Reducing the ecological footprint of surgical hand scrub: it is time to act!

fibre realignment into parallel configurations), recruiting greater length from a given area of tissue and overall subtle migration of tissue in the direction of the applied force vector. Siebert’s study demonstrated expansion of 10%/h to a maximum of 15–20%. Sustained mechanical creep leads to biological creep – synthesis of new tissue elements stimulated by activating subcellular molecular pathways, driving processes like angiogenesis and fibroblast recruitment and activation. This work suggests that to derive only 1 mm from (assumed) ≥25*mm flaps, Douglas and Morris employed either suboptimal surgical or quantification techniques; or did not assess their KPIFs after a sufficiently long time frame. We feel this represents a misinterpretation of the visco-elastic properties of skin and of the principles of soft-tissue handling. An incremental flap inset technique is also critical to the KPIF method. Initially, interrupted stitches are placed – one, central leading edge; two offset at the trailing edge so maximal tension lines distribute obliquely across the flap, not in the same vector of maximal tension of the defect. After V–Y advancements are performed to close secondary defects at both ends of the flap, HEMMING sutures are used for optimal dermal apposition. Total release of the least compliant soft-tissue layer – the deep fascia – is performed with preservation of deep perforators and longitudinal neurovascular structures. Aside from skin and fascia islanding providing mechanical advantage, the KPIF may provide additional benefits to wound-healing; such as improving flap vascularity (correlating with observed flap hyperaemia/hyperperfusion leading to observations described as the ‘red-dot’ sign). This hyperaemia and apparent increased KPIF vascularity is too acute to be attributable to angiogenesis. It may, however, be mediated by mural smooth-muscle tone relaxation causing vasculature dilation, driven by hypoxia, release of presynthesized mediators (known vasodilators such as nitric oxide or prostaglandin E2), or inhibition of noradrenaline release from sympathetic nerve terminals. One theory is that skin-islanding removes the most sympathetic autonomic nerve fibres, contributing to a ‘sympathectomy-effect’ and reducing baseline vasoconstrictor tone to result in dermal capillary and perforator dilation. Similar skin hyperaemia is described in lumber sympathectomy. In conclusion, we agree that more rigorous science is needed in the surgical literature. Unfortunately criticisms of the KPIF technique because in their limited ‘model’ Douglas and Morris observed minimal soft-tissue gain, are invalid. They utilize non-standardized techniques, insufficient numbers and no scientific methodology, quantification or analysis. In addition to this, they entirely miss the point of the KPIF, which predominantly works by redistribution of laxity. Their study seeks to address only one of numerous ways in which KPIF design aids wound closure, and due to the study design, contributes little to the field. We feel that in the right indications, the KPIF is a clinically useful method of definitive wound closure.