Abstract

Background. Approximately 200,000 incisional hernias are repaired annually in the United States. The high incidence (11–20%) and recurrence rate (24–54%) for incisional hernias have not changed appreciably in 75 years. Mechanical advances in suture material, incision orientation, and closure technique have failed to eliminate this common surgical complication. A biological approach to acute wound failure may offer a new strategy.Methods. A rodent incisional hernia model was used. Seventy rats underwent 5-cm midline celiotomies and were closed with fine, fast-absorbing sutures to induce intentional acute wound failure. Group 1 received no other treatment. The midline fascia in groups 2 and 3 was injected immediately prior to incision with 100 μl of vehicle alone or vehicle containing 1 μg of transforming growth factor β2 (TGF-β2). Necropsy was performed on Postoperative Day 28 and the wounds were examined for herniation.Results. Incisional hernias developed in 88% (35/40) and 79% (11/14) of untreated incisions and those treated with vehicle alone. No hernias formed in the TGF-β2-treated incisions (0/16, P < 0.05). Standard histology and immunohistochemistry demonstrated enhanced macrophage, lymphocyte, and fibroblast chemotaxis and increased collagen I and III production in TGF-β2 treated incisions.Conclusions. Treatment of abdominal wall fascial incisions with TGF-β2 prevented the development of incisional hernias in this rat model. TGF-β2 stimulated fascial macrophage and fibroblast chemotaxis as well as acute wound collagen production. A biological approach such as this may reduce the incidence of incisional hernia formation in humans.

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