Hyperbarics and Wound Care: A Perfect Partnership Juan O Bravo MD CWSP UHM Medical Director Center for Wound Care and Hyperbaric Medicine at Broward Health Coral Springs
Disclosures I am part of the advisory committee for Hollister I am part of the Speakers Bureau for Organogenesis, Hollister, Mimedix
What is Hyperbaric Oxygen Therapy? Hyperbaric oxygen (HBO2) is a treatment, in which the patient breathes 100% oxygen intermittently while inside a treatment chamber at a pressure higher than sea level pressure (i.e., > 1 atmosphere absolute; atm abs).
Mechanism of action The mechanism of action of Hyperbarics can be divided in primary and secondary mechanism. Primary mechanism- effects of hyper-oxygenation and pressure (oxygen is dissolved into plasma and tissue fluids by the pressure) (Transient) Secondary - results due to the hyper-oxygenation Will cause changes at cellular level to improve healing and fight infection causing (Permanent changes and wound healing).
Primary Mechanism The increase in partial pressure of Oxygen will drive the O2 into hard to reach areas like fibrotic tissue, cicatrix or edema. The distance at which the Oxygen will travel in the tissue will be directly proportional to Oxygen partial pressure. Angiogenesis, Fibroblasts function, White blood cells and peroxidase killing will not occur if there is lack of Oxygen.
Primary Mechanism Hyperoxygenation- It occurs quickly but effects are transient. 10 min plasma, 1-2 hrs for muscle, 6 hrs for subcutaneous tissue. If the blood flow is inadequate the tissue fluid will saturate more slowly.
PRIMARY MECHANISM Oxygen in high concentrations is able to wash out other gases and poisons like CO and He Decompression illness. Also Oxygen under pressure will be dissolved in plasma and will help keep tissues alive in the case that blood is needed and not available.
SECONDARY MECHANISM related to Wound Healing This secondary mechanisms results in more permanent changes. Vasoconstriction resulting in edema reduction, Gas wash out/decrease in bubble size, re-perfusion injury mitigation, antimicrobial killing and inhibition are some of the secondary effects of HBO.
SECONDARY MECHANISM related to Wound Healing The effects on microbial killing are one of the most important secondary mechanisms of action in wound healing. Adequate levels of Oxygen are needed for the Leucocytes to engulf and kill bacteria. Oxydative killing will not occur in the absence of Oxygen. This mechanism increases O2 consumption 100 folds. Fibroblast proliferation and function (collagen production, migration and proliferation) are O2 dependent as well as wound matrix production.
SECONDARY MECHANISM related to Wound Healing Another secondary mechanism that helps with wound healing is the enhancement of fibroclastic function to digest dead and infected bone. This increases O2 consumption 100 folds and in many patients is only noted when HBO is started. Angiogenesis, improve antimicrobial activity and reabsorption of dead bone are all integral part of wound healing and all of these procedures are O2 dependent.
Now, lets be real HBO will not help this!!!!
Plasma Dissolved Oxygen Increases with Partial Pressure ~ 2 vol% increase with each atmosphere
Oxygen Therapy in Current Wound Management: Oxygen and Wound Healing: Oxygen clearly plays a large role in wound healing. It is one of the most versatile and powerful agents available in the management of chronic wounds. All of the major components of wound healing, collagen formation, angiogenesis, epithelization, and bacterial killing proceed in proportion to the amount of oxygen available.
Neovascularization and Angiogenesis: Neovascularization / Angiogenesis represents an indirect and delayed response to serial hyperbaric oxygenation. New tissue striving to fill dead space needs to be supplied by blood vessels, which follows the formation of collagen. Collagen forms a basement membrane that provides structure support for these budding vessels. Capillaries then grow into hypoxic areas and collagen synthesis is carried further into the wound forming new granulation tissue and further decreasing dead space. Increasing capillary po 2 tension with HBO increases the amount of oxygen reaching these advancing cells. Thereby allowing granulation tissue to migrate further from functioning capillaries. Hyperbaric oxygen enables this new vascular supply to advance quickly, thereby ensuring faster wound closure.
Oxygen Consumption and Infected Wounds: As oxygen tension falls, infection begins to dominate. Leukocyte bacterial killing is further impaired. This downward spiral can be interrupted in several ways. Warmth (enhance perfusion) Debridement (remove infected tissue) Drainage of abscesses (remove infection) Antibiotics (reduce infection) Reduction in sympathetic stimuli (reduce vasoconstriction) Edema control (enhance perfusion) Each of these interventions either increases supply of or decreases demand for oxygen thereby enhancing oxidative killing and tissue perfusions.
Re-perfusion Injury: Most of the damage associated with re-perfusion is brought about by the inappropriate activation of leukocytes. Following an ischemic interval, the total injury pattern is a result of two components: Direct irreversible injury component from hypoxia. Indirect injury which is largely mediated by the inappropriate activation of leukocytes. HBOT reduces the indirect component of the injury by preventing activation through the down regulation of leukocyte receptor sites. Basically HBO inhibits leukocyte endothelial intravascular adhesions. This effect has been reported to last up to 8 hours post-hbo. 2 The net effect is the preservation of marginal tissues that may otherwise have been lost to a ischemia-re-perfusion injury.
Stem Cell Mobilization by HBO HBO mobilizes stem/progenitor cell release from bone marrow through a nitric oxide dependent mechanism Population of CD34 cells in peripheral circulation doubled in response to single HBO treatment (2 ATA, 120 min) Over course of 20 treatments circulating CD34 cells increased 8 fold, total WBC count unchanged Number of colony-forming cells increased from 16±2 to 20±3 CFCs/100,000 monocytes plated Increased cell growth occurred only in samples obtained immediately post treatment Thom SR, et al. Stem cell mobilization by hyperbaric oxygen. Am J Physiol Heart Circ Physiol 2006; 290:H1378-H1386.
The PO 2 Wave: 1400 mmhg Base-line tcpo 2 25 mmhg Increased tissue po 2 last 2-8 hrs After 16-20 treatments the baseline tcpo 2 level starts to move up. The base-line level will continue moving up to within 80% of normal tissue/post HBO Level required for normal wound healing 40 mmhg 20 mmhg HBO Tx 120 min Tx # 1 Tissue po 2 levels 2-6 hrs post therapy Tx # 2 Approximately 16-18 hrs until next treatment Tx # 16-20
Brian Sigal DPM