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General Considerations
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Most cases of acute pancreatitis are related to biliary tract disease (a passed gallstone, usually < 5 mm in diameter) or heavy alcohol intake The exact pathogenesis is not known but may include edema or obstruction of the ampulla of Vater, reflux of bile into pancreatic ducts, and direct injury of pancreatic acinar cells by prematurely activated pancreatic enzymes Among the numerous other causes or associations are hypercalcemia, hyperlipidemias (chylomicronemia, hypertriglyceridemia, or both), abdominal trauma (including surgery), drugs (including azathioprine, mercaptopurine, asparaginase, pentamidine, didanosine, valproic acid, tetracyclines, estrogen and tamoxifen [by raising serum triglycerides], sulfonamides, mesalamine, thiazides, and possibly glucocorticoids), vasculitis, infections (eg, mumps, cytomegalovirus, Mycobacterium avium complex), peritoneal dialysis, cardiopulmonary bypass, ERCP, and genetic mutations that also predispose to chronic pancreatitis (see below) In patients with pancreas divisum, a congenital anomaly in which the dorsal and ventral pancreatic ducts fail to fuse, acute pancreatitis may result from stenosis of the minor papilla with obstruction to flow from the accessory pancreatic duct, although concomitant mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene have also been reported to account for acute pancreatitis in some patients with pancreas divisum Acute pancreatitis may also result from anomalous union of the pancreaticobiliary duct Rarely, acute pancreatitis may be the presenting manifestation of a pancreatic or ampullary neoplasm Apparently idiopathic acute pancreatitis is often caused by occult biliary microlithiasis and may be caused by sphincter of Oddi dysfunction involving the pancreatic duct No more than 20% of cases are truly idiopathic Smoking may increase the risk of alcoholic and idiopathic pancreatitis, and older age and obesity increase the risk of a severe course
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Prognosis
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Survival of patients with primary sclerosing cholangitis averages 12 17 years Adverse prognostic markers are older age, hepatosplenomegaly, higher serum bilirubin and AST levels, lower albumin levels, a history of variceal bleeding, a dominant bile duct stricture, and extrahepatic duct changes Variceal bleeding is also a risk factor for cholangiocarinoma Actuarial survival rates with liver transplantation are as high as 85% at 3 years, but rates are much lower once cholangiocarcinoma has developed Following transplantation, patients have an increased risk of nonanastomotic biliary strictures and in those with ulcerative colitis colon cancer The retransplantation rate is higher than that for primary biliary cirrhosis Those patients who are unable to undergo liver transplantation will ultimately require high-quality palliative care (see 5)
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Abdalian R et al Sclerosing cholangitis: a focus on secondary causes Hepatology 2006 Nov;44(5):1063 74 [PMID: 17058222] Berstad AE et al Diagnostic accuracy of magnetic resonance and endoscopic retrograde cholangiography in primary sclerosing cholangitis Clin Gastroenterol Hepatol 2006 Apr;4(4):514 20 [PMID: 16616358] LaRusso NF et al Primary sclerosing cholangitis: summary of a workshop Hepatology 2006 Sep;44(3):746 64 [PMID: 16941705] Prytz H et al; Swedish Internal Medicine Liver Club Dynamic FDG-PET is useful for detection of cholangiocarcinoma in patients with PSC listed for liver transplantation Hepatology 2006 Dec;44(6):1572 80 [PMID: 17133469] Tischendorf JJ et al Characterization, outcome, and prognosis in 273 patients with primary sclerosing cholangitis: a single center study Am J Gastroenterol 2007 Jan;102(1):107 14 [PMID: 17037993]
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A Symptoms and Signs
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Epigastric abdominal pain, generally abrupt in onset, is steady, boring, and severe and often made worse by walking and lying supine and better by sitting and leaning forward The pain usually radiates into the back but may radiate to the right or left Nausea and vomiting are usually present Weakness, sweating, and anxiety are noted in severe attacks There may be a history of alcohol intake or a heavy meal immediately preceding the attack, or a history of milder similar episodes or biliary pain in the past The abdomen is tender mainly in the upper part, most often without guarding, rigidity, or rebound The abdomen may be distended, and bowel sounds may be absent with associated ileus Fever of 384 39 C, tachycardia,
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