly lower triglycerides. Heparin boluses are no longer recommended. Target TG < 500 mg/dL.
Complications
Pseudocyst: Encapsulated fluid collection that develops >4 weeks after acute pancreatitis. Most are asymptomatic and resolve spontaneously. Intervention (endoscopic or surgical drainage) only for symptomatic, infected, or >6 cm pseudocysts.[1]
Infected necrosis: Suspect when a patient with known necrotizing pancreatitis develops new fever, leukocytosis, or clinical deterioration at 2–4 weeks. Gas within a necrotic collection on CT is pathognomonic. Treatment is antibiotics (carbapenems penetrate necrotic tissue best) ± endoscopic/surgical necrosectomy — delayed intervention (>4 weeks) when possible improves outcomes.
Pseudoaneurysm and hemorrhage: Pancreatic enzymes can erode adjacent vessels (splenic, gastroduodenal, pancreaticoduodenal arteries) causing pseudoaneurysm and life-threatening hemorrhage. Suspect with sudden hemodynamic deterioration or sentinel bleed. CTA followed by IR embolization is the treatment.
Disposition
Admit if: Cannot tolerate PO, uncontrolled pain, organ failure or BISAP ≥3, gallstone pancreatitis (needs cholecystectomy), concurrent cholangitis, first presentation (to confirm diagnosis and establish etiology), significant comorbidities, or social factors limiting safe discharge.
Discharge if: Mild pancreatitis with pain controlled on oral medications, tolerating low-fat diet, no organ failure, no biliary etiology (or prior cholecystectomy), reliable follow-up within 48 hours. This is reasonable for known recurrent pancreatitis in a patient who recognizes the disease and has good follow-up.
References
- Tenner S et al. American College of Gastroenterology guideline: management of acute pancreatitis. Am J Gastroenterol. 2013;108(9):1400-1415. PubMed
- Lippi G et al. Ceruloplasmin, lipase, and amylase in the diagnosis of acute pancreatitis. Clin Chem Lab Med. 2012;50(8):1325-1330.
- de-Madaria E et al. Aggressive or moderate fluid resuscitation in acute pancreatitis (WATERFALL). N Engl J Med. 2022;387(11):989-1000. PubMed
- Wu BU et al. The early prediction of mortality in acute pancreatitis: a large population-based study. Gut. 2008;57(12):1698-1703. PubMed
- van Baal MC et al. Systematic review of percutaneous catheter drainage as primary treatment for necrotizing pancreatitis. Br J Surg. 2011;98(1):18-27. PubMed
- Tenner SM et al. Predicting gallstone pancreatitis with laboratory parameters: a meta-analysis. Am J Gastroenterol. 1994;89(10):1863-1866. PubMed
- Bakker OJ et al. Early versus on-demand nasoenteric tube feeding in acute pancreatitis. N Engl J Med. 2014;371(21):1983-1993. PubMed
- Basurto Ona X et al. Opioids for acute pancreatitis pain. Cochrane Database Syst Rev. 2013;(7):CD009179. PubMed
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