Description

Acute inflammation of the pancreas with variable involvement of regional tissue or remote organ systems

• Symptoms relate to intrapancreatic activation of enzymes with pain, nausea and vomiting, and associated intestinal ileus
• Complete structural and functional recovery if there is no necrosis or pancreatic ductal disruption

Epidemiology

Etiology and Pathophysiology

• Together, gallstones (including microlithiasis) and chronic alcohol use account for >80% of cases.
• Postendoscopic retrograde cholangiopancreatography (post-ERCP)
• Medications (most common)
  • ACE inhibitors; angiotensin receptor blockers (ARBs); thiazide diuretics and furosemide
  • Antimetabolites (mercaptopurine and azathioprine) and checkpoint inhibitors
  • Corticosteroids; glyburide; exenatide
  • Mesalamine; sulfamethoxazole/trimethoprim, pentamidine; valproic acid; statins
  • NSAIDs, opiates
• Metabolic causes
  • Hypertriglyceridemia (classically >1,000 mg/dL); even nonfasting levels as low as ~≥177 mg/dL (third overall most common cause, ~10% of cases)
  • Hypercalcemia; acute renal failure
  • Diet with high glycemic load
  • Systemic lupus erythematosus/polyarteritis/other vascular disease
  • Autoimmune; type I with elevated IgG4 and type II with normal IgG4
  • Infections: mumps, coxsackie, CMV, EBV, cryptosporidiosis, ascaris, Clonorchis; SARS CoV-2
• Penetrating peptic ulcer (rare)
• AIDS
• Cystic fibrosis, CFTR gene mutations, and other mutations
• Tumors (e.g., pancreatic, ampullary)
• Trauma/surgery
• Miscellaneous obstruction: celiac disease; Crohn disease; pancreas divisum; sphincter of Oddi dysfunction; choledochocele
• Scorpion venom
• Acute fatty liver of pregnancy
• Pancreatic fat deposition
• Associated coexisting risk factors: obesity; type II diabetes; smoking
• Pathophysiology—enzymatic autodigestion of the pancreas with interstitial edema and third spacing of fluid.
• Cellular injury alters membrane trafficking, which alters lysosomal function leading to trypsin formation and zymogen activation. A robust inflammatory response ensues resulting in increased vascular permeability, hemorrhage, edema, and necrosis.
• The severity of the first episode of acute pancreatitis, alcohol abuse, and smoking all increase the risk of acute recurrent pancreatitis, which, in turn, increases the risk of progression to chronic pancreatitis.
• Clinical features associated with an increasing severity of acute pancreatitis: age ≥60 years; obesity; long-term, heavy alcohol use; altered mental status

General Prevention

• Avoid excess alcohol consumption.
• Tobacco cessation
• Correct underlying metabolic processes (hypertriglyceridemia or hypercalcemia).
• Discontinue offending medications.
• Cholecystectomy (symptomatic cholelithiasis)
• Diet: There is an increased risk of gallstone pancreatitis with diets high in saturated fats, cholesterol, red meat, and eggs.

Commonly Associated Conditions

• Alcohol withdrawal, alcoholic hepatitis, diabetic ketoacidosis, and ascending cholangitis
• Morbid obesity, a pro-inflammatory state, increases severity and adverse outcomes (organ failure, mortality).

History

• Acute onset of epigastric pain, which may radiate posteriorly
• Nausea/vomiting
• Alcohol use
• Personal or family history of gallstones
• Medication use—look for inciting medications
• Abdominal trauma
• Recent significant rapid weight loss

Physical Exam

• Vital signs—Assess hemodynamic stability; fever; tachycardia; hypotension.
• Abdominal findings: epigastric tenderness, loss of bowel sounds, peritoneal signs
• Other findings: jaundice, rales/percussive dullness
• Rare (with hemorrhagic pancreatitis): flank discoloration (Grey Turner sign) or umbilical discoloration (Cullen sign)

Differential Diagnosis

• Penetrating peptic ulcer
• Acute cholecystitis or cholangitis
• Macroamylasemia, macrolipasemia
• Mesenteric vascular occlusion and/or infarction
• Intestinal obstruction; perforated viscus
• Aortic aneurysm (dissecting or rupturing)
• Inferior wall myocardial infarction
• Lymphoma

Diagnostic Tests & Interpretation

• Interpret laboratory and radiographic findings in the context of the clinical history.
• Diagnosis typically requires two of the following three criteria:
  • Upper abdominal pain
  • Serum lipase or amylase >3× ULN
  • Characteristic findings on CT
• There are several scoring systems to assess severity (BISAP, Ranson criteria, HAPS, etc.); however, none have been shown to be superior.
• Presence of SIRS is more easily adaptable and its presence for ≥48 hours indicates poor prognosis.
• Lipase is more specific to the pancreas than amylase. In addition, lipase has a longer half-life, and is preferred in patients who present later after pain onset.
• Elevated total bilirubin. If >3 mg/dL, consider common bile duct obstruction.
• A 3-fold elevation in the alanine aminotransferase (ALT) in the setting of acute pancreatitis has a 95% positive predictive value for gallstone pancreatitis. Triglyceride levels >1,000 mg/dL suggest hypertriglyceridemia as the cause.
• Glucose and calcium increased in severe disease.
• WBC elevation to 10,000 to 25,000/μL possible and not indicative of active infection
• Elevated baseline hematocrit >44 or rising hematocrit is poor prognostic sign (severe third spacing with associated hemoconcentration).

General Measures

Many cases of acute pancreatitis require hospitalization; ICU if multiorgan dysfunction or hypotension/respiratory failure; 15–20% of cases of acute pancreatitis progress from mild to severe (including persistent organ failure).

