Non-invasive physical therapy as salvage measure for ischemic skin flap: A literature review

Abstract

This review focuses on the available evidence regarding the molecular mechanisms and treatment potential of several non-surgical physical therapies for managing flap ischemia to propose a non-invasive, economical, and simple treatment to improve flap survival. A review of the literature was conducted on the topics of various non-invasive methods for the treatment of ischemic necrosis of the distal end of the flap between 1988 and 2019. A total of 52 published studies were reviewed on the applications of hyperbaric oxygen therapy, electrical stimulation therapy, heat stress pretreatment, phototherapy, and vibration therapy to manage skin flap necrosis. The underlying molecular mechanisms of these physical therapies on revitalizing the dying skin flaps were discussed and preliminary clinical uses of these therapies to salvage the necrotic skin flaps were pooled and summarized for clarifying the safety and feasibility of these methods. Various physical therapy regimens have been ushered to manage necrotic development in cutaneous flaps. With the refinement of these new technologies and enhancement of related basic science research on vascular revitalization, the prevention and treatment of flap ischemia will enter a new era.

Keywords: Electrical stimulation therapy; Heat stress pretreatment; Hyperbaric oxygen; Phototherapy; Physiotherapy; Skin flap; Vibration therapy.

Figure 1

Putative mechanism of physiotherapy on the dying skin flap as induction of angiogenesis through inhibiting sympathetic nerve for vasodilation and promoting the secretion of vascular endothelial growth factor secretion. Akt/PKB: Protein kinase B; Erk: Extracellular signal-regulated kinase; MEK: Mitogen-activated protein kinase kinase; Pl3K: Phosphatidylinositol 3-kinase; VEGF: Vascular endothelial growth factor; VEGFR: Vascular endothelial growth factor receptor; Raf: Rapidly accelerated fibrosarcoma.

Figure 2

Putative molecular mechanism of physiotherapeutic methods for upregulation of heat shock protein 32 and heat shock protein 70 in the skin flap, which promotes vasodilation and inhibition of apoptosis. Apaf-1: Apoptosis protease-activating factor-1; HSP: Heat shock protein; JNK: Jun N-terminal kinase; p38: Protein 38.