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ACUTE PAIN
 

Pre-treatment with morphine does not prevent the development of remifentanil-induced hyperalgesia.

McDonnell C. et al

2009/4

Can J. Anesth 2008;55(12):813-8 > read the abstract
   

BACKGROUND:
Remifentanil, an ultra short-acting opioid commonly used to supplement general anesthesia, is associated with the development of hyperalgesia that manifests clinically as an increase in postoperative analgesic requirement. This study involving adolescents undergoing scoliosis surgery evaluated whether pre-treatment with morphine prior to commencing remifentanil infusion would decrease the initial 24-hr morphine consumption and pain scores.

METHODS:
Forty ASA I-II pediatric patients undergoing surgical correction of idiopathic scoliosis were recruited in a prospective, randomized, double-blind fashion to receive 150 microg x kg(-1) morphine or an equal volume saline prior to commencing remifentanil by infusion. The primary outcome was the initial 24-hr postoperative morphine consumption. Numeric rating scale (NRS) pain scores at rest and on coughing were recorded, as were scores for nausea, vomiting, and sedation and incidences of pruritus.

RESULTS:
The groups were demographically similar. No differences were observed between groups vis-a-vis the initial 24-hr morphine consumption, NRS pain scores, sedation, nausea, or vomiting.

CONCLUSION:
Pre-treatment with 150 microg x kg(-1) morphine did not decrease the initial 24-hr morphine consumption in adolescents who received remifentanil by infusion for surgical correction of idiopathic scoliosis.

◊ Reviewed by C. Stein, MD, PhD
Chairman, Dept. of Anesthesiology and Critical Care Medicine
Freie Universität and Charité Campus Benjamin Franklin, Berlin, Germany.

This paper investigates the effects of supplemental treatment with morphine before and after remifentanil infusion on the requirements for postoperative analgesic medication in scoliosis surgery. At the outset, some issues regarding terminology have to be considered: “Hyperalgesia” is defined as an increased response to painful stimuli. Thus, to evaluate hyperalgesia, one needs to apply painful stimuli (e.g. noxious pressure or heat) and to measure patient’s response. The current study did not do so. Only reports of spontaneous pain were recorded and, as the primary outcome, the amount of postoperative morphine requested by the patient was measured. An increased postoperative consumption of analgesic medication is not synonymous with hyperalgesia either, but may well be the result of acute opioid tolerance.

The term “remifentanil-induced” is also misleading. In fact, remifentanil was terminated at the end of surgery and pain scores were taken thereafter, i.e. during withdrawal of remifentanil. Finally, in the discussion the authors mention that the study group received morphine divided into a pre-remifentanil dose (0.15 mg/kg) and a post-remifentanil dose (0.1 mg/kg). Thus, a more accurate title of this paper would be: “Intraoperative supplemental morphine does not decrease postoperative morphine consumption during withdrawal from remifentanil”.

The results show no differences between groups receiving supplemental intraoperative treatment with 0.25 mg/kg morphine or saline with regard to postoperative morphine consumption, spontaneous pain scores or side effects. This has to be interpreted in light of the average total duration of surgery of about 400 min and the patients’ weight of about 52 kg. Thus, the average verum patient received a supplemental intraoperative morphine dose of 13 mg over 6.5 h. This is not exceptionally high and, as might be expected, did not have a major influence on postoperative morphine consumption. Clinical practice does not need to change as a consequence of this study but the readership should become aware of the incorrect use of terminology in the field of “opioid-induced hyperalgesia”. The increasing confusion of terms such as “opioid-induced”, “withdrawal-induced”, “hyperalgesia” or “tolerance” is alarming and steadily produces misleading conclusions.

 
   
 
     
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