HBOT For Central retinal artery occlusion

Central retinal artery occlusion (CRAO) is an uncommon eye disorder, but one that typically produces severe and irreversible vision loss in the affected eye. Emboli dislodged from the carotid artery are the most common cause of CRAO, from either an unstable atherosclerotic plaque or a cardiac source. Central retinal artery occlusion is a blockage of the central retinal artery. The blockage usually comes from a blood clot or cholesterol in your blood vessel. The retina has a dual blood supply, with the retinal circulation supplying the inner layers and the choroidal circulation supplying the outer layers. In CRAO, vision loss results from cell death in the inner retinal layers despite relative sparing of the outer layers. When one of the vessels that carry blood to your eye’s retina gets blocked, it can cause you to lose your eyesight. This problem often happens suddenly and without any pain. Your retina is the layer of nerve tissue at the back of your inner eye that senses light. Like a tiny video camera, your retina turns images into electrical signals. Your optic nerve carries these signals to your brain. If a blockage of a blood vessel happens in your retina, it can be very serious. The blockage usually comes from a blood clot or cholesterol deposit in your blood vessel. This is a serious condition. You should seek prompt medical attention. If a blood clot breaks free and moves to the brain, it could cause a stroke.

If supplemental oxygen is provided, however, oxygen from the choroidal circulation may diffuse in adequate quantities to the inner layers of the retina to maintain retinal function and restore vision. In some patients this can be achieved with normobarichyperoxia; in others, hyperbaric oxygen (HBO2) may be required. The challenge is to provide the supplemental oxygen early enough after the onset of vision loss to prevent irreversible damage to the retina. In experimental models of complete CRAO, the ischemic time window before permanent retinal damage occurs is just over 90 minutes; in the clinical setting where occlusion may be incomplete, return of vision may be achieved even after delays of eight to 24 hours. Experts say that if you arrive at the hospital with at least 20/40 vision, you may have fairly good eyesight later on. If your vision in the eye is 20/200 or worse, the outlook for recovery is not good. In patients with a clinical picture of CRAO who present within 24 hours of vision loss, supplemental oxygen should be started immediately at the highest possible fraction of inspired oxygen (FiO2). If vision is not quickly restored, emergent HBO2 should be undertaken if feasible. If the patient responds to HBO2, follow-up treatment with supplemental oxygen should be customized to maintain retinal viability until the obstructed retinal artery recanalized, which typically occurs within the first 72 hours. This treatment has not been proven to be reliably effective. How well this works depends on the type of blockage. It also depends on how quickly therapy begins after the blockage forms. This therapy may work best if started within 8 hours after the blockade begins.