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Acute inflammatory process of the pancreas with variable involvement of regional tissue or remote organ systems
- Inflammatory episode with symptoms related to intrapancreatic activation of enzymes with pain, nausea and vomiting, and associated intestinal ileus
- Varies widely in severity, complications, and prognosis, accounting for ~280,000 hospital admissions per year in the United States
- Complete structural and functional recovery if there is no necrosis or pancreatic ductal disruption
- 1 to 5/10,000
- Predominant age: none
- Predominant sex: male = female
- Acute: 19/10,000
- Acute pancreatitis is the most common gastrointestinal diagnosis for inpatient hospitalization.
Etiology and Pathophysiology
- Gallstones (including microlithiasis)
- Acute discontinuation of medications for diabetes or hyperlipidemia
- Following endoscopic retrograde cholangiopancreatography (ERCP)
- Medications (most common, not an exhaustive list)
- ACE inhibitors; angiotensin receptor blockers (ARBs); thiazide diuretics and furosemide
- Antimetabolites (mercaptopurine and azathioprine)
- Corticosteroids; glyburide; exenatide
- Mesalamine; pentamidine
- Valproic acid
- HMG-CoA reductase inhibitors
- Review all medications and continue only if benefit outweighs risk.
- Metabolic causes
- Hypertriglyceridemia (classically >1,000 mg/dL); even nonfasting levels as low as ~≥177 mg/dL have been associated with acute pancreatitis.
- Hypercalcemia; acute renal failure
- Diet with high glycemic load
- Systemic lupus erythematosus/polyarteritis
- Autoimmune; with/without elevated IgG4
- Mumps, coxsackie, CMV, EBV, cryptosporidiosis, ascaris, clonorchis
- Penetrating peptic ulcer (rare)
- Cystic fibrosis and CFTR gene mutations
- Tumors (e.g., pancreatic, ampullary)
- Miscellaneous obstruction
- Celiac disease
- Crohn disease
- Pancreas divisum
- Sphincter of Oddi dysfunction
- Scorpion venom; vascular disease
- Acute fatty liver of pregnancy
- Associated coexisting risk factors
- Type II Diabetes
- Pathophysiology—enzymatic “autodigestion” of the pancreas, interstitial edema with severe interstitial acute fluid accumulation (“3rd spacing”), hemorrhage, necrosis, release of vasoactive peptides (within 6 weeks), pseudocyst or acute necrotic collection (>6 weeks), pancreatic ductal disruption, injury to surrounding vascular structures-splenic vein (thrombosis) and splenic artery (pseudoaneurysm)
- 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 increasing severity of acute pancreatitis: age ≥ 60 years; obesity; long-term, heavy alcohol use.
- Hereditary pancreatitis is rare; autosomal dominant
- Polymorphisms and mutations in multiple genes
- 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. Decreased risk of gallstone pancreatitis with diet high in fiber and vitamin D. There is a decreased risk of non-gallstone pancreatitis with diets high in fiber, coffee, and caffeine.
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).