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.
Most common causes 
- Biliary pancreatitis; (∼ 40% of cases; mostly caused by gallstones)
- Alcohol-induced (∼ 20% of cases)
- Idiopathic (∼ 25% of cases)
Other causes 
- Hypertriglyceridemia-induced pancreatitis: caused by severe hypertriglyceridemia (> 1,000 mg/dL)
- Drug-induced pancreatitis
- Scorpion stings
- Viral infections (e.g., coxsackievirus B, mumps)
- Trauma (especially in children)
- Autoimmune and rheumatological disorders (e.g., Sjögren syndrome)
- Pancreas divisum
- Hereditary (e.g., mutation of PRSS1 gene, cystic fibrosis) 
- Cholesterol embolism
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.
Sequence of events
- 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)
- Increased proteolytic and lipolytic enzyme activity → destruction of pancreatic parenchyma
- Attraction of inflammatory cells (neutrophils, macrophages) → release of inflammatory cytokines → pancreatic inflammation (pancreatitis)
Sequelae of pancreatitis
- Capillary leakage; : release of inflammatory cytokines and vascular injury by pancreatic enzymes → vasodilation and increased vascular permeability → shift of fluid from the intravascular space into the interstitial space (third-space fluid loss) → hypotension, tachycardia, warm and flushed skin →
- Pancreatic necrosis: uncorrected hypotension and third-spacing → decreased end-organ perfusion → multiorgan dysfunction (mainly renal) and pancreatic necrosis
- Hypocalcemia: lipase breaks down peripancreatic and mesenteric fat; → release of free fatty acids that bind calcium → hypocalcemia (fatty saponification) 
Constant, severe epigastric pain
- Classically radiating towards the back
- Worse after meals and when supine
- Improves on leaning forwards
- Nausea, vomiting
- If pulmonary complications are present: chest pain, dyspnea
- Abdominal examination
- Pulmonary examination: signs of and/or may be present
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 
Two of the three following criteria should be met for a diagnosis of acute pancreatitis to be made.
- Characteristic abdominal pain
- ↑ Serum pancreatic enzymes: lipase or amylase ≥ 3× ULN
- Characteristic findings of acute pancreatitis on cross-sectional imaging (e.g., contrast-enhanced CT abdomen)
- All patients
- Diagnostic uncertainty: Perform contrast-enhanced CT (CECT) abdomen.
- Perform further diagnostics as needed to determine the etiology (e.g., MRCP for suspected biliary pancreatitis).
- Calculate severity scores of acute pancreatitis to estimate severity and prognosis.
- In patients with severe pancreatitis, consider CECT abdomen 5–7 days after the onset of symptoms to assess for .
|Laboratory studies in acute pancreatitis|
|Findings and interpretation|
|Serum pancreatic enzymes |
|Inflammatory markers |
|Liver chemistries |
|Serum triglycerides |
Ultrasound abdomen 
- Indications: first-line imaging modality for all patients
- Features of acute pancreatitis (visible in 20% of cases) 
- Features of biliary pancreatitis
- Evidence of complications: pancreatic pseudocysts, walled-off necrosis (typically > 4 weeks from symptom onset) 
CT abdomen and pelvis with IV contrast 
- Diagnostic uncertainty (e.g., typical clinical features in a patient with moderately elevated pancreatic enzymes)
- Severe pancreatitis : optimally performed > 5–7 days after symptom onset 
- Lack of improvement (after > 7 days) or sudden acute deterioration
- To evaluate for underlying etiology if routine diagnostic studies are negative 
- Features of acute pancreatitis
- Evidence of complications
- Necrotizing pancreatitis: nonenhancing areas of pancreatic parenchyma
- Acute necrotic collections: ill-defined, heterogeneous appearance with varying densities
- Walled-off necrosis: an encapsulated collection of necrotic material, usually occurring > 4 weeks after the onset of necrotizing pancreatitis
- Infection: air within the pancreatic or peripancreatic tissue or fluid collections
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. 
