Pancreas - Acute pancreatitis

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Pancreas

Pancreatitis

Acute pancreatitis

Reviewer: Deepali Jain, M.D. (see Reviewers page)
Revised: 22 November 2012, last major update August 2012
Copyright: (c) 2001-2012, PathologyOutlines.com, Inc.

General
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● Acute onset of abdominal pain due to enzymatic necrosis and inflammation of pancreas (Wikipedia)
● Symptoms: abdominal pain, high white blood count, DIC, ARDS, diffuse fat necrosis, peripheral vascular collapse, acute tubular necrosis, shock (blood loss, electrolyte disturbances, endotoxemia, release of cytokines), hypocalcemia, hyperglycemia
● Complications: sterile pancreatic abscess, pancreatic pseudocyst, infected pancreatic necrosis, large vessel thrombi in nearby vessels, distant fat necrosis
● Unexpected deaths may occur in early phase of disease (Am J Forensic Med Pathol 2007;28:267)

Terminology
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● Acute interstitial pancreatitis: mild, with edema and fat necrosis only
● Acute necrotizing pancreatitis: more severe, may get hemorrhagic pancreatitis as well as fat necrosis
● Bile pancreatitis: bile reflux through common bile duct into pancreatic duct due to abnormal junction (Arch Pathol Lab Med 1985;109:433)
● Infected pancreatic necrosis: secondary infection of necrotic foci
● Postoperative pancreatitis: due to trauma of exploration of common bile duct, gastric resection, papillary stenosis plus sphincterotomy

Epidemiology
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● 20 cases/100,000 in US, 80% associated with biliary tract disease or alcoholism
● Note: 1/3 to 2/3 of patients have gallstones, but only 5% with gallstones develop pancreatitis
● 75% of gallstone related cases occur in women
● 86% of alcohol related cases occur in men
● Alcoholism associated: 2/3 of all cases in US, 5% in UK

Pathophysiology
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● Due to autodigestion by inappropriately activated enzymes
● Trypsin activates digestive enzymes as well as prekallikrien, which activates clotting and complement systems, amplifying small vessel thrombosis
● Obstruction from gallstones or alcohol associated concretions increases intraductal pressure, causing enzyme-rich interstitial fluid to accumulate, which causes fat necrosis, which attracts neutrophils that release cytokines and cause interstitial edema, which impairs blood flow and causes ischemia and acinar cell injury
● Acinar cell injury also caused by infections, drugs, trauma, shock, premature release of proenzymes and lysosomal hydrolases
● Obstruction or alcohol cause proenzymes to be delivered in an intracellular compartment with lysosomal hydrolases, which may activate them prematurely
● Alcohol may also reactivate chronic pancreatitis due to secretion of protein-rich pancreatic fluid, which causes deposition of inspissated protein plugs, causing obstruction of small pancreatic ducts

Etiology
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● Common channel between common bile duct and main pancreatic duct due to migrating gallstone, biliary sludge, spasm of sphincter of Oddi (although 50% of normals also have a common channel)
● Infectious causes: Actinomyces, adenovirus in immunocompromised (Hum Pathol 1993;24:1145), AIDS related toxoplasmosis, Ascaris lumbricoides, aspergillus, Campylobacter jejuni, Clonorchis sinensis, CMV, coccidioides, coxsackie virus, cryptococcus, EBV, Echinococcus granulosus, Hepatitis A and B, herpes simplex, histoplasma, HIV, mumps, mycobacterium, Mycoplasma pneumoniae, nocardia, rubella, paracoccidioides, Pneumocystis jiroveci, Rocky Mountain spotted fever/Rickettsiae (Arch Pathol Lab Med 1984;108:963), Salmonella typhi, Strongyloides stercoralis, Yersinia enterocolitica
● Drugs: antiretroviral, azathioprine, estrogen, furosemide, methyldopa, pentamidine, procainamide, sulfa, thiazides
● Other: acute ischemia (thromboemboli, vasculitis, shock), anatomic abnormalities such as pancreas divisum, hyperlipidemia, hyperparathyroidism or other causes of hypercalcemia, hyperthyroidism, idiopathic (10%), SLE, trauma (including post-operative)

Diagnosis
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● Elevated amylase (also seen in abdominal aortic aneurysm, duodenal ulcer, gangrenous cholecystitis, mesenteric thrombosis, volvulus), elevated lipase, elevated C reactive protein, Xray (large and inflamed pancreas)

Prognostic factors
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● 5% die of shock during first week
● Overall mortality is 20% (10% if swollen/edematous vs. 50% if hemorrhagic/necrotic)
● Acute respiratory distress syndrome or acute renal failure are poor prognostic factors

Treatment
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● Rest the pancreas by food/fluid restriction

Gross description
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● Swollen, indurated, edematous or hemorrhagic/necrotic, yellow nodules represent fat necrosis in pancreas, mesenteric and peritoneal fat
● May spread to colon and cause ileus, stenosis, perforation, fistulas

Gross images
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Fat necrosis

Micro description
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● Classified as either acute interstitial or acute hemorrhagic types
● Acute interstitial: typically an acute inflammatory cell infiltrate admixed with edema and fibrinous exudate
● Acute hemorrhagic: patchy necrosis typically in a periductal or perilobular distribution with a sparing of portions of the pancreas; diffuse interstitial edema due to microvascular leakage, fat necrosis, neutrophils, acinar and blood vessel destruction, interstitial hemorrhage
● Also acinar cell homogenization, ductal dilation with mucinous or squamous metaplasia, fibroblasts, thrombi in capillaries and venules
● Initially neutrophils are present, then macrophages and later lymphocytes
● Calcification occurs early and extensively

Micro images
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Hemorrhage, necrosis, fat necrosis, neutrophils

Differential diagnosis
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● Acute abdomen, including acute cholecystitis with rupture, appendicitis, occlusion of mesenteric vessels with bowel infarction, perforated peptic ulcer

End of Pancreas > Pancreatitis > Acute pancreatitis

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