Deep sedation with dexmedetomidine in a porcine model does not compromise the viability of free microvascular flap as depicted by microdialysis and tissue oxygen tension.

BACKGROUND

Deep sedation is often necessary after major reconstructive plastic surgery in the face and neck regions to prevent sudden spontaneous movements capable of inflicting mechanical injury to the transplanted musculocutaneous flap(s). An adequate positioning may help to optimize oxygenation and perfusion of the transplanted tissues. We hypothesized that dexmedetomidine, a central alpha2-agonist and otherwise potentially ideal postoperative sedative drug, may induce vasoconstriction in denervated flaps, and thus increase the risk of tissue deterioration.

METHODS

Two symmetrical myocutaneous flaps were raised on each side of the upper abdomen in 12 anesthetized pigs. The sympathetic nerve fibers were stripped from the arteries in one of the flaps (denervated flap), while nerve fibers were kept untouched in the other (innervated flap). After simulation of ischemia and reperfusion periods, the animals were randomized to deep postoperative sedation with either propofol (n = 6) or dexmedetomidine (n = 6). Flap tissue metabolism was monitored by microdialysis and tissue-oxygen partial pressure. Glucose, lactate, and pyruvate concentrations were analyzed from the dialysate every 30 min for 4 h.

RESULTS

Mean arterial blood pressure was higher in the dexmedetomidine group (P = 0.036). Flap tissue metabolism remained stable throughout the experiment as measured by lactate-pyruvate and lactate-glucose ratios (median ranges 14.3-24.5 for lactate-pyruvate and 0.3-0.6 for lactate-glucose) and by tissue-oxygen partial pressure, and no differences were found between groups.

CONCLUSIONS

Our data suggest that dexmedetomidine, even if used for deep sedation, does not have deleterious effects on local perfusion or tissue metabolism in denervated musculocutaneous flaps.