Pancreas
Pancreatitis
Acute pancreatitis

Author: Deepali Jain, M.D. (see Authors page)

Revised: 8 December 2017, last major update August 2012

Copyright: (c) 2002-2017, PathologyOutlines.com, Inc.

PubMed Search: Acute pancreatitis[TI] pancreas[TI] free full text[sb]

Cite this page: Jain, D. Acute pancreatitis. PathologyOutlines.com website. http://www.pathologyoutlines.com/topic/pancreasacute.html. Accessed February 19th, 2018.
Definition / general
  • Acute onset of abdominal pain due to enzymatic necrosis and inflammation of pancreas (Wikipedia: Acute Pancreatitis [Accessed 8 December 2017])
  • 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
  • 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
  • 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
  • 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
  • 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, coxsackievirus, 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 / Rickettsia (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 postoperative)
Diagnosis
  • 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
  • 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
  • Rest the pancreas by food / fluid restriction
Gross description
  • 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

Microscopic (histologic) description
  • 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
Microscopic (histologic) images

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Hemorrhage, necrosis, fat necrosis, neutrophils

Differential diagnosis