X-ray chest and abdomen 
- Indications: not routinely indicated; may be performed as part of the initial workup of undifferentiated abdominal pain 
- On abdominal x-ray
- On chest x-ray: pleural effusion, pulmonary edema suggesting ARDS
MRI abdomen 
- Supportive findings
- Indications: prior to therapeutic ERCP in suspected biliary pancreatitis
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 
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. 
CT severity index 
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 and MCTSI|
|CTSI score ||MCTSI score |
|Degree of inflammation||Normal pancreas||0||0|
|Localized or diffuse enlargement||1||2|
|Single acute fluid collection||3||4|
|Multiple or extensive acute fluid collections||4|
|Degree of parenchymal necrosis||None||0||0|
|Presence of extrapancreatic complications||n/a||2|
| || |
Ranson criteria 
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 |
|Parameter||Nonbiliary pancreatitis||Biliary pancreatitis|
|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|
- Mainly used in the ICU setting to determine the severity of acute pancreatitis
- Scores ≥ 8 indicate severe pancreatitis with a guarded prognosis. 
Bedside index of severity of acute pancreatitis (BISAP) 
- Used to estimate in-hospital mortality due to pancreatitis
- Each criterion is worth one point.
- BISAP ≥ 2 indicates severe pancreatitis.
The initial management is identical for all etiologies of acute pancreatitis and should be administered without delay. 
Acute stabilization 
- ABCDE survey
- Hemodynamic and respiratory support
- Maintain NPO status until potential causes of acute abdomen that require emergency surgery have been ruled out.
Goal-directed IV fluid therapy 
Fluids and infusion rate
- Crystalloids such as normal saline (NS) or lactated Ringer's solution (LR) are preferred. 
- Hemodynamically stable patients 
- 5–10 mL/kg/hour or 250–500 mL/hour
- Exercise caution in patients with renal or cardiovascular disease.
Hemodynamically unstable patients
- Administer rapid fluid bolus (e.g., for adults NS or LR 500–1000 mL IV bolus over 10–30 minutes).
- Repeat as needed based on response.
- See also “Fluid resuscitation” for further detail.
- Monitor vitals, oxygen saturation, and urine output every 1–2 hours during the initial period of fluid resuscitation.
- Obtain laboratory studies (CBC, BMP, HCT) every 6–12 hours to monitor adequacy of fluid resuscitation and tissue perfusion.
- Perform serial physical examination every 4–6 hours to assess for abdominal compartment syndrome.
- Fluid therapy goals in acute pancreatitis 
- Replete electrolytes as needed.
- Antiemetics as needed (e.g., ondansetron , metoclopramide )
- Multidisciplinary care is ideal.
- Urgent gastroenterology, surgery, and/or interventional radiology for cholangitis, choledocholithiasis, or localized complications.
- 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. 
- Early oral feeding: Begin as soon as tolerated (i.e., not causing pain, nausea, or vomiting), ideally within 24 hours. 
- Enteral tube (nasogastric or nasojejunal): preferred over parenteral nutrition if patients cannot tolerate oral intake 
- Parenteral nutrition (total or partial): only in patients who cannot tolerate enteral feeds (e.g., those with persistent paralytic ileus) 
Management of the underlying cause
Therapeutic ERCP 
- Indication: biliary pancreatitis associated with cholangitis or persistent CBD obstruction
- Timing: Urgent therapeutic ERCP (within < 24 hours) is indicated if there is concurrent cholangitis.
- Procedure: sphincterotomy and stone removal; see “Treatment of choledocholithiasis”
- Complications: aggravation of pancreatitis, perforation, hemorrhage 
- Cholecystectomy 
- Initiate measures to rapidly decrease triglyceride levels alongside fluid resuscitation and analgesia.
- Evaluate for secondary causes of hypertriglyceridemia ; consider screening for familial hypertriglyceridemia if none are present.
- Long-term management
- Initiate long-term lipid-lowering therapy e.g., with fibrates, as soon as tolerated to prevent recurrences.
