Acute pancreatitis

Last updated: September 11, 2023

Summarytoggle arrow icon

Acute pancreatitis is an inflammatory condition of the pancreas most commonly caused by gallstones and alcohol use. The typical manifestation includes sudden, severe epigastric pain that radiates to the back, nausea and vomiting, and epigastric tenderness on palpation. Elevation of serum lipase or amylase ≥ 3× ULN and/or characteristic findings of acute pancreatitis on cross-sectional imaging (e.g., contrast-enhanced CT abdomen) confirm the diagnosis. Clinical scores (e.g., Ranson criteria, APACHE II) are used to predict the severity and prognosis of pancreatitis. Initial management is primarily supportive and includes fluid resuscitation, analgesia, antiemetics, and early enteral nutrition as tolerated. The underlying cause should be identified and managed to prevent recurrence (e.g., cholecystectomy for biliary pancreatitis, long-term lipid-lowering therapy for hypertriglyceridemia-induced pancreatitis). Localized complications of pancreatitis include necrosis (necrotizing pancreatitis), which may become infected, pancreatic pseudocysts, and walled-off necrosis. Systemic complications include sepsis, ARDS, organ failure, and shock. Complications of pancreatitis are associated with significant morbidity and mortality.

Etiologytoggle arrow icon

Most common causes [1]

  • Biliary pancreatitis; (∼ 40% of cases; mostly caused by gallstones)
  • Alcohol-induced (∼ 20% of cases)
  • Idiopathic (∼ 25% of cases)

Other causes [1]

I GET SMASHED: Idiopathic, Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmune, Scorpion venom, Hypercalcemia and hypertriglyceridemia, ERCP, and Drugs are the most common causes of acute pancreatitis.

Pathophysiologytoggle arrow icon

Sequence of events

  1. Intrapancreatic activation of pancreatic enzymes: secondary to pancreatic ductal outflow obstruction (e.g., gallstones, cystic fibrosis) or direct injury to pancreatic acinar cells (e.g., alcohol, drugs)
  2. Increased proteolytic and lipolytic enzyme activity → destruction of pancreatic parenchyma
  3. Attraction of inflammatory cells (neutrophils, macrophages) → release of inflammatory cytokines pancreatic inflammation (pancreatitis)

Sequelae of pancreatitis

Clinical featurestoggle arrow icon


Examination findings

Diagnosticstoggle arrow icon

Acute pancreatitis should be managed as a medical emergency as it is a potentially fatal condition. Initiate fluid resuscitation as soon as this diagnosis is suspected (see “Treatment of acute pancreatitis”). Simultaneously conduct diagnostics to establish the diagnosis, assess severity, and rule out potential differential diagnoses of acute abdominal pain.

Diagnostic criteria for acute pancreatitis [4][5]

Two of the three following criteria should be met for a diagnosis of acute pancreatitis to be made.

Approach [6][7][8]

Laboratory studies

Laboratory studies in acute pancreatitis


Findings and interpretation
Serum pancreatic enzymes [4][9]
Inflammatory markers [9][10]
Liver chemistries [18][19]
LDH [20]
Serum triglycerides [9][21]

The degree of lipase and/or amylase elevation does not necessarily correlate with the severity of or prognosis for acute pancreatitis. [22]

Measure serum triglycerides promptly after symptom onset, as levels decrease rapidly with fasting. [23]

Determining calcium values is very important: Hypercalcemia may cause pancreatitis, which may then, in turn, cause hypocalcemia!


Ultrasound abdomen [8][24]

Abdominal ultrasound for suspected acute pancreatitis is primarily used to identify gallstones as features of acute pancreatitis are only visible in approximately 20% of cases. [8]

CT abdomen and pelvis with IV contrast [6][8][14]

CT abdomen is not routinely required to establish a diagnosis of acute pancreatitis. If performed to evaluate for necrotic pancreatitis, the optimal timing to perform a CT abdomen is at least 5–7 days after symptom onset. [8]

Suspect pancreatic tumor as the underlying cause for idiopathic acute pancreatitis in patients aged > 40 years; see “Pancreatic cancer.” [25]

X-ray chest and abdomen [8][26][27]

MRI abdomen [6][8]

Magnetic resonance cholangiopancreatography [4][6][8]

Endoscopic retrograde cholangiopancreatography

Endoscopic ultrasound [31]

Severity grading and prognostic scorestoggle arrow icon

There are several scores used to assess the severity and prognosis of acute pancreatitis. The most commonly used and validated scores are described here.

Revised Atlanta grades of severity [5]

The revised Atlanta grades of severity classify pancreatitis as mild, moderate, or severe, depending on the presence of organ failure. Organ failure can be determined using the modified Marshall scoring system for organ dysfunction.

  • Mild acute pancreatitis: no organ failure and no local or systemic complications
  • Moderate acute pancreatitis: transient organ failure (< 48 hours) and/or local or systemic complications
  • Severe acute pancreatitis: persistent organ failure (> 48 hours)

Patients with organ failure at presentation or within the first 24 hours of admission should be classified as having severe pancreatitis. If organ failure resolves within 48 hours, patients can be reclassified as having moderately severe acute pancreatitis. [5]

CT severity index [7][23][32]

The CT severity index for acute pancreatitis (CTSI) and modified CT severity index (MCTSI) can be used to estimate the severity, mortality, and morbidity of acute pancreatitis based on the extent of pancreatic inflammation and necrosis on a CT abdomen performed ideally > 5–7 days (or at least 72 hours) after symptom onset.

