Spinal catheter observer effect and surgical technique.

gesic effect after oxycodone administration based on published information on blood concentrations of oxycodone and metabolites, protein binding, blood–brain barrier behaviour (animal data), and opioid receptor affinity. Using these data, we found that oxycodone itself is responsible for 83.0% and 94.8% of the analgesic effect after p.o. and i.v. administration, respectively. In contrast, the potent oxycodone metabolite oxymorphone only played a minor role (15.8% after p.o. and 4.5% after i.v. administration). We took the opportunity using the new human data from the study by Kokki and colleagues to re-calculate the contribution of oxycodone and its metabolites to the analgesic effect. Therefore, the cerebrospinal fluid (CSF)/plasma ratio of oxycodone and its metabolites based on AUC or Cmax values available 1 were calculated (Table 1). We applied these ratios to the data available after i.v. administration 4 and compared the results with our previous calculations using animal data for the CSF/plasma ratio. The contribution of oxycodone itself decreased from 94.8% to 77.3% and consequently, oxymorphone contribution increased from 4.5% to 18.9%. However, this was based on the ratios obtained for Cmax, which is probably not the best parameter, but only AUC values of oxycodone itself are reported. It is quite obvious that after epidural oxycodone administration, the analgesic effect must result from the very high oxycodone concentrations in CSF, in relation only negligible concentrations of the metabolites are observed. Using Cmax concentration in CSF, our calculations result in .99% contribution of oxycodone to the overall analgesic effect. The data provided by Kokki and colleagues substantially support the current understanding that active oxycodone metabolites only have a minor contribution to the analgesia after oxycodone administration.