- Dietary and lifestyle modifications
- See “Treatment of hypertriglyceridemia in adults” for details.
Hypercalcemia-induced pancreatitis 
- Initial treatment: See “Treatment of hypercalcemia.”
- Definitive management: Investigate for primary hyperparathyroidism; if this is the underlying cause, perform parathyroidectomy.
- Check magnesium and phosphorus levels and replete as needed. 
- Vitamin supplementation (thiamine, pyridoxine)
- See “Treatment of alcohol use disorder” for details.
- Provide before discharge. 
- Start oxygen therapy if hypoxic.
- Establish IV access with two large-bore cannulas.
- Commence goal-directed IV fluid resuscitation.
- Replete electrolytes as needed.
- Administer supportive therapy: analgesics (e.g., NSAIDs), antiemetics
- Obtain ultrasound abdomen for all patients and CT abdomen in cases of diagnostic uncertainty.
- Establish the diagnosis based on the diagnostic criteria for acute pancreatitis.
- Assess severity, e.g., revised Atlanta grades of severity, BISAP , APACHE II
- Urgent consults as needed, e.g.,
- Admit to hospital; consider ICU admission if any of the following are present:
- Monitor vitals, urine output, laboratory studies, and perform serial abdominal examinations (see “Fluid therapy goals for acute pancreatitis”).
- Initiate enteral nutrition (either PO or via nasogastric or nasojejunal tube) as early as tolerated.
- Identify and treat the underlying cause.
Special patient groups
Acute pancreatitis during pregnancy 
- Etiology: most commonly gallstones, heavy alcohol use, and familial hypertriglyceridemia
- Clinical features: See “ ” above.
- Imaging: abdominal ultrasound or MRI are preferred (e.g., to identify choledocholithiasis or complications of acute pancreatitis such as hemorrhage, edema, or pseudocysts)
- Identical to that for nonpregnant individuals (see “” above)
- See “” for further details.
|Overview of acute and chronic pancreatitis|
|Acute pancreatitis||Chronic pancreatitis|
|Characteristics|| || |
|Etiology||Most common causes|
|Less common causes|
|Course|| || |
|Clinical features||Main symptoms|
|Imaging|| || |
| || |
Necrotizing pancreatitis 
- Definition: necrosis of pancreatic and peripancreatic tissue
- Clinical features: fever, persistent tachycardia, or insufficient symptomatic improvement over several days
- Diagnostics: nonenhancing areas of pancreatic parenchyma on CECT abdomen 
- Treatment 
Infected necrotizing pancreatitis 
- Definition: bacterial superinfection of necrotic pancreatic parenchyma
- Clinical features: similar to those of necrotizing pancreatitis
- Supportive care: fluid therapy, analgesics, nutritional support
- Broad-spectrum empiric antibiotics with good tissue penetration (e.g., carbapenems ) for 4 weeks 
- Drainage of infected material if there is clinical deterioration or persistence of symptoms despite antibiotic therapy
- Prognosis: high mortality rate (30%) 
- Diagnostics: CT abdomen with IV contrast showing an encapsulated heterogeneous collection containing fluid and debris 
- Treatment (of symptomatic walled-off necrosis): percutaneous drainage or transmural endoscopic necrosectomy 
Other localized complications 
Systemic complications 
- Shock, SIRS, sepsis,
- Pneumonia, respiratory failure, 
- Pleural effusion
- Prerenal failure due to volume depletion
- Paralytic ileus
- Pancreatic ascites
We list the most important complications. The selection is not exhaustive.
Important predictors of severity
- Age > 55
- Gastrointestinal bleeding
- Fall in Hct within 48 hours
- Hypocalcemia and/or hyperglycemia
- Inflammatory markers: ↑↑ CRP, ↑ IL-6, ↑ IL-8
- Evidence of shock and/or organ failure
- CT findings: pancreatic edema, peripancreatic fluid collection, and/or necrosis of > 33% of the pancreas
- See “Severity scores for acute pancreatitis” for details.