INTRODUCTION:Rare intraoperative microvascular anastomotic failure by intractable vasospasm/thrombosis has been explained by reactive thrombocytosis and/or hypercoaguability. A third hypothesis involves a genetic predisposition to vasospasm: patients with mutations in the endothelial nitrous oxide synthase (eNOS) gene exhibit a propensity for systemic vasospastic conditions.

METHODS:In 14 flap-failures from 171 microsurgical procedures, 2/3 intraoperative failures revealed a possible etiology. Case 1, a male Type-II-diabetic who underwent lower extremity free-tissue-transfer exhibited intractable vasospasm/thrombosis of the anastomosis. Case 2 (non-diabetic male) exhibited a similar clinical course. Case 1's DNA was analyzed by RT-PCR for the presence of the T-786-C-single-nucleotide-polymorphism of the eNOS gene, a mutation associated with vasospastic conditions. Cases 1 and 2 were tested for a full hypercoaguability panel, reactive thrombocytosis, and aspirin and/or heparin resistance.

RESULTS:Case 1: heterozygosity(T/C) for the eNOS gene; Case 2: Reactive thrombocytosis coinciding with the timing of the attempted free tissue transfer; Cases 1&2: Platelets, hypercoagulability, aspirin/heparin resistance studies normal(Figures1,2).

CONCLUSIONS:These data suggest two distinct etiologies for intraoperative microvascular vasospastic/thrombotic failures and may predict patients at increased risk for free-flap loss. eNOS-mediated vascular dysfunction is an established cause of vasospastic/thrombotic conditions, as is reactive thrombocytosis. Both represent possible molecular targets for prevention of intraoperative vasospasm/thrombosis in microsurgery.