Meperidine vs. Ketorolac for Biliary Colic
Meperidine vs. Ketorolac for Biliary Colic
Abstract & Commentary
Source: Dula DJ, et al. A prospective study comparing I.M. ketorolac with I.M. meperidine in the treatment of acute biliary colic. J Emerg Med 2001;20:121-124.
To evaluate the potential efficacy of ketorolac (previously untested in biliary colic), Dula and colleagues studied 30 patients in an academic emergency department (ED) in Pennsylvania. All had right upper quadrant pain and tenderness to palpation, with ultrasound-documented gallstones. Patients with fever, narcotic or non-steroidal anti-inflammatory drug (NSAID) allergy, who were on warfarin therapy, or who were pregnant were excluded. Patients were evaluated by means of a 10-point visual analog pain scale before and 30 minutes after injection of analgesia. A global assessment score was completed two hours later at the time of ED discharge, and by telephone follow-up in 7-14 days. Ages ranged from 18 to 65 years (mean = 42). Females comprised 80% of cases. Patients were randomized prospectively in double-blind fashion to either meperidine (MEP) 1.5 mg/kg intramuscular (IM) (maximum dose: 100 mg) or to ketorolac (KET) 60 mg IM.
Average initial pain scores were 7.6 and 7.3 for MEP and KET, respectively. Pain relief score at 30 minutes was reduced to 3.9 for MEP vs. 3.8 for KET (P = 0.96); scores at discharge two hours later were 1.8 for MEP vs. 1.9 for KET (P = 0.79). At 30 minutes, rescue medication (MEP 1 mg/kg) was required for four of 14 patients (29%) in the MEP group vs. two of 16 (12%) in the KET group (P = 0.38). All patients achieved pain relief sufficient for ED discharge. Over a two-week follow-up period, emergency cholecystectomy was required for two patients in each group. The authors conclude that KET is as effective as MEP for pain relief in acute biliary colic.
Comment by Michael Felz, MD
Each agent reduced pain scores by 50% at 30 minutes and by 70% at two hours, such that no patient required hospital admission. KET was associated with less need for rescue medication than MEP, but not to the level of statistical significance. The authors postulate that NSAIDs such as KET, by blocking cyclooxygenase, inhibit prostaglandins responsible for pain, cystic duct inflammation, and local smooth muscle spasm, and that these properties account for ketorolac’s efficacy in biliary colic. In contrast, the pharmacologic properties of opioids such as MEP and morphine involve centrally-mediated analgesia, with central nervous system sedation and spasm of the sphincter of Oddi as possible side effects. To support these claims, Dula and associates cite an earlier series of 60 patients with acute biliary colic in whom another NSAID, diclofenac (Voltaren), not only achieved pain relief in 85% of cases, but also markedly reduced the incidence of cholecystitis, hospitalization, and urgent cholecystectomy. Whether these therapeutic and preventive benefits extend to KET is intriguing but, as yet, unproven. So what is the bottom line? KET is not our newest ED bullet, but perhaps we have a brand new target: symptomatic gallstones.
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