Surgical errors in the length and orientation of a flap pedicle can result in kinks, twists, or tension on the pedicle vessels. When these errors occur together with the microvascular repairs associated with free flap transfer, thrombosis and flap failure may be the outcome. A model was designed to simulate these events. The rabbit central ear artery and vein were dissected and all other tissue connections were severed in a near-complete amputation. The artery was transected, shortened by 2 mm, and repaired standardly. The ear was then rotated 360 degrees, twisting the vein around the repaired artery. The ear cartilage was shortened by 6 mm, then sutured, and the skin was closed. In a series of 20 ears, 95% necrosed, 18 from arterial thrombosis and 1 from venous thrombosis. Several other groups were used in which aspects of the basic model were modified to determine the factors influencing failure. When the arterial anastomosis was not performed and the vascular pedicle was rotated with cartilage shortening, all ears survived; when the cartilage was not resected in this paradigm, leaving tension on the pedicle, 50% of the ears necrosed from venous thrombosis. In counterpoint, when the artery was repaired without twisting the pedicle, all ears survived, whether or not the cartilage was shortened. When the artery was repaired without shortening it and with rotation of the ear, 50% of the ears necrosed when the cartilage was shortened, 40% from venous thrombosis and 10% from arterial thrombosis; all ears necrosed (of venous thrombosis) when the cartilage was not shortened. These findings demonstrate the combined effects of a twisted pedicle, microvascular anastomosis, and vascular tension on thrombotic failure. This new model offers a clinically relevant experimental method for evaluating therapies for the prevention of thrombosis-related free flap failure.
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