Am Fam Physician. 2001 Jul 15;64(2):219-220.
to the editor: I found the review of pancreatitis by Drs. Munoz and Katerndahl1 to be thorough and informative; however, I take issue with the authors stating that meperidine [Demerol] is the preferred analgesic for treating the pain of acute pancreatitis because morphine may cause spasm of the sphincter of Oddi and worsen the pain. The authors cite a review article as the source of this contention.2 Close scrutiny, however, reveals that this review cites two additional reviews in turn as the basis for this claim.3,4 Is there experimental evidence that meperidine causes less sphincter of Oddi spasm than morphine or hydromorphone? Moreover, are there data to link this physiologic mechanism with the clinical outcome of worsening pain? I believe the evidence is lacking on these points. A recent review of the literature could identify only a small number of trials addressing this issue and, after weighing the evidence, could not draw a firm conclusion.5 An additional review concluded that there is “no good evidence” to support giving priority to meperidine for acute pancreatitis and called the practice “outdated.”6
Why is this important? Meperidine has several disadvantages when compared with other narcotic preparations. In particular, there is potential for a neurotoxic metabolite, normeperidine, to accumulate and cause seizures, myoclonus and tremors. This may be of specific concern for patients with alcoholic pancreatitis who are already at risk for developing neurologic complications of ethanol withdrawal. Furthermore, meperidine has a shorter duration of action than morphine or hydromorphone and is, therefore, less effective for sustained analgesia and more likely to result in a potentially avoidable “rebound” effect. Finally, meperidine is more likely to cause muscle fibrosis than competing narcotics when administered intramuscularly. For these reasons, the pharmacy at my institution explicitly prohibits the use of meperidine for any reason other than amphotericin-induced rigors or documented intolerance to alternative narcotics.
In short, it appears that the well-established drawbacks of meperidine may outweigh the anecdotal benefits. Evidence-based practice dictates that we value methodologically sound experimental data over dogma propagated by review articles and hearsay. It may be time to reconsider the age-old dogma that meperidine is the “analgesic of choice,” not only for acute pancreatitis, but for any disorder marked by severe pain.
REFERENCESshow all references
1. Munoz A, Katerndahl DA. Diagnosis and management of acute pancreatitis. Am Fam Physician. 2000;62:164–74....
2. Marshall JB. Acute pancreatitis: a review with an emphasis on new developments. Arch Intern Med. 1993;153:1185–98.
3. Geokas MC, Baltaxe HA, Banks PA, Silva J, Frey CF. Acute pancreatitis. Ann Intern Med. 1985;103:86–100.
4. Glazer G. Contentious issues in acute pancreatitis. In: Glazer G, Ranson JH, eds. Acute pancreatitis: experimental and clinical aspects of pathogenesis and management. London, England: Bailliere Tindall, 1988:1–36.
5. Isenhower HL, Mueller BA. Selection of narcotic analgesics for pain associated with pancreatitis. Am J Health Syst Pharm. 1998;55:480–6.
6. van Voorthuizen T, Helmers JH, Tjoeng MM, Otten MH. Meperidine (pethidine) outdated as analgesic in acute pancreatitis. Ned Tijdschr Geneeskd. 2000;144:656–8.
in reply:We wish to thank Dr. Spiegel for his thoughtful comments about our article.1 We must confess that we, too, like other authors before us, stuck to the “party line” concerning the use of narcotics in acute pancreatitis. Our sources were indeed previous reviews and not original research. Today, Micromedex still states that meperidine's spasmogenic effect on intestinal smooth muscle may cause biliary tract spasm; however, it is still the drug of choice for biliary pain because it can produce less increase in biliary pressure than other analgesics.
In attempting to identify the origin of this lore, we were able to track this “wisdom” back to Bailey and Love,2 who said, “the spasmodic side effects of morphine have been recognized for many years, and it is standard teaching that this drug should not be used to treat patients with pancreatitis since it causes a rise in biliary and pancreatic pressure.” Without a copy of this textbook, we lost the trail there.
The review by Isenhower and Mueller3 was indeed excellent. Although they did not draw a firm conclusion, they did state that morphine increases intraluminal pressure in the sphincter of Oddi. The prevailing assumption that morphine may increase the pain associated with pancreatitis or mask resolution of disease cannot be discounted. The assertion that meperidine does not increase sphincter of Oddi pressure is opposed by some evidence, but the only study conducted with endoscopic retrograde cholangiopancreatography (ERCP) showed no increase in pressure.”3 Hence, Isenhower and Mueller3 leave the issue unsettled. We found no research since 1998 to clarify the issue further.
The current status appears to be that meperidine may cause less spasm in the sphincter of Oddi and, therefore, a lesser rise in intraluminal pressure than does morphine. Although Isenhower and Mueller3 found some evidence that morphine-induced rise in biliary pressure can be associated with pain, the link between spasm in the sphincter of Oddi and abdominal pain is unproved. It then remains an individual choice whether to avoid a theoretic risk of increasing pain or masking resolution by using meperidine in patients with acute pancreatitis, or to avoid the risk of the complications of meperidine administration by using another narcotic.
1. Munoz A, Katerndahl DA. Diagnosis and management of acute pancreatitis. Am Fam Physician. 2000;62:164–74.
2. Bailey H, Love R. Short practice of surgery. 13th ed. Rains AJ, Capper WM, eds. London: Lewis, 1965:886.
3. Isenhower HL, Mueller BA. Selection of narcotic analgesics for pain associated with pancreatitis. Am J Health Syst Pharm. 1998;55:480–6.
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