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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When the fetuss trophoblast does not fully extend into the uterine wall, the spiral arteries do not become fully converted into low-resistance channels. It has been found that this incomplete conversion of spiral arteries increases the resistance to uterine blood flow during pregnancy, and that this occurrence was associated with gestational hypertension. One potential cause of this incomplete breach of the spiral arteries that leads to gestational hypertension is a mistaken immune response by the maternal tissue, reaction to the alien fetal tissue. Therefore, it is clear that the complication of gestational hypertension has roots in the early implantation of the fetus in the uterine wall, an implantation technique that is unique to humans.The highly invasive placenta that is found in humans is thought to be linked to humans high circulating levels of the hormones CG and hCG. It has been shown that the higher the levels of these hormones, the deeper the trophoblasts invasion into the uterine wall. Instances of gestational hypertension and pre-eclampsia have been shown to occur when the invasion of the uterine wall is not deep enough, because of lower CG and hCG levels in the mother. Evolutionary tradeoff
Despite these risks for gestational hypertension, the hemochorial placenta has been favored because of its advantages in the way that it aids in diffusion from mother to fetus later in pregnancy. The bipedal posture that has allowed humans to walk upright has also led to a reduced cardiac output, and it has been suggested that this is what necessitated humans aggressive early placental structures.