Reconstruction of Wrist Defects with Free Flaps in High Tension Electrical Burn Patients

High tension electrical burns affecting the wrist are likely to produce full thickness necrosis of the skin and to damage deep vital structures beneath the eschar, affecting he local tendons, nerves, vessels, even bones and joints which result in serious dysfunction of the hand. An aggressive approach to the treatment of these severe wounds and adequate wound coverage are essential for the successful result. From October 1997 to February 2000, we had treated 23 electrical wrist injuries in 20 patients with free flaps. Among these, 13 anterolateral thigh flaps, 5 forearm flaps, 2 scapular flaps, 2 parascapular flaps, and 1 medial leg flap were executed. About 2-4 weeks after initial injury, we tried free flaps. Preoperative debridement was not carried out. At the time of surgery, debridement of all nonviable tissue was done, but nerves, tendons, and bones were left in place with minimal or no debridement when they had anatomic continuity, regardless of their appearance of viability. In all cases, successful soft tissue coverage and wound healing were achieved, and we obtained the following conclusions. 1. Flap coverage should be executed before damage of the tendons, nerves, vessels. 2. As long as the free flap survives, the infected tendons, nerves, and denuded bone can be salvaged. 3. For later reconstruction of the wrist, fasciocutaneous flap should be preferred to promise tendon gliding and endure several operative procedures.

The Effect of Freezing on Acute Damaged Endothelium in Rat Femoral Vein

In the case of crush injury, the failure rate of replantation of free tissue transfer is high. Recently, the freezing of intact and repaired microarteries has been known to relieve spasm without inducing thrombosis in vivo. Therefore, the author thought that the vascular freezing of crushed vein showing only unrecognized endothelial damage after adequate debridement of a damaged vessel can also relieve spasm without inducing thrombosis and improve the patency rate of microvascular anastomosis. In this study, the process of vascular freezing was investigated in veins with acutely damaged endothelium using ethly chloride in a rat model. Two experiments were performed in 30 Sprague-Dawley rats, weighing about 250 gm. In the first experiment, a new crush model was established on the femoral vein of the rats. The degree of vessel injury was evaluated as crush energy. The proper crush energy was determined only by the endothelial damage without inducing thrombosis(0.037 J). In the second experiment, femoral veins were crushed with the energy of 0.037 J on the left side and then frozen after inflicted crush injury with the same energy on the right side. The gross and pathologic findings and patency rates were observed at postoperative day 2, 10 and 30. Patency in both the crushed and crush-freezing group was 100%. Pathlolgic findings in the crush-freezing group were more severe loss of the intima and most parts of the media, as well as cellular depopulation of the media when compared to the crushed group. Microthrombi adherent to the wall were demonstrated in several crush-freezing specimens, but the crush-freezing group showed relief of crush-induced vasopasm and endothelial regeneration. In conclusion, the freezing of microveins with acute endothelial damage relieves spasm without inducing thrombosis. Therefore, this study presents the posslbility of clinical application of vascular freezing in a case of crush injury requiring microvascualr anastomosis.