In our study, there was no difference in the use of oral codeine or oxycodone for the control of postoperative pain in our post-craniotomy patients. This is in contrast to many of the previous studies done4,6 and may be attributed to: lower pain scores in the local population and the pharmacokinetic profile of either drug in the local population.
In most studies, the incidence of moderate to severe post-craniotomy pain (VAS > 5) especially in the first 24 hours was high2,6 ranging from 50 to 80%1. However, in our study, most patients reported a VAS score of 1 to 3, which conventionally can be treated with simple analgesics, hence the requirement for strong opiates such as oxycodone might be reduced. Although codeine is thought to have a weaker analgesic effect compared to oxycodone, there was no statistically significant increase in the cumulative dose of codeine used compared with oxycodone from POD 0 to 3. Again, this is likely attributable to the low VAS scores reported in our population since regular paracetamol is served as a baseline with codeine or oxycodone being given on an as needed basis.
The low incidence of severe pain postoperatively at 24 hours could be postulated to be due to scalp infiltration by the surgeon as well as the use of intravenous fentanyl intra and postoperatively as transitional analgesia, both of which might provide early, post-surgical pain relief. Nemergut suggested in his review that the incidence of severe postcraniotomy pain could be reduced with local anaesthetic infiltration by the surgeons together with transitional analgesia after intravenous remifentanil infusion intraoperatively1.
Another factor which might explain why there was no statistically significant difference in pain scores in both groups could be due to the fact that most of our patients did not have preoperative pain. Sudheer found that patients who required opioids preoperatively were more likely to report significantly higher levels of postoperative pain hence requiring higher amounts of opioid analgesics6.
In terms of pharmacokinetic profiles, the metabolism of codeine or oxycodone in the local population may play a part in explaining why we did not find a difference in the use of either drug. It is well known that only 1% of Asians compared to 7% of Caucasians are poor metabolisers of CYP2D67, which prevent them from metabolizing drugs that are substrates of this enzyme such as codeine. Codeine is metabolized to morphine, its active substrate, and poor metabolisers of codeine will experience minimal analgesia with its use. The main opioid effects of oxycodone are realized through its parent drug, although oxycodone is metabolized to noroxycodone by CYP3A4 and to oxymorphone by CYP2D68; both of which have negligible analgesic effects due to the small amount produced. It is plausible that being effective metabolisers of codeine, the patients in the codeine group would be able to use codeine as effectively as oxycodone for the control of post-craniotomy pain.
Comparing codeine and oxycodone, we did not show an increase in adverse events such as sedation, respiratory depression or nausea after the use of oxycodone. Although the study may not have been powered to look at secondary objectives, there was no statistically significant difference in adverse effects between the 2 drugs, hence this could suggest the safety of prudent and titrated use of oral opioids with adequate monitoring.