Pancreatitis, Acute

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Basics

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

Incidence
1 to 5/10,000, with no predominant age or sex

Prevalence
  • 19/10,000
  • It is the most common gastrointestinal diagnosis for inpatient hospitalization.

Etiology and Pathophysiology

  • Alcohol—most common in adults (ages 30–50)
  • Gallstones (including microlithiasis)–most common in adults (median age of 69)
  • Trauma/surgery–most common in adults (median age of 65)
  • 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
    • Sulfamethoxazole/trimethoprim, pentamidine
    • Valproic acid
    • Statins
  • Metabolic causes
    • Hypertriglyceridemia (classically >1,000 mg/dL); even nonfasting levels as low as ~≥177 mg/dL.
    • 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
  • Penetrating peptic ulcer (rare)
  • AIDS
  • Cystic fibrosis, CFTR gene mutations, and other mutations
  • Tumors (e.g., pancreatic, ampullary)
  • Miscellaneous obstruction
    • Celiac disease
    • Crohn disease
    • Pancreas divisum
    • Sphincter of Oddi dysfunction
    • Choledochocele
  • Scorpion venom
  • Acute fatty liver of pregnancy
  • Idiopathic
  • Associated coexisting risk factors
    • Obesity
    • Type II diabetes
    • Smoking
  • Pathophysiology—enzymatic autodigestion of the pancreas with interstitial edema and third spacing of fluid. Possible sequalae 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 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

Genetics
  • Hereditary pancreatitis is rare; autosomal dominant
  • Polymorphisms and mutations in multiple genes

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. Decreased risk of gallstone pancreatitis with diet high in fiber and vitamin D. There is a decreased risk of nongallstone 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).

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Basics

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

Incidence
1 to 5/10,000, with no predominant age or sex

Prevalence
  • 19/10,000
  • It is the most common gastrointestinal diagnosis for inpatient hospitalization.

Etiology and Pathophysiology

  • Alcohol—most common in adults (ages 30–50)
  • Gallstones (including microlithiasis)–most common in adults (median age of 69)
  • Trauma/surgery–most common in adults (median age of 65)
  • 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
    • Sulfamethoxazole/trimethoprim, pentamidine
    • Valproic acid
    • Statins
  • Metabolic causes
    • Hypertriglyceridemia (classically >1,000 mg/dL); even nonfasting levels as low as ~≥177 mg/dL.
    • 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
  • Penetrating peptic ulcer (rare)
  • AIDS
  • Cystic fibrosis, CFTR gene mutations, and other mutations
  • Tumors (e.g., pancreatic, ampullary)
  • Miscellaneous obstruction
    • Celiac disease
    • Crohn disease
    • Pancreas divisum
    • Sphincter of Oddi dysfunction
    • Choledochocele
  • Scorpion venom
  • Acute fatty liver of pregnancy
  • Idiopathic
  • Associated coexisting risk factors
    • Obesity
    • Type II diabetes
    • Smoking
  • Pathophysiology—enzymatic autodigestion of the pancreas with interstitial edema and third spacing of fluid. Possible sequalae 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 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

Genetics
  • Hereditary pancreatitis is rare; autosomal dominant
  • Polymorphisms and mutations in multiple genes

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. Decreased risk of gallstone pancreatitis with diet high in fiber and vitamin D. There is a decreased risk of nongallstone 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).

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