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Pancreatitis<br />

STEPHEN H. THOMAS AND JONATHAN S. ILGEN<br />

n Agents<br />

n Opioids<br />

n NSAIDs<br />

n Cholecystokinin receptor agents<br />

n Octreotide<br />

n Glucagon<br />

n Evidence<br />

Opioids remain the most commonly used, and most commonly recommen-<br />

ded, treatment for acute (and acute-on-chronic) pancreatitis. 1 Evidence<br />

addressing opioids’ effect on the sphincter of Oddi and biliary tract pain<br />

(see the chapter on biliary tract pain) may also be applicable in pancreatitis.<br />

The data show little difference in efficacy between various opioids. Authors<br />

criticizing the widespread practice of using meperidine (pethidine) for pan-<br />

creatitis pain have noted that there is no contraindication to routine use of<br />

morphine. 2,3<br />

While most opioids are acceptable, there are reasons to select the mixed<br />

agonist–antagonist buprenorphine. Buprenorphine appears to have advantages<br />

related to a paucity of effect on Oddi’s sphincter. Perhaps related to this<br />

property are reports of buprenorphine success when pure-agonist opioids<br />

fail to control pancreatitis pain. 4,5 For instance, a trial has found that buprenorphine<br />

achieves better analgesia than meperidine. 6 Use of an agent with<br />

limited effects on the sphincter of Oddi can reduce confusion about the<br />

etiology of the pancreatitis, by eliminating the opioid as a possible cause. 7<br />

(In the rare instance in which mu receptor agonists cause pancreatitis,<br />

naloxone is the indicated therapy.)<br />

There may be situations in which oral agents may be appropriate for ED<br />

therapy (e.g. chronic or less-severe pancreatitis). In these cases, PO tramadol<br />

339

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