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Evaluation of Acute Pancreatitis in the Older Patient

  • Fri, 9/5/08 - 4:54pm
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  • 3763 reads
Citation: 

Pages 30 - 35

Author(s): 

Adam H. Skolnick, MD, Edward R. Feller, MD, FACP, and Aman Nanda, MD, CMD

Introduction
As many as 30% of acute pancreatitis occurs in patients older than age 65 years.1 A minority are severe, with local complications and organ failure with or without morphologic changes on computed tomography (CT) scan indicative of pancreatic necrosis.2 Severe acute pancreatitis is associated with an 8-10% mortality; in older patients, the mortality is as high as 20-25%.3 A greater propensity to fulminant disease in old age has been attributed to diminished organ function reserve, comorbid illness, diminishing ability to tolerate fluid shifts, and susceptibility to ischemia and infection.4 Age-associated changes in the pancreas and biliary system are listed in Table I. We review the etiology, evaluation, and management of pancreatic inflammation in the elderly to alert clinicians to the unique features of acute pancreatitis in this age group.

Age-Related Structural Changes in the Pancreas
Diagnosis may be complicated by changes in organ structure with normal aging. Pancreatic ducts have been reported to dilate with age at an average of 8% per decade after age 40.5 Hastier and coworkers6 reported that only 31.4% (33 of 105) of patients older than age 70 years without pancreatic pathology had duct diameters within defined normal limits. The main pancreatic duct in some older patients may reach 1 cm in diameter without evidence of obstruction or clinical chronic pancreatitis. The dilation is generally insidious and uniform throughout the pancreas, unlike the subacute, irregular dilation commonly seen in chronic pancreatitis. In some older patients, ductal ectasia may be cystic, mimicking a pancreatic pseudocyst or cystic neoplasm. Ductal or parenchymal calculi may form, unassociated with chronic pancreatitis.7 In a Japanese review of 130,000 abdominal ultrasound examinations of asymptomatic patients, 84% of main pancreatic duct dilatations, 87% of cystic areas, and half of all calcifications were considered to be purely age-related, unassociated with any pathology.8

In an autopsy study of pancreatograms in 60 older patients without clinical history or histologic evidence of pancreatic disease, false-positive duct changes consistent with those of chronic pancreatitis were found in 81% of cases.9 Caution must be exercised in interpretation of pancreatograms because normal aging changes may simulate those of chronic pancreatitis or pancreatic carcinoma ( Table I). Increased diameter of the common bile duct of up to 10 mm has also been reported in aging, with normal levels post-cholecystectomy as high as 14 mm.10 On a gross level, the aged pancreas also atrophies.5 An atrophic gland, terminating abruptly on endoscopic or magnetic resonance pancreatography, may be misdiagnosed as an obstruction at that point.

Etiology
Pancreatitis in older patients, as compared with a younger cohort, is much more likely to be due to gallstone pancreatitis (Table II). In the elderly patient, the etiology of as many as 75% of episodes of acute pancreatitis is biliary disease. Contributing factors may include increased lithogenicity of bile, increased likelihood of infected bile, and increased propensity for gallstone formation.11

Although excessive alcohol use is a common cause of pancreatic inflammation in younger patients, only 5% of episodes in the older patient are due to alcohol abuse. Alcohol abuse is, however, the most common cause of chronic pancreatitis, which may present as an episode of acute pancreatitis unaccompanied by exocrine or endocrine insufficiency. Because covert alcohol use is common, routine evaluation of every older patient should include age-adjusted alcohol screening questions.12

Metabolic and medication-induced etiologies must also be assessed. Older women taking hormone replacement therapy are at risk for hypertriglyceridemic pancreatitis, thought to be due to free fatty acid release from serum triglycerides by the action of pancreatic lipase.

References: 

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2. Baron TH, Morgan DE. Acute necrotizing pancreatitis. N Engl J Med 1999;340:1412-1417.

3. Uomo G, Talamini G, Rabitti PG, et al. Influence of advanced age and related comorbidity on the course and outcome of acute pancreatitis. Ital J Gastroenterol Hepatol 1998;30:616-621.

