When oxygen is breathed at high partial pressures, a hyperoxic condition will rapidly spread, with the most vascularised tissues being most vulnerable. During times of environmental stress, levels of reactive oxygen species can increase dramatically, which can damage cell structures and produce oxidative stress.While all the reaction mechanisms of these species within the body are not yet fully understood, one of the most reactive products of oxidative stress is the hydroxyl radical (·OH), which can initiate a damaging chain reaction of lipid peroxidation in the unsaturated lipids within cell membranes. High concentrations of oxygen also increase the formation of other free radicals, such as nitric oxide, peroxynitrite, and trioxidane, which harm DNA and other biomolecules. Although the body has many antioxidant systems such as glutathione that guard against oxidative stress, these systems are eventually overwhelmed at very high concentrations of free oxygen, and the rate of cell damage exceeds the capacity of the systems that prevent or repair it. Cell damage and cell death then result. Diagnosis
Diagnosis of central nervous system oxygen toxicity in divers prior to seizure is difficult as the symptoms of visual disturbance, ear problems, dizziness, confusion and nausea can be due to many factors common to the underwater environment such as narcosis, congestion and coldness. However, these symptoms may be helpful in diagnosing the first stages of oxygen toxicity in patients undergoing hyperbaric oxygen therapy.
Central retinal vein occlusion, also CRVO, is when the central retinal vein becomes occluded, usually through thrombosis. The central retinal vein is the venous equivalent of the central retinal artery and both may become occluded. Since the central retinal artery and vein are the sole source of blood supply and drainage for the retina, such occlusion can lead to severe damage to the retina and blindness, due to ischemia (restriction in blood supply) and edema (swelling).CRVO can cause ocular ischemic syndrome. Nonischemic CRVO is the milder form of the disease. It may progress to the more severe ischemic type. CRVO can also cause glaucoma. Diagnosis
Despite the role of thrombosis in the development of CRVO, a systematic review found no increased prevalence of thrombophilia (an inherent propensity to thrombosis) in patients with retinal vascular occlusion. Treatment
Treatment consists of Anti-VEGF drugs like Lucentis or intravitreal steroid implant (Ozurdex) and Pan-Retinal Laser Photocoagulation usually. Underlying conditions also require treatment. CRVO without ischemia has better visual prognosis than ischemic CRVO. A systematic review studied the effectiveness of the anti-VEGF drugs ranibizumab and pagatanib sodium for patients with non-ischemic CRVO. Though there was a limited sample size, participants in both treatment groups showed improved visual acuity over 6 month periods, with no safety concerns. See also
Central retinal artery occlusion
Branch retinal artery occlusion
Branch retinal vein occlusionEylea
Iridodialysis
Ischemic optic neuropathy

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