Chapter 2 - SKIN FLAP PHYSIOLOGY

Abstract

The “take” of a skin flap is very dependent on adequate vascular perfusion and sufficient wound healing. The ultimate goal is to have the skin flap integrate at its recipient wound bed and peripheral margins. Once the skin flap has been transposed, the wound healing cascade requires angiogenesis, collagen formation and remodeling, and epithelialization of the flap edges. This chapter describes important concepts in skin flap physiology to maximize skin flap survival. Attempts to improve flap survival have involved improving flap design, altering the early physiologic impairment of blood flow, and increasing tissue resistance to ischemia. Staging the skin flap by surgical flap delay is the most effective clinical technique to improve distal flap survival. Pharmacologic manipulations designed to improve blood flow or to increase tissue tolerance of ischemia have not achieved significant and reproducible results. Newer strategies to improve skin flap neovascularization include administering supplemental angiogenic cytokines such as vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) to the flap by a variety of delivery modalities. If therapeutically effective, a cytokine strategic approach to improve soft tissue revascularization could make a major impact in improving skin flap survival in patients who have compromised healing.