• Fluid resuscitation
  • Patients may have significant volume deficit due to third spacing
  • Infuse bolus of 10 mL/kg, followed by 1.5 mL/kg/hr. Larger volumes may be required for patients presenting with severe pancreatitis, preferably with CVP monitoring (1)[A].
  • Lactated Ringer solution preferred over normal saline for initial fluid resuscitation, in patients without hypercalcemia, to decrease risk of systemic inflammation/SIRS and due to its less acidic pH
  • Target urine output should be 0.5 to 1.0 mL/kg/hr. 4 L should be the maximum total fluid on day 1.
  • Fluid resuscitation is of limited value after 24 hours, and fluid overload results in significant complications.
    • Eliminate unnecessary medications, especially those implicated as causes of pancreatitis.
    • Nasogastric (NG) tube for intractable emesis
    • Follow renal function, volume status, calcium, and oxygenation. Organ failure is more important prognostic indicator than pancreatic necrosis.
    • Nutritional support: Begin oral alimentation after pain, tenderness, and ileus have resolved; small amounts of high-carbohydrate, low-fat, and low-protein foods; advance as tolerated. In cases of mild pancreatitis, a soft low-fat diet may be started as soon as tolerated even before enzymes elevation and pain have completely resolved. Enteral nutrition can be considered for severe pancreatitis at 72 hours (or earlier if tolerated); nasogastric, nasoduodenal, and nasojejunal are all safe routes that can be used. However, nasojejunal tube route is preferred if there is digestive intolerance from gastric outlet obstruction or delayed gastric emptying. Discontinue with increases in pain, increases in amylase/lipase levels, or fluid retention; TPN (without lipids if triglycerides are elevated) if oral or nasoenteric feedings are not tolerated

Medication

Issues for Referral

Refer to a tertiary center if pancreatitis is severe or actively evolving and when advanced imaging or endoscopic therapy is being considered.

Surgery/Other Procedures

• Consider cholecystectomy before discharge in patients with uncomplicated acute biliary (nonnecrotizing) pancreatitis to reduce risk of recurrence.
• Necrosectomy should be performed nonsurgically for either infected or noninfected necrosis. Walled-off necrosis should be observed for 4 weeks and treated with antibiotics if infected.
• ERCP early if evidence of acute cholangitis or at 72 hours if evidence of ongoing biliary obstruction; ERCP with pancreatic ductal stent placement, if ductal disruption persists longer than 1 to 2 weeks.
• Plasma exchange with insulin within 24 hours of presentation if severe necrotizing pancreatitis secondary to hypertriglyceridemia

Admission, Inpatient, and Nursing Considerations

Discharge criteria

• Pain controlled
• Tolerating oral diet
• Alcohol rehabilitation and tobacco cessation
• Low-grade fever and mild leukocytosis do not necessarily indicate infection and may take weeks to resolve. Infections may occur even after 10 days (33% of patients with necrotizing pancreatitis) due to secondary infection of necrotic material, requiring surgical débridement.

Follow-up Recommendations

• Follow-up imaging in several weeks if the original CT scan showed a fluid collection or necrosis or if the amylase/lipase continue to be elevated. Follow-up findings may include:
  • Pseudocyst (occurs in 10%) or abscess (sudden onset of fever)
  • Splenic vein thrombosis in 16–18% with necrotizing pancreatitis
  • Pseudoaneurysm (splenic, gastroduodenal, intrapancreatic) hemorrhage can be life-threatening.
• Mild exocrine and endocrine dysfunction is usually subclinical. Patients with necrotizing pancreatitis, steatorrhea, or ductal obstruction should receive enzyme supplementation.
• After the first episode of acute pancreatitis, the risk of lifetime diabetes doubles, the risk of developing acute recurrent pancreatitis is ~17%, and the risk for developing chronic pancreatitis is ~8%.

Diet

Advance diet as tolerated; reduce fat, alcohol, and added sugars.

Prognosis

85–90% of cases of acute pancreatitis resolve spontaneously; 3–5% mortality (17% in necrotizing pancreatitis)

Complications

AKI, ARDS, ascites, chronic pancreatitis/pancreatic insufficiency, DIC, multiorgan failure, necrotizing pancreatitis, pancreatic abscess, intestinal or bowel obstruction, pseudocyst, pseudoaneurysm, venous thrombosis

Additional Reading

• Beij A, Verdonk RC, van Santvoort HC, et al. Acute pancreatitis: an update of evidence-based management and recent trends in treatment strategies. United European Gastroenterol J. 2025;13(1):97–106.  [PMID:39804691]
• Trikudanathan G, Yazici C, Evans Phillips A, et al. Diagnosis and management of acute pancreatitis. Gastroenterology. 2024;167(4):673–688.  [PMID:38759844]

ICD-10

• K85.9 Acute pancreatitis, unspecified
• K85.8 Other acute pancreatitis
• K85.2 Alcohol induced acute pancreatitis
• K85.3 Drug induced acute pancreatitis
• K85.1 Biliary acute pancreatitis
• K85.0 Idiopathic acute pancreatitis

SNOMED

• 197456007 Acute pancreatitis (disorder)
• 235949005 Familial acute pancreatitis (disorder)
• 235942001 Alcohol-induced acute pancreatitis (disorder)
• 235944000 Drug-induced acute pancreatitis
• 235943006 Idiopathic acute pancreatitis (disorder)
• 235941008 Gallstone acute pancreatitis (disorder)
• 235950005 Traumatic acute pancreatitis