BACKGROUND
Wound healing is a complex process during which the skin and underlying tissues are repaired through several well-defined phases.1 One of the key factors in the healing process is tissue oxygenation, especially during the early phases of healing.2 Although initial hypoxia is required to initiate the healing process,3 increased oxygen tension becomes necessary to stimulate phagocytosis, provide mitochondrial energy, enhance angiogenesis, increase keratinocyte differentiation, migration, and re-epithelialization, enhance fibroblast proliferation and collagen synthesis, and promote wound contraction. Oxygen is also essential for producing superoxide by polymorphonuclear leukocytes which is necessary for destroying invading pathogens.2-5
Unfortunately, wounds are typically hypoxic with diminished oxygen delivery to the healing tissue.6 It has been estimated that wounds require a tissue oxygen tension ≥20 mm Hg to heal while non-healing wounds have transcutaneous oxygen pressure (tcpO2) as low as 5 mm Hg.7 In one study, tcpO2 ≥30 mm was a predicter of healing success.8 The tcpO2 is especially worrisome for wounds associated with peripheral arterial occlusive disease and diabetic foot ulcers.9 Consequently, the use of occlusive dressings can increase the oxygen deficit and further diminish wound healing.10 Since oxygenation of the outer layers of skin to a depth of 250 to 400 μM is almost exclusively provided by the atmosphere with little coming from circulating blood,11 increasing the presence of external oxygen will enhance the healing process.
Hyperbaric Oxygen
Hyperbaric oxygen therapy (HBOT) refers to the administration of 100% oxygen at ≥1.4 atmosphere within a pressurized chamber.12 During HBOT, tissue oxygen levels of 200 to 400 mm Hg can be achieved.13
HBOT has been shown to upregulate the production of vascular endothelial growth factor (VEGF), variants of platelet-derived growth factor (PDGF), and fibroblast growth factor (FGF) partially through nitric oxide modulation. VEGF and PDGF are responsible for stimulating capillary budding and wound granulation by altering signaling pathways leading to cell proliferation and migration. FGF plays a similar role in angiogenesis, but also induces neural development, keratinocyte organization, and fibroblast proliferation leading to wound granulation and epithelialization.14
HBOT can also enhance the antibacterial effects of oxygen at wound sites. As neutrophils and macrophages enter these environments to kill bacteria and remove necrotic material, they require large amounts of oxygen which is used to create hy-
Unfortunately, wounds are typically hypoxic with diminished oxygen delivery to the healing tissue.6 It has been estimated that wounds require a tissue oxygen tension ≥20 mm Hg to heal while non-healing wounds have transcutaneous oxygen pressure (tcpO2) as low as 5 mm Hg.7 In one study, tcpO2 ≥30 mm was a predicter of healing success.8 The tcpO2 is especially worrisome for wounds associated with peripheral arterial occlusive disease and diabetic foot ulcers.9 Consequently, the use of occlusive dressings can increase the oxygen deficit and further diminish wound healing.10 Since oxygenation of the outer layers of skin to a depth of 250 to 400 μM is almost exclusively provided by the atmosphere with little coming from circulating blood,11 increasing the presence of external oxygen will enhance the healing process.
Hyperbaric Oxygen
Hyperbaric oxygen therapy (HBOT) refers to the administration of 100% oxygen at ≥1.4 atmosphere within a pressurized chamber.12 During HBOT, tissue oxygen levels of 200 to 400 mm Hg can be achieved.13
HBOT has been shown to upregulate the production of vascular endothelial growth factor (VEGF), variants of platelet-derived growth factor (PDGF), and fibroblast growth factor (FGF) partially through nitric oxide modulation. VEGF and PDGF are responsible for stimulating capillary budding and wound granulation by altering signaling pathways leading to cell proliferation and migration. FGF plays a similar role in angiogenesis, but also induces neural development, keratinocyte organization, and fibroblast proliferation leading to wound granulation and epithelialization.14
HBOT can also enhance the antibacterial effects of oxygen at wound sites. As neutrophils and macrophages enter these environments to kill bacteria and remove necrotic material, they require large amounts of oxygen which is used to create hy-
