The Efficacy of Prophylactic Low-Molecular-Weight Heparin to Prevent Pulmonary Thromboembolism in Immediate Breast Reconstruction Using the TRAM Flap

Abstract

Sir: We read with great interest the recent publication by Kim et al. entitled “The Efficacy of Prophylactic Low-Molecular-Weight Heparin to Prevent Pulmonary Thromboembolism in Immediate Breast Reconstruction Using the TRAM Flap” (Plast Reconstr Surg. 2009;123:9–12). The authors compared a group of 450 patients receiving a free microvascular transverse rectus abdominis musculocutaneous (TRAM) flap without medical prophylaxis with 200 patients receiving low-molecular-weight heparin for prophylaxis of deep vein thrombosis, and found a significant decrease in asymptomatic pulmonary thromboembolism in the latter group. Because antithrombotic therapy may influence not only deep vein thrombosis but also anastomotic patency and the incidence of microvascular anastomosis thrombosis, we would like to ask the authors about the incidence of anastomotic failure, requiring surgical revision, in their series. Did the authors observe a reduction of either venous or arterial anastomotic thrombosis in the heparin group? Finally, did the authors observe a difference in flap survival between the two groups? In large studies of microvascular breast reconstruction, the incidence of anastomotic venous and arterial thrombosis is reported to be 1.5 and 0.6 percent, respectively.1 Arterial anastomotic thrombosis is associated with flap loss in 11.1 percent of the cases, whereas venous anastomotic thrombosis may lead to flap loss in 26.7 percent of these cases.1 In concordance with the results from Kim et al., these data suggest a need for medical prophylaxis of vascular thrombosis following microvascular free tissue transfer. However, postoperative anticoagulation and antiaggregation regimens are not standardized, and it is unclear which thromboembolic risk factors may contribute to anastomotic thrombosis. In this context, we would like to point out the possible role of hereditary thrombophilia in postoperative thrombosis of both deep leg veins and microvascular anastomosis. Factor V Leiden mutation was first described in 1994 and has since been identified as a major risk factor for thromboembolic complications.2 Heterozygous carriers of the gene mutation carry a 5- to 10-fold higher risk for deep vein thrombosis, and the risk is 80-fold higher in homozygous carriers. In the white population, the prevalence of the factor V Leiden mutation is between 2 and 10 percent, thus resembling the most common type of hereditary thrombophilia in the Western world.2 We have recently published a case in which a patient with factor V Leiden mutation suffered from recurrent venous and arterial thrombosis at the microvascular anastomosis following breast reconstruction with a TRAM flap.3 Other authors also suggest a possible impact of factor V Leiden mutation on thrombotic occlusion of microvascular anastomosis.4,5 Because of the relatively high prevalence of factor V Leiden mutation in whites, further research on the impact of this thrombophilic disorder in patients undergoing free microvascular tissue transfer is warranted. Alexander E. Handschin, M.D. Kay Busch, M.D. Peter M. Vogt, M.D., Ph.D. Plastic, Hand, and Reconstructive Surgery Medical School Hannover Hannover, Germany