A Hyperbaric Warm Perfusion System Preserves Tissue Composites Ex vivo and Delays the Onset of Acute Rejection.

BACKGROUND: Ischemia-reperfusion injury (IRI) precipitates acute rejection of vascularized composite allografts (VCA). Hyperbaric preservation of tissues ex vivo, between harvest and revascularization, may reduce IRI and mitigate acute rejection of VCA. METHODS: A porcine heterotopic musculocutaneous gracilis flap model was used. In phase 1, control autografts (n = 5) were infused with University of Wisconsin Solution (UWS) and stored at 4°C for 3 hours. Intervention autografts (n = 5) were placed in a hyperbaric oxygen organ preservation system for 5 hours and infused with hyperoxygenated UWS at 20°C and 3 atm. Grafts were replanted into the animals' necks. In phase 2, similarly treated control (n = 8) and intervention grafts (n = 8) were allotransplanted into the necks of animals separated by a typed and standardized genetic mismatch. No systemic immunosuppression was given. Systemic markers of IRI, and clinical and histopathological assessments of necrosis and rejection were performed. RESULTS: Autotransplanted tissue composites preserved in the hyperbaric chamber showed histopathological evidence of less muscle necrosis at 3 hours (p = 0.05). Despite a longer period of ischemia, no evidence was found of a difference in systemic markers of IRI following revascularization in these groups. Allotransplanted tissues supported ex vivo within the hyperbaric perfusion device experienced acute rejection significantly later than corresponding controls. CONCLUSION: Hyperbaric warm perfusion preserves musculocutaneous tissue composites ex vivo for longer than standard cold preservation in this model. This translates into a delay in acute rejection of allotransplanted tissue composites.

Free flap failure secondary to dual thrombophilia.

Much has been learned over the past several decades regarding thrombophilic conditions. Thrombotic complications, such as deep venous thrombosis, pulmonary embolus, myocardial infarction, and stroke, are sometimes attributed to a diagnosable thrombophilia. Less has been written with regard to their effect on reconstructive outcomes. Fortunately, it is rare to encounter a notable intraoperative thrombophilia while performing reconstructive microsurgery. When this does occur, salvage can be difficult and outcome can be compromised. It is imperative that microsurgeons be knowledgeable of both major and minor thrombogenic conditions to optimize intraoperative outcome and postoperative care. We present a case of a failed free flap for lower extremity reconstruction associated with hyperhomocysteinemia in conjunction with markedly elevated Factor VIII levels.