Surgical errors in the length and orientation of a flap pedicle can re
sult in kinks, twists, or tension on the pedicle vessels. When these e
rrors occur together with the microvascular repairs associated with fr
ee flap transfer, thrombosis and flap failure may be the outcome. A mo
del was designed to simulate these events. The rabbit central ear arte
ry and vein were dissected and all other tissue connections were sever
ed in a near-complete amputation. The artery was transected, shortened
by 2 mm, and repaired standardly. The ear was then rotated 360 degree
s, 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 veno
us 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 ped
icle was rotated with cartilage shortening, all ears survived; when th
e cartilage was not resected in this paradigm, leaving tension on the
pedicle, 50% of the ears necrosed from venous thrombosis. In counterpo
int, when the artery was repaired without twisting the pedicle, all ea
rs survived, whether or not the cartilage was shortened. When the arte
ry was repaired without shortening it and with rotation of the ear, 50
% of the ears necrosed when the cartilage was shortened, 40% from veno
us thrombosis and 10% from arterial thrombosis; all ears necrosed (of
venous thrombosis) when the cartilage was not shortened. These finding
s demonstrate the combined effects of a twisted pedicle, microvascular
anastomosis, and vascular tension on thrombotic failure. This new mod
el offers a clinically relevant experimental method for evaluating the
rapies for the prevention of thrombosis-related free flap failure.