Pathology of warm ischaemia and reperfusion injury in adipomusculocutaneous flaps

In-vivo assessment and histological analysis after 168 hours of reperfusion were used to determine the normothermic (37 degrees C) ischaemic tolerance of adipomusculocutaneous, free flap, isotransplants in inbred AS rats. Flaps stored for up to 2 hours under normothermic conditions survived; flaps stored for 4 hours partially survived but those which had been stored for more than 6 hours became totally necrotic. Neither treatment with the iron chelator desferrioxamine (DFX) nor hypertonic citrate (HCA) flush increased the ischaemic tolerance of flaps which had been stored for 4 hours since neither diminished the amount of necrosis. Treated and untreated flaps stored for 4 hours were also assessed 0, 0.5, 24, 48, 96 and 168 hours after isotransplantation. They were compared to control flaps which had not been stored prior to reperfusion and negative control flaps which were not stored but isotransplanted without a blood supply. Oedema reached a peak at 24 hours and there was progressive increase in general severe necrosis, reaching a plateau by 48 hours. Suture line epidermalization and thickening was established by 48 hours. Among flaps stored for 4 hours, those treated with DFX had the most necrosis. Adipose tissue and striated muscle proved the least tolerant to warm ischaemic stress. These experiments suggest reperfusion injury contributes to eventual flap necrosis, but the role of free radicals has not been established. The 4-hour stored flap is a useful model to study the effects of ischaemia both in flap tissue and at the suture line.