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Biliary tract pain<br />

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

n Agents<br />

n Opioids<br />

n NSAIDs<br />

n Cholecystokinin receptor agents<br />

n Spasmolytics/anticholinergics<br />

n Calcium channel blockers<br />

n Evidence<br />

OPIOIDS<br />

Opioids are the benchmark against which other biliary tract analgesics are<br />

assessed. Historically, the distinction between opioids used for biliary tract<br />

pain (BTP) has been based upon differential effects on Oddi’s sphincter. We<br />

believe that clinical tradition has tended to exaggerate the magnitude of, and<br />

even mischaracterize, these differential effects. The evidence reveals that, in<br />

terms of Oddi sphincter effects and induction of biliary tract spasm, there are<br />

no significant differences between morphine and other pure mu receptor<br />

agonists. 1 There is thus no evidence basis for the common practice of substituting<br />

meperidine (pethidine) for morphine when treating BTP.<br />

While the pure mu agonists are generally equivalent for BTP, there are other<br />

opioid considerations that clinicians should keep in mind. Pentazocine is to be<br />

avoided, since it increases frequency and duration of bile duct sphincter contraction;<br />

there are no such untoward effects from tramadol or buprenorphine.<br />

2,3,4 In fact, buprenorphine is arguably the opioid of choice for BTP,<br />

since it even relieves pain from meperidine-induced spasm of Oddi’ssphincter. 5<br />

The well-known association between pure mu agonism and biliary tract<br />

spasm translates into an occasional role for naloxone for BTP in patients<br />

(including those post-cholecystectomy) who have received opioids. 6,7<br />

111

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