CTSI score [33] MCTSI score [34]
Degree of inflammation Normal pancreas 0 0
Localized or diffuse enlargement 1 2
Peripancreatic inflammation 2
Single acute fluid collection 3 4
Multiple or extensive acute fluid collections 4
Degree of parenchymal necrosis None 0 0
< 30% 2 2
≥ 30%–50% 4 4
> 50% 6
Presence of extrapancreatic complications n/a 2


  • Mild: 0–3 points
  • Moderate: 4–6 points
  • Severe: 7–10 points
  • Mild: 0–2 points
  • Moderate: 4–6 points
  • Severe: 8–10 points

Ranson criteria [7][28]

The Ranson criteria is one of the oldest predictive models used to estimate severity and prognosis of biliary and nonbiliary pancreatitis; , but full assessment is only possible after 48 hours, and sensitivity for predicting severity and outcome can be as low as 70%.

Ranson criteria for acute pancreatitis [22]
Parameter Nonbiliary pancreatitis Biliary pancreatitis
On admission
Age > 55 years > 70 years
WBC > 16,000/mm3 > 18,000/mm3
Blood glucose > 200 mg/dL > 220 mg/dL
Serum LDH > 350 U/L > 400 U/L
Serum AST > 250 U/L > 250 U/L
After initial 48 hours
Hct decrease > 10% > 10%
BUN increase > 5 mg/dL > 2 mg/dL
Serum calcium < 8 mg/dL < 8 mg/dL
Arterial pO2 < 60 mm Hg n/a
Fluid sequestration > 6 L > 4 L
Serum base deficit > 4 mmol/L > 5 mmol/L

Interpretation [35]

Acute physiology and chronic health evaluation II (APACHE II score) [7]

Bedside index of severity of acute pancreatitis (BISAP) [10]

Treatmenttoggle arrow icon

The initial management is identical for all etiologies of acute pancreatitis and should be administered without delay. [4][6][10][25]

Acute stabilization [4][6][10][25]

Goal-directed IV fluid therapy [4][6][10][25]

Intravenous fluid resuscitation in the first 12–24 hours has the greatest impact on the clinical outcome of patients with acute pancreatitis. [25]

Supportive therapy

In concurrent acute kidney injury, avoid NSAIDs and use opioids with caution because of the risk of accumulation. [10]

Prophylactic antibiotics are not recommended, and should only be used in patients with evidence of infected necrosis. [10]


Disposition [6][28]

  • Hospital admission is usually required.
  • Consider ICU admission in the following cases:
  • Refer to a specialist center if the need for surgical or interventional procedures is anticipated. [6]


Bowel rest is no longer routinely recommended. Enteral nutrition, via oral route or enteral tube, should be initiated as early as tolerated. [4]

Management of the underlying cause

Biliary pancreatitis

Urgent ERCP is not indicated in acute biliary pancreatitis unless acute cholangitis is present. [4]

Hypertriglyceridemia-induced pancreatitis [23]

Hypercalcemia-induced pancreatitis [17]

Alcohol-induced pancreatitis

"PANCREAS": Perfusion (fluid replacement), Analgesia, Nutrition, Clinical (observation), Radiology (imaging), ERCP, Antibiotics (if indicated), Surgery (surgical intervention, if necessary)

Acute management checklisttoggle arrow icon

Special patient groupstoggle arrow icon

Acute pancreatitis during pregnancy [47]

Differential diagnosestoggle arrow icon


The differential diagnoses listed here are not exhaustive.

Acute pancreatitis vs. chronic pancreatitistoggle arrow icon

Overview of acute and chronic pancreatitis
Acute pancreatitis Chronic pancreatitis
  • Progressive inflammation
  • Irreversible damage with impairment of exocrine and endocrine function
Etiology Most common causes
Less common causes
  • Sudden onset
  • Recurrent, progressive episodes
Clinical features Main symptoms
Further symptoms
Diagnostics Laboratory studies
  • Mortality
    • In patients without organ failure: < 1%
    • In patients with organ failure: ∼ 30% [7]
  • Dependent on alcohol use, smoking, and presence of end-stage liver disease [48]

Complicationstoggle arrow icon

Necrotizing pancreatitis [14]

Infected necrotizing pancreatitis [14]

Walled-off necrosis

  • Definition
  • Diagnostics: CT abdomen with IV contrast showing an encapsulated heterogeneous collection containing fluid and debris [8]
  • Treatment (of symptomatic walled-off necrosis): percutaneous drainage or transmural endoscopic necrosectomy [14]

Other localized complications [49][50]

Systemic complications [51]

We list the most important complications. The selection is not exhaustive.

Prognosistoggle arrow icon

Amylase and lipase, which are used for the diagnosis of pancreatitis, cannot be used to predict the prognosis!


Referencestoggle arrow icon

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