Even though the time to first analgesic requirement was prolonged significantly by magnesium, the addition of intrathecal magnesium sulfate to spinal anesthesia is not desirable in patients undergoing knee arthroscopy due to the prolonged time to ambulation and the lack of effect of magnesium on postoperative analgesic consumption.

Background:Spinal administration of dexmedetomidine has been proposed as an adjuvant in spinal anesthesia. However, there is limited information about its possible neurotoxic effect after its neuraxial administration. Potential spinal neurotoxicity should be investigated in animals before administering drugs through the spinal cord. Our aim was to investigate the neurotoxic effects of intrathecal dexmedetomidine in rats.Methods:Two groups were performed: the dexmedetomidine (D) group (n = 10) received 10 μg (0.5 ml), whereas the control (C) group (n = 10) received 0.9% (0.5 ml) sodium chloride through indwelling intrathecal catheter. Seven days after the injection, the medulla spinalis was extracted. Samples were withdrawn from both groups for histologic, electron microscopic examination. The histologic examination was performed separately on each of the four sites. The findings were categorized as follows: 0 - normal neuron; 1 - intermediate neuron damage; and 2 - neurotoxicity.Results:Intrathecal administration of dexmedetomidine sensorial block was seen in the dexmedetomidine group and significant differences in the dexmedetomidine group than control group in 15th and 30th min (P < 0.05). Histological examination did not show evidence suggestive of neuronal body or axonal lesion, gliosis, or myelin sheath damage in any group. In all animals, there were observed changes compatible with unspecific inflammation at the tip of the needle location. On the four-area scoring histologic examination, the scores of both groups were 0–1, and no statistical difference was observed between the groups.Conclusions:A single dose of intrathecal dexmedetomidine did not produce histologic evidence of neurotoxicity.

intubation may accentuate any unrecognized preload deficit and further depress the cardiac output. It is plausible that in our patient the use of propofol as induction agent and the addition of positive pressure ventilation may have provided the setting for peripheral vasodilatation, alterations in preload, and finally, the decrease in cardiac output, enough to decrease coronary perfusion pressure. Unrecognized delayed dilated cardiomyopathy has important anesthetic implications, awareness of the potential for this pathophysiology to occur, recognition of its existence and a well-thought anesthetic plan is warranted. Luis M . Zab ala M D M D T ar i q Pa r r ay M D M D