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What is Central Retinal
Artery Occlusion (CRAO)
Central Retinal Artery Occlusion (CRAO) is a serious ocular emergency characterized by a sudden, painless loss of vision in one eye due to the blockage of blood flow through the central retinal artery. This condition results in ischemia and potential irreversible damage to the retina if not treated promptly.
Common Sources of
Central Retinal
Artery Occlusion (CRAO)
Include:
Key characteristics of CRAO include:
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Sudden, profound vision loss, often described as a “curtain falling” over the eye
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Painless ocular condition
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Typically unilateral (affecting one eye)
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Potential presence of a cherry-red spot in the macula on fundoscopic examination
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Retinal whitening due to ischemia
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Possible presence of an embolus visible in retinal arterioles
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Occasional occurrence of transient vision loss episodes (amaurosis fugax) prior to CRAO
Types of retinal artery occlusions:
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Complete CRAO
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Partial CRAO
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Transient retinal artery occlusion
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Branch retinal artery occlusion (BRAO)
Factors contributing to CRAO:
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Embolism (most common cause)
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Thrombosis
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Vasculitis
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Giant cell arteritis
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Atherosclerosis
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Hypercoagulable states
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Cardiac valvular disease
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Carotid artery disease
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Rare causes: trauma, vasospasm, hypertensive crisis
Prompt recognition and treatment of CRAO is crucial, as the retina can only tolerate ischemia for a limited time (estimated 90-100 minutes) before irreversible damage occurs.
How HBOT Helps with
Central Retinal
Artery Occlusion (CRAO)
Hyperbaric Oxygen Therapy (HBOT) has emerged as a promising adjunctive treatment for CRAO. Here’s how HBOT specifically addresses the challenges of this condition:
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Rapid Oxygenation of Ischemic Retina: HBOT dramatically increases oxygen levels in the blood, allowing oxygen to reach the ischemic retina through alternate routes such as the choroidal circulation, potentially preserving retinal function until blood flow is restored.
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Reduction of Retinal Edema: The hyperbaric environment helps reduce edema in the retina, which can alleviate pressure on retinal cells and improve their function.
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Promotion of Retinal Vessel Vasodilation: HBOT can induce vasodilation in retinal vessels, potentially improving blood flow around the site of occlusion.
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Enhancement of Fibrinolysis: HBOT may enhance the body’s natural fibrinolytic processes, potentially aiding in the dissolution of the occluding embolus or thrombus.
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Mitigation of Ischemia-Reperfusion Injury: When blood flow is restored to the retina, HBOT can help mitigate reperfusion injury by modulating the inflammatory response and reducing free radical damage.
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Stimulation of Retinal Angiogenesis: HBOT promotes the formation of new blood vessels, which may help establish collateral circulation to the affected retina.
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Neuroprotection of Retinal Cells: The hyperoxic environment provided by HBOT may have neuroprotective effects on retinal neurons, potentially preserving visual function.
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Extension of the Treatment Window: While early intervention is crucial, HBOT may extend the window of opportunity for treatment, offering hope for patients with delayed diagnosis.
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Synergy with Conventional Treatments: HBOT can be used in conjunction with other treatments such as ocular massage, anterior chamber paracentesis, and intra-arterial thrombolysis, potentially enhancing overall outcomes.
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Reduction of Intraocular Pressure: HBOT may help reduce intraocular pressure, which can be beneficial in improving retinal perfusion in CRAO.
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Modulation of Retinal Gene Expression: HBOT has been shown to influence gene expression, potentially activating genes involved in cellular repair and protection in the context of retinal ischemia.
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Enhancement of Retinal Pigment Epithelium Function: By improving oxygenation, HBOT may support the function of the retinal pigment epithelium, which is crucial for photoreceptor health.
What Happens in Our Bodies During HBOT for
Central Retinal
Artery Occlusion (CRAO)
During HBOT treatment for Central Retinal Artery Occlusion, several physiological processes occur that specifically address the unique challenges of this condition:
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Hyperoxia Induction in Ocular Tissues: Blood oxygen levels increase dramatically, with oxygen dissolved directly in the plasma. This leads to significantly increased oxygen levels in ocular tissues, including the retina, choroid, and vitreous.
