n e w e ng l a n d j o u r na l
m e dic i n e
David C. Whitcomb, M.D., Ph.D.
This Journal feature begins with a case vignette highlighting a common clinical problem. Evidence supporting various strategies is then presented, followed by a review of formal guidelines, when they exist. The article ends with the author’s clinicalrecommendations.
A 56-year-old woman presents with severe epigastric pain and vomiting of 14 hours’ duration, symptoms that had developed shortly after dinner the previous night. She has no history of alcohol use, takes no medications, and has no family history of pancreatitis. On physical examination, she has a heart rate of 110 beats per minute and moderate epigastric abdominal tenderness withoutperitoneal signs. The white-cell count is 16,500 per cubic millimeter, and the hematocrit is 49 percent. The serum amylase level is 1450 IU per liter, the serum lipase level is 3200 IU per liter, the serum alanine aminotransferase level is 280 IU per liter, and the serum lactate dehydrogenase level is 860 IU per liter. Calcium, albumin, triglyceride, and electrolyte values are normal. How should thepatient be further evaluated and treated?
The Cl inic a l Probl e m
From the Division of Gastroenterology, Hepatology, and Nutrition, University of Pittsburgh, Pittsburgh. Address reprint requests to Dr. Whitcomb at the University of Pittsburgh Medical Center Presbyterian, Mezzanine Level 2, C Wing, 200 Lothrop St., Pittsburgh, PA 15213, or at firstname.lastname@example.org. N Engl J Med 2006;354:2142-50.Copyright © 2006 Massachusetts Medical Society.
Acute pancreatitis accounts for more than 220,000 hospital admissions in the United States each year.1 The disease occurs at a similar frequency among various age groups, but the cause of the condition and the likelihood of death vary according to age, sex, race, body-mass index (the weight in kilograms divided by the square of the height inmeters), and other factors. The most important risk factors for pancreatitis in adults are gallstones and excessive alcohol use, although clinically detected pancreatitis never develops in most persons with these risk factors.2,3 The incidence of gallstone pancreatitis is increased among white women over the age of 60 years4,5 and is highest among patients with small gallstones (less than 5 mm indiameter) or microlithiasis.3,5 Excessive alcohol use as a cause of pancreatitis is more common among men than women6; the association between alcohol consumption and acute pancreatitis is complex but appears to be dose-dependent. Other causes include metabolic aberrations (e.g., hypertriglyceridemia), duct obstruction (e.g., related to a tumor or pancreas divisum), medications (e.g., azathioprine,thiazides, and estrogens), and trauma. In children, the distribution of causes differs from that in adults, with systemic diseases and trauma particularly common.7 About 20 percent of cases in adults remain idiopathic, although this classification is expected to become less common as factors of genetic predisposition and environmental susceptibility are elucidated.8 Overall, about 20 percent ofpatients with acute pancreatitis have a severe course, and 10 to 30 percent of those with severe acute pancreatitis die. Despite improvements in intensive care treatment during the past few decades, the rate of death has not significantly declined.9 The pathogenesis of acute pancreatitis relates to inappropriate activation of trypsinogen to trypsin (the key enzyme in the activation of pancreaticzymogens) and a lack of prompt elimination of active trypsin inside the pancreas.8 Activation of diges-
n engl j med 354;20
may 18, 2006
Downloaded from www.nejm.org on March 10, 2009 . Copyright © 2006 Massachusetts Medical Society. All rights reserved.
clinical pr actice
tive enzymes causes pancreatic injury and results in an inflammatory response that is out...