The central retinal vein is the venous equivalent of the central retinal artery and, like that blood vessel, it can suffer from occlusion (central retinal vein occlusion, also CRVO, similar to that seen in ocular ischemic syndrome. 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). It can also cause glaucoma. Nonischemic CRVO is the milder form of the disease. It may progress to the more severe ischemic type.

In the wet, or exudative, form of age-related macular degeneration (AMD or ARMD), pathologic choroidal neovascular membranes (CNVM) develop under the retina. The CNVM can leak fluid and blood and, if left untreated, ultimately cause a centrally blinding disciform scar. Approximately 10-20% of patients with nonexudative AMD eventually progress to the exudative form, which is responsible for the majority of the estimated 1.75 million cases of advanced AMD in the United States.AMD usually occurs bilaterally, but it is often asymmetrical. Patients with exudative AMD present with the following: Subretinal fluid Retinal pigment epithelial (RPE) detachments Subretinal hemorrhage Choroidal neovascularization Subretinal lipid deposits (occasionally) Patients with exudative AMD typically describe painless, progressive blurring or distortion of their central visual acuity, which can be acute or insidious in onset.Patients who develop subretinal hemorrhage from choroidal neovascularization (CNV), for example, typically report an acute onset. Other patients with CNV may experience insidious blurring secondary to shallow subretinal fluid or RPE detachments. They also report relative or absolute central scotomas, metamorphopsia, and difficulty reading.The natural history of exudative AMD (and occasionally nonexudative AMD) results in a stable central scotoma in which the patient’s visual acuity falls below the reading level and the legal driving level. However, peripheral visual acuity is usually retained.

The retina is a thin tissue inside the eye. It is delicate and can be torn by trauma or wear associated with age. Retinal gets plucked by vitreous traction, during sintomatic posterior vitreous detachment (PVD) associated with the aging process, or by some kind of ocular trauma. A break in the retina predisposes to its detachment, therefore it must be identified and treated in time. There are retina tear predisposing conditions and it is important to determine them. The sight of sparks, lights or lightning are especially important signs.. Risk factors include short sightedness, previous cataract surgery, eye trauma, family history of retinal detachment. But any person after age 40 could get a retina break without any known cause. Diagnosis is made by ocular fundus examination through a dilated pupil with an ophthalmoscope, or sometimes by ultrasound. In case of a retinal tear, efforts to prevent progression to retinal detachment include cryotherapy using a cold probe or retinal photocoagulation using a laser. The incidence of retinal tears in eyes with an acute symptomatic PVD ranges near 8.0% (18 out of 223). The average length of time from onset of symptoms to examination was 11 days with a range of 1 to 30 days. late–onset retinal breaks present in 1.4% of cases (2 out of 138) Timely diagnosis is key to effective treatment.

Epiretinal membrane is a disease of the eye in response to changes in the vitreous humor or more rarely, diabetes. It is also called macular pucker. Sometimes, as a result of immune system response to protect the retina, cells converge in the macular area as the vitreous ages and pulls away in posterior vitreous detachment (PVD). PVD can create minor damage to the retina, stimulating exudate, inflammation, and leucocyte response. These cells can form a transparent layer gradually and, like all scar tissue, tighten to create tension on the retina which may bulge and pucker (e.g., macular pucker), or even cause swelling or macular edema. Often this results in distortions of vision that are clearly visible as bowing when looking at lines on chart paper (or an Amsler grid) within the macular area, or central 1.0 degree of visual arc. Usually it occurs in one eye first, and may cause binocular diplopia or double vision if the image from one eye is too different from the image of the other eye. The distortions can make objects look different in size (usually larger = macropsia), especially in the central portion of the visual field, creating a localized or field dependent aniseikonia that cