Prolonged spasm in arteries, veins, and vein grafts has been described as a physiologic complication in microsurgery for over 20 years.6,14 Vasospasm results from several processes including intrinsic smooth muscle contraction,15 local noradrenaline metabolism, 16 neurogenic and hormonal processes,l7 and prostaglandin metabolism.18,19 Topical agents, such as magnesium sulfate,20 lidocaine,17,21 papaverine,22,23 and chlorpromazine6 have been reported to successfully relieve vasospasm. Other described methods for relieving vasospasm include nerve blocks,24,25 systemic adrene agents,26,27 and systemic vasodilating agents such as sodium nitroprusside.28

Acland attributed early clot formation following experimental microvascular repair to platelet aggregation at the site of the vascular repair.5 Later clinical and experimental investigations have continued to emphasize the role of platelets in microvascular thrombosis and clinical failures. 7,29,30 Acland in 1972, experimentally aborted early microvascular clot formation with topical magnesium sulfate.5 Subsequently, agents that interfere with platelet function have been widely used in microsurgery and have included aspirin, 1,31

Other aspects of thrombosis have also been considered significant to the outcome of microsurgical procedures. Improved characteristics of blood flow (including decreased blood viscosity7 and volume expansion 34) have provided another rationale for the widespread use of dextran. Heparin, which neutralizes activated clotting factors 34 and decreases platelet adhesion,38,39 has been used as a systemic anticoagulant adjunct in replantation of injured tissue 1,36,40 and in situations where anastomotic revisions have been required.31,36 Heparin is called upon in these cases to prevent pedicle and microcirculatory clot formation in instances of prolonged low flow or stasis.41 Experimental studies42,43 and anecdotal clinical reports 4,37 propose the use of fibrinolytics in similar circumstances.

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