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.
• Acute discontinuation of medications for diabetes or hyperlipidemia
• Following endoscopic retrograde cholangiopancreatography (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 (3rd 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 virus, 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; possible sequelae include necrosis, pseudocyst formation, pancreatic ductal disruption, pancreatic ascites, multiorgan failure (early or late), walled-off necrosis (late), and injury to surrounding vascular structures such as splenic vein thrombosis and splenic artery pseudoaneurysm.
• 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 1st 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

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).