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Diffusion of Oxygen to Ischemic Retina: The increased oxygen tension in the blood allows for diffusion of oxygen from the choroidal circulation to the inner retinal layers, bypassing the occluded central retinal artery.
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Reduction of Retinal Edema: HBOT causes vasoconstriction in normal tissues, which helps reduce edema in the retina. This can alleviate pressure on retinal cells and improve their function.
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Stimulation of Retinal Blood Flow: The alternating hyperoxic and relative hypoxic states during and after HBOT stimulate the release of nitric oxide and other vasoactive substances, promoting vasodilation in retinal vessels.
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Enhancement of Fibrinolytic Activity: HBOT may enhance the activity of endogenous tissue plasminogen activator (tPA), potentially aiding in the dissolution of the occluding embolus or thrombus.
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Modulation of Retinal Inflammation: HBOT affects the production and activity of various inflammatory mediators, potentially dampening harmful inflammatory responses in the ischemic retina.
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Stimulation of Antioxidant Defenses: While HBOT increases oxygen levels, it also upregulates antioxidant defenses, helping to protect retinal cells from oxidative stress during reperfusion.
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Mobilization of Stem Cells: The hyperbaric environment activates and mobilizes stem cells from the bone marrow, which may contribute to repair processes in the damaged retina.
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Enhancement of Mitochondrial Function: Increased oxygen availability supports improved mitochondrial function in retinal cells, potentially aiding in cellular survival during ischemia.
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Modulation of Retinal Neurotransmitter Activity: HBOT may influence the activity of neurotransmitters in the retina, potentially affecting signal transmission and visual processing.
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Stimulation of Retinal Neuroplasticity: The hyperoxic environment may promote neuroplasticity in the visual system, potentially aiding in the reorganization of visual processing in response to retinal ischemia.
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Alteration of Retinal Metabolism: HBOT shifts retinal metabolism towards aerobic pathways, potentially reducing the accumulation of harmful metabolites during ischemia.
Protocol
HBOT treatment for CRAO typically involves pressurizing the chamber to 2.0-2.5 atmospheres absolute (ATA) for about 90-120 minutes. In acute cases, treatments may be administered multiple times within the first 24-48 hours, followed by daily sessions for several days.
It’s important to note that the physiological responses to HBOT in CRAO can continue for some time after each treatment session. The cumulative effect of multiple treatments leads to sustained improvements in retinal oxygenation, reduction of edema, and enhancement of cellular function, potentially improving the chances of visual recovery.
References
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Murphy-Lavoie, H., Butler, F., & Hagan, C. (2012). Central retinal artery occlusion treated with oxygen: a literature review and treatment algorithm. Undersea & Hyperbaric Medicine, 39(5), 943-953.
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Hadanny, A., Maliar, A., Fishlev, G., Bechor, Y., Bergan, J., Friedman, M., … & Efrati, S. (2017). Reversibility of retinal ischemia due to central retinal artery occlusion by hyperbaric oxygen. Clinical ophthalmology (Auckland, NZ), 11, 115.
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Cope, A., Eggert, J. V., & O’Brien, E. (2011). Retinal artery occlusion: visual outcome after treatment with hyperbaric oxygen. Diving and Hyperbaric Medicine, 41(3), 135-138.
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Weiss, J. N. (2010). Hyperbaric oxygen treatment of nonacute central retinal artery occlusion. Undersea & Hyperbaric Medicine, 37(3), 167-172.
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Menzel-Severing, J., Siekmann, U., Weinberger, A., Roessler, G., Walter, P., & Mazinani, B. (2012). Early hyperbaric oxygen treatment for nonarteritic central retinal artery obstruction. American journal of ophthalmology, 153(3), 454-459.
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Soares, A., Gomes, N. L., Mendonça, L., & Ferreira, C. (2017). The efficacy of hyperbaric oxygen therapy in the treatment of central retinal artery occlusion. BMJ case reports, 2017, bcr-2017.
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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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Wu, X., Chen, S., Li, S., Zhang, Y., Wang, T., Xiao, J., … & Xu, X. (2014). Oxygen therapy in acute coronary syndrome: are the benefits worth the risk? Vascular health and risk management, 10, 665.