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What are
Acute Thermal Burn Injuries?
Acute thermal burn injury is tissue damage caused by exposure to extreme heat, typically from sources such as flames, hot liquids, or heated objects. This type of injury results in immediate and potentially severe damage to the skin and underlying tissues.
Common Sources of
Acute Thermal Burn Injuries
Include:
Key characteristics of acute thermal burn injury include:
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Rapid tissue destruction due to protein denaturation
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Formation of distinct burn zones (coagulation, stasis, and hyperemia)
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Potential for systemic inflammatory response
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Risk of compartment syndrome in circumferential burns
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Fluid shifts leading to hypovolemia and edema
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Increased susceptibility to infection
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Potential for inhalation injury in cases involving fire or smoke
Classification of thermal burns:
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First-degree (superficial): Affects only the epidermis
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Second-degree (partial thickness): Involves epidermis and part of the dermis
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Superficial partial thickness
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Deep partial thickness
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Third-degree (full thickness): Destroys epidermis and full thickness of dermis
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Fourth-degree: Extends beyond the skin into underlying fat, muscle, or bone
Factors influencing the severity of thermal burns:
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Temperature of the heat source
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Duration of exposure
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Total body surface area (TBSA) affected
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Location of the burn (e.g., face, hands, genitals)
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Age of the patient (children and elderly at higher risk)
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Pre-existing medical conditions
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Presence of inhalation injury
Immediate and proper management of acute thermal burn injuries is crucial to minimize tissue damage, prevent complications, and optimize healing outcomes.
How HBOT Helps with
Acute Thermal Burn Injuries
Hyperbaric Oxygen Therapy (HBOT) has shown promise as an adjunctive treatment for acute thermal burn injuries. Here’s how HBOT specifically addresses the challenges of these injuries:
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Reduction of Burn Edema: HBOT helps reduce edema in the burn area by causing vasoconstriction in non-injured tissues, which can help limit the progression of tissue damage in the zone of stasis.
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Preservation of Dermal Appendages: By improving oxygenation to the burn area, HBOT can help preserve dermal appendages such as hair follicles and sweat glands, which are crucial for skin regeneration.
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Enhancement of Burn Wound Healing: HBOT stimulates angiogenesis and fibroblast activity, promoting faster and more effective healing of the burn wound.
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Mitigation of Ischemia-Reperfusion Injury: In thermal burns, tissue damage can continue even after the heat source is removed due to ischemia-reperfusion injury. HBOT helps mitigate this secondary damage.
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Reduction of Burn Depth Progression: By improving tissue oxygenation, HBOT can help prevent the conversion of partial-thickness burns to full-thickness burns, potentially reducing the need for skin grafting.
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Modulation of the Inflammatory Response: HBOT helps regulate the inflammatory process in burn injuries, potentially reducing the risk of systemic inflammatory response syndrome (SIRS).
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Enhancement of Skin Graft and Flap Survival: When skin grafting is necessary, HBOT can improve the survival and take of skin grafts and flaps in burn reconstruction.
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Improvement of Inhalation Injury Outcomes: In cases of concomitant inhalation injury, HBOT can help reduce pulmonary edema and improve oxygenation.
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Reduction of Burn-Related Pain: Some studies suggest that HBOT may help reduce pain associated with burn injuries, potentially decreasing the need for analgesics.
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Prevention of Burn Wound Infection: HBOT enhances the oxygen-dependent killing capacity of neutrophils, helping to prevent infection in the vulnerable burn wound.
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Acceleration of Epithelialization: HBOT promotes faster re-epithelialization of partial-thickness burns, which can lead to earlier wound closure.
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Mitigation of Hypertrophic Scarring: By promoting more efficient healing, HBOT may help reduce the formation of hypertrophic scars in thermal burn injuries.
What Happens in Our Bodies During HBOT for
Acute Thermal Burn Injuries
During HBOT treatment for acute thermal burn injury, several physiological processes occur that specifically address the unique challenges of these injuries:
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Hyperoxia Induction in Burn Zones: Blood oxygen levels increase dramatically, with oxygen dissolved directly in the plasma. This is particularly crucial for the zone of stasis in the burn injury, where tissue survival is precarious.
