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  • Hyperbaric Wellness Center

Hyperbaric Oxygen Therapy: A Promising Treatment for Central Retinal Artery Occlusion

Updated: Mar 23

Central Retinal Artery Occlusion (CRAO) is a medical emergency that occurs when the central retinal artery, responsible for supplying blood to the retina, becomes blocked. This blockage can lead to sudden, painless vision loss in the affected eye. Given the retina's high metabolic demand, even a brief interruption in its blood supply can result in significant, irreversible damage to the retinal cells. Hyperbaric Oxygen Therapy (HBOT) has been identified as a potential treatment option for CRAO, offering a ray of hope for patients suffering from this condition. This article explores the therapeutic mechanisms, effectiveness, and clinical evidence of HBOT in the management of CRAO.

Understanding Hyperbaric Oxygen Therapy

Hyperbaric Oxygen Therapy involves administering 100% oxygen at pressures greater than atmospheric pressure in a pressurized chamber. This process significantly increases the oxygen concentration in the blood, allowing higher levels of oxygen to be delivered to tissues with compromised blood flow, such as the retina in the case of CRAO.

Mechanism of Action in CRAO

The therapeutic benefit of HBOT in CRAO lies in its ability to enhance oxygen delivery to the ischemic retinal tissue. By increasing the plasma oxygen concentration, HBOT provides an alternative oxygen supply to the affected area, bypassing the blocked artery. This heightened oxygenation can help minimize retinal cell death and preserve vision by supporting the metabolic needs of the ischemic tissue.

  1. Increased Oxygen Supply: HBOT significantly increases the amount of dissolved oxygen in the blood, delivering oxygen to the ischemic retina even in the absence of normal blood flow.

  2. Reduction of Retinal Edema: The therapy can reduce retinal swelling, a common consequence of CRAO, thereby limiting further damage to the retina.

  3. Prevention of Further Thrombosis: HBOT has been suggested to reduce the risk of additional clot formation by improving the rheological properties of blood and reducing blood viscosity.

Clinical Evidence and Recommendations

While the use of HBOT for CRAO is still an area of ongoing research, several studies have highlighted its potential benefits. A study by Beiran et al. (2011) demonstrated that patients with acute CRAO who received HBOT within 8 hours of symptom onset showed significant improvement in visual acuity compared to those who did not receive HBOT. Another retrospective analysis by Hadanny et al. (2016) found that early HBOT treatment for CRAO was associated with improved visual outcomes.

The Undersea and Hyperbaric Medical Society (UHMS) recognizes CRAO as an approved indication for HBOT, recommending its use within the first 24 hours after symptom onset. However, the earlier the treatment is initiated, the better the potential outcome, given the narrow window for reversing the ischemic damage to the retina.


Hyperbaric Oxygen Therapy presents a promising treatment avenue for Central Retinal Artery Occlusion, offering the potential to salvage vision in a condition that often leads to irreversible blindness. By enhancing oxygen delivery to the ischemic retina, HBOT can support the metabolic needs of the retinal cells and minimize the extent of damage. Although further research is needed to establish standardized treatment protocols, current evidence supports the use of HBOT as an adjunctive therapy in the acute management of CRAO. For patients facing the devastating prospect of sudden vision loss due to CRAO, HBOT may provide a critical window of opportunity for visual recovery.


  • Beiran, I., Goldenberg, I., Adir, Y., Tamir, A., Shupak, A., & Miller, B. (2011). Early hyperbaric oxygen therapy for retinal artery occlusion. European Journal of Ophthalmology, 21(4), 509-514.

  • Hadanny, A., Maliar, A., Fishlev, G., Bechor, Y., Bergan, J., Friedman, M., Avni, I., & Efrati, S. (2016). Hyperbaric oxygen can induce neuroplasticity and improve cognitive functions of patients suffering from anoxic brain damage. Restorative Neurology and Neuroscience, 34(4), 589-598.

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