Anticoagulants37

Technical error including inadequate vessel anastomoses, inappropriate selection of recipient vessels, pedicle kink, twist or tension and compression from wound closure, are the most common causes of anastomotic clotting. Occasionally, other factors, such as a true hypercoagulable state in patients with multiple injuries may be present.49 There is no unanimous agreement among microsurgeons about the anticoagulant regimen to be followed because of absence of complete data about the antithrombotic power of each anticoagulant.

Heparin inhibits fibrin formation, which is needed for platelet adhesiveness, by binding to antithrombin III and inactivating thrombin. Thrombin bound to the vessel wall, however, may be resistant to heparin and this may be responsible for the occasional failure of the prophylactic administration of systemic heparin. Topical administration of heparin may be more effective and avoids bleeding complications from donor and recipient site.57

For inhibition of thrombus formation an antiplatelet drug is also needed. Aspirin by preventing the production of postaglandins reduces the production of throm-boxane A2, which is an aggregant and vasoconstrictor agent, that affects not only the anastomosis itself, but also the downstream flap circulation. The role of aspirin on the microsurgical anastomosis is not completely defined, but clinically seems to be effective. Its use should be omitted in debilitated patients and where potential bleeding may be detrimental, such as in intracranial reconstruction.

Dextran19 of low molecular weight (40.000 MW) in 10% solution has been used in microsurgery as a pharmacologic adjunct because it is a volume expander, increases blood flow, interferes with platelet attachment to vessel wall and it has antifibrin function. It may be dangerous however, because of allergic reactions and tissue edema, including cerebral and pulmonary edema.

Occasionally fibrinolysins14,50—streptokinase, urokinase and recombinant human tissue-type plasminogen activator (rt-Pa)—may be useful in salvaging a failing free flap, by local infusion. If however the problem is anastomotic clotting, reanastomosis should always be done. Prophylactic local infusion of recombinant human tissue type plasminogen activator has been proven effective in experimental setting.3,51,51 Its use appears to be safer, because of its unique ability to electively activate the fibrinolytic system only at the site of fibrin presence. This localized thrombolytic effect does not deplete clotting proteins and diminishes the risk for hemorrhagic complications.

Other substances such as recombinant hirudin, which is contained in leech saliva and inactivates thrombin in the absence of antithrombin III, monoclonal antibodies against platelet adhesion receptors and substances that inhibit the coagulation pathway, are under investigation.

In conclusion, each team has established its own practice but routine postoperative use of full anticoagulation, except in complicated situations, is discouraged. We prefer to administer one intravenous bolus of heparin (5000 units in adults) at the time of completion of the anastomoses (the 30 minutes following opening of the anastomosis are the most critical for clot formation) and one aspirin per day postop-eratively for 3 weeks.

Patients undergoing elective reconstruction may be started on aspirin preopera-tively. Recently, severely injured or bedridden patients are kept on low molecular weight heparins. Anticoagulant substances must be used judiciously, because they may cause bleeding and wound hematomas that may adversely effect the surgical outcome.

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