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What is
Decompression Sickness?
Decompression sickness (DCS), also known as “the bends,” is a condition that occurs when dissolved gases (mainly nitrogen) come out of solution in the blood and tissues as bubbles, due to a rapid decrease in ambient pressure. This typically happens when a diver ascends too quickly from depth or when an aircraft suddenly loses cabin pressure at high altitude.
Common Sources of
Decompression Sickness
Include:
Key characteristics of decompression sickness include:
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Joint pain (often severe), known as “the bends”
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Skin manifestations, including itching and marbling
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Neurological symptoms such as numbness, paralysis, or confusion
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Pulmonary symptoms like chest pain and shortness of breath
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Extreme fatigue
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In severe cases, shock and death
DCS is typically categorized into two types:
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Type I (mild): Involves only the skin, joints, and lymphatic system
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Type II (serious): Affects the nervous system, respiratory system, or circulatory system
Factors that increase the risk of decompression sickness include:
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Rapid ascent from depth
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Multiple dives within a short period
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Flying too soon after diving
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Dehydration
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Obesity
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Age (older divers are at higher risk)
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Cold water diving
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Strenuous exercise during or immediately after a dive
Early recognition and treatment of DCS are crucial for the best outcomes.
How HBOT Helps with
Decompression Sickness
Hyperbaric Oxygen Therapy (HBOT) is the primary and most effective treatment for decompression sickness. Here’s how HBOT helps:
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Bubble Size Reduction: The increased pressure during HBOT reduces the size of nitrogen bubbles according to Boyle’s Law, allowing them to be more easily absorbed or eliminated.
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Enhanced Nitrogen Elimination: Breathing 100% oxygen under pressure creates a steep diffusion gradient that accelerates the removal of excess nitrogen from tissues.
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Improved Tissue Oxygenation: HBOT dramatically increases the amount of dissolved oxygen in the blood plasma, supporting oxygen delivery to tissues even if blood flow is compromised by bubbles.
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Reduced Inflammation: The anti-inflammatory effects of HBOT can help mitigate tissue damage caused by bubbles.
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Edema Reduction: HBOT helps reduce swelling in affected tissues, which can be particularly important in neurological DCS.
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Ischemia-Reperfusion Injury Prevention: By providing high levels of oxygen, HBOT can help prevent or reduce damage that occurs when blood flow is restored to oxygen-starved tissues.
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Promotion of Healing: Increased oxygen levels stimulate the body’s healing processes, including angiogenesis and stem cell mobilization.
What Happens in Our Bodies During HBOT for
Decompression Sickness
During HBOT treatment for decompression sickness, several physiological processes occur:
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Pressure Effects:
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As pressure increases, gas bubbles compress and shrink (Boyle’s Law).
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Smaller bubbles are more likely to dissolve back into the bloodstream or be eliminated through the lungs.
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Oxygen Saturation:
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The partial pressure of oxygen in the blood increases dramatically.
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Hemoglobin becomes fully saturated with oxygen.
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Significant amounts of oxygen dissolve directly into the blood plasma.
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Nitrogen Elimination:
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The high oxygen concentration creates a diffusion gradient that promotes the movement of nitrogen out of tissues and into the bloodstream.
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Nitrogen is then exhaled through the lungs.
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Tissue Oxygenation:
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The increased oxygen in the blood reaches tissues that may have been oxygen-deprived due to bubble obstruction.
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This can help prevent or reverse hypoxic tissue damage.
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Vasoconstriction:
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HBOT causes vasoconstriction in normal tissues, which can help reduce edema in affected areas.
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Immune Response Modulation:
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HBOT modulates the body’s inflammatory response, potentially reducing secondary tissue damage.
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Cellular Repair Activation:
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The increased oxygen levels stimulate cellular repair mechanisms and the production of growth factors.
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Bubble Surface Tension Alteration:
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The high oxygen environment may alter the surface tension of bubbles, making them more likely to dissolve.
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Protocol
HBOT treatment for decompression sickness typically involves pressurizing the chamber to 2.8-3.0 atmospheres absolute (ATA) for about 4-6 hours for the initial treatment, followed by shorter treatments over the next few days. The exact protocol may vary based on the severity of the condition and the patient’s response to treatment.
It’s crucial to begin HBOT treatment as soon as possible after the onset of DCS symptoms, as early intervention significantly improves outcomes. In many cases, symptoms begin to improve during or shortly after the first treatment, but multiple treatments are often necessary for complete resolution.
References
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Vann, R. D., Butler, F. K., Mitchell, S. J., & Moon, R. E. (2011). Decompression illness. The Lancet, 377(9760), 153-164.
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Gempp, E., & Blatteau, J. E. (2010). Risk factors and treatment outcome in scuba divers with spinal cord decompression sickness. Journal of Critical Care, 25(2), 236-242.
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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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Undersea and Hyperbaric Medical Society. (2014). Hyperbaric Oxygen Therapy Indications. 13th Edition. Best Publishing Company.
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Moon, R. E. (2014). Hyperbaric oxygen treatment for decompression sickness. Undersea and Hyperbaric Medicine, 41(2), 151-157.
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Bennett, M. H., Lehm, J. P., Mitchell, S. J., & Wasiak, J. (2012). Recompression and adjunctive therapy for decompression illness. Cochrane Database of Systematic Reviews, (5).
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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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Jain, K. K. (2016). Textbook of Hyperbaric Medicine. Springer International Publishing.
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Pollock, N. W., & Buteau, D. (2017). Updates in decompression illness. Emergency Medicine Clinics, 35(2), 301-319.
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Levett, D. Z., & Millar, I. L. (2008). Bubble trouble: a review of diving physiology and disease. Postgraduate Medical Journal, 84(997), 571-578.