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Edema Reduction Through Vasoconstriction: HBOT causes vasoconstriction in non-injured tissues, which helps reduce edema in the burn area. This is vital for limiting the progression of tissue damage and improving microcirculation in the burn wound.
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Stimulation of Heat Shock Proteins: The hyperoxic environment stimulates the production of heat shock proteins, which play a protective role in burn injuries by stabilizing cellular proteins and enhancing cell survival.
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Enhancement of Fibroblast and Keratinocyte Activity: Increased oxygen levels stimulate fibroblast proliferation and keratinocyte migration, crucial for wound closure and re-epithelialization in partial-thickness burns.
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Modulation of Cytokine Production: HBOT affects the production and activity of various cytokines involved in the burn wound healing process, helping to optimize the inflammatory response.
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Improvement of Neutrophil Function: HBOT enhances the oxygen-dependent killing capacity of neutrophils, which is essential for preventing infection in the vulnerable burn wound.
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Stimulation of Angiogenesis: The alternating hyperoxic and relative hypoxic states during and after HBOT stimulate the release of angiogenic factors, promoting the formation of new blood vessels in the healing burn wound.
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Reduction of Lactate Accumulation: HBOT helps reduce tissue lactate levels, which can accumulate in the burn wound due to anaerobic metabolism, potentially improving the local metabolic environment.
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Enhancement of Antioxidant Defenses: While HBOT increases oxygen levels, it also upregulates antioxidant defenses, helping to mitigate oxidative stress in the burn wound.
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Modulation of Nitric Oxide Production: HBOT influences nitric oxide synthesis, which plays a role in vasodilation and tissue perfusion, potentially benefiting the microcirculation in the burn wound.
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Preservation of ATP Levels: By improving oxygen delivery, HBOT helps maintain ATP levels in burn-injured tissues, supporting cellular function and survival.
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Reduction of Leukocyte Adhesion: HBOT can reduce leukocyte adhesion to capillary walls, potentially limiting additional tissue damage in the burn area.
Protocol
HBOT treatment for acute thermal burn injuries typically involves pressurizing the chamber to 2.0-2.5 atmospheres absolute (ATA) for about 90-120 minutes. Treatments are usually administered daily, with the total number of sessions ranging from 5 to 20 or more, depending on the severity of the burn and the clinical response.
It’s important to note that the physiological responses to HBOT in acute thermal burn injuries can continue for some time after each treatment session. The cumulative effect of multiple treatments leads to sustained improvements in tissue oxygenation, edema reduction, and cellular function, ultimately enhancing the healing process and potentially improving long-term outcomes.
References
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Cianci, P., Sato, R., & Slade, J. B. (2013). Adjunctive hyperbaric oxygen therapy in the treatment of thermal burns. Undersea & Hyperbaric Medicine, 40(1), 89-108.
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Thom, S. R. (2011). Hyperbaric oxygen: its mechanisms and efficacy. Plastic and Reconstructive Surgery, 127(Suppl 1), 131S-141S.
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Bhutani, S., & Vishwanath, G. (2012). Hyperbaric oxygen and wound healing. Indian Journal of Plastic Surgery, 45(2), 316-324.
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Villanueva, E., Bennett, M. H., Wasiak, J., & Lehm, J. P. (2004). Hyperbaric oxygen therapy for thermal burns. Cochrane Database of Systematic Reviews, (3).
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Zamboni, W. A., Browder, L. K., & Martinez, J. (2003). Hyperbaric oxygen and wound healing. Clinics in Plastic Surgery, 30(1), 67-75.
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Slade, J. B., Hattori, T., Ray, C. S., Baumgartner, T. J., & Hemba, E. (2001). Statewide experience with adjunctive hyperbaric oxygen therapy for thermal burns. Undersea & Hyperbaric Medicine, 28(Suppl), 62.
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Mathieu, D., Marroni, A., & Kot, J. (2017). Tenth European Consensus Conference on Hyperbaric Medicine: recommendations for accepted and non-accepted clinical indications and practice of hyperbaric oxygen treatment. Diving and Hyperbaric Medicine, 47(1), 24-32.
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Roeckl-Wiedmann, I., Bennett, M., & Kranke, P. (2005). Systematic review of hyperbaric oxygen in the management of chronic wounds. British Journal of Surgery, 92(1), 24-32.