4. Mayer KL, Frey CF. Benign diseases of the pancreas in the elderly. Probl Gen Surg 1997;3:91-107.

5. Kreel L, Sandin B. Changes in pancreatic morphology associated with aging. Gut 1973;14:962-970.

6. Hastier P, Buckley MJ, Dumas R, et al. A study of the effect of age on pancreatic duct morphology. Gastrointest Endosc 1998;48:53-57.

7. Nagai H, Ohtsubo K. Pancreatic lithiasis in the aged. Its clinicopathology and pathogenesis. Gastroenterology 1984;86:331-338.

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10. Kaim A, Steinke K, Frank M, et al. Diameter of the common bile duct in the elderly patient: Measurement by ultrasound. Eur Radiol 1998;8:1413-1415.

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14. Dassopoulos T, Ehrenpreis ED. Acute pancreatitis in human immunodeficiency virus-infected patients: A review. Am J Med 1999;107:78-84.

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20. Mohiuddin J, Katrak A, Junglee D, et al. Serum pancreatic enzymes in the elderly. Ann Clin Biochem 1984;21 (Pt 2):102.

21. Royse VL, Jensen DM, Corwin HL. Pancreatic enzymes in chronic renal failure. Arch Intern Med 1987;147:537-539.

22. Yadav D, Nair S, Norkus EP, Pitchumoni CS. Nonspecific hyperamylasemia and hyperlipasemia in diabetic ketoacidosis: Incidence and correlation with biochemical abnormalities. Am J Gastroenterol 2000;95:3123-3128.

23. Lankisch PG, Burchard-Reckert S, Lehnick D. Underestimation of acute pancreatitis: Patients with only a small increase in amylase/lipase levels can also have or develop severe acute pancreatitis. Gut 1999;44:542-544.

24. Clavien PA, Robert J, Meyer P, et al. Acute pancreatitis and normoamylasemia. Not an uncommon combination. Ann Surg 1989;210:614-620.

25. Spechler SJ, Dalton JW, Robbins AH, et al. Prevalence of normal serum amylase levels in patients with acute alcoholic pancreatitis. Dig Dis Sci 1983;28:865-869.

26. Balthazar EJ. Acute pancreatitis: Assessment of severity with clinical and CT evaluation. Radiology 2002;223:603-613.

27. MacEneaney P, Mitchell MT, McDermott R. Update on magnetic resonance cholangio-pancreatography. Gastroenterol Clin North Am 2002;31:731-746.

28. Beger HG, Rau B, Isenmann R. Natural history of necrotizing pancreatitis. Pancreatology 2003;3:93-101.

29. Andersson R, Andren-Sandberg A. Fatal acute pancreatitis. Characteristics of patients never reaching the hospital. Pancreatology 2003;3:64-66.

30. Fan ST, Choi TK, Lai CS, Wong J. Influence of age on the mortality from acute pancreatitis. Br J Surg 1988;75:463-465.

31. Sullivan DH, Bopp MM, Roberson PK. Protein energy underutilization and life-threatening complications among the hospitalized elderly. J Gen Intern Med 2002;17:923-932.

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35. Berzin TM, Mortele KJ, Banks PA. The management of suspected pancreatic necrosis. Gastroenterol Clin North Am 2007;35:393-407.

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38. Uhl W, Warshaw A, Imrie C, et al; International Association of Pancreatology. IAP Guidelines for the Surgical Management of Acute Pancreatitis. Pancreatology 2002;2:565-573.

39. Shemesh E, Czerniak A, Schneabaum S, Nass S. Early endoscopic sphincterotomy in the management of acute gallstone pancreatitis in elderly patients. J Am Geriatr Soc 1990;38:893-896.

40. Rosenthal RA, Zenilman ME. Surgery in the elderly. Townsend CM, Beauchamp RD, Evers BM, Mattox KL, eds. Sabiston Textbook of Surgery. 16th ed. Philadelphia, PA: W.B. Saunders; 2001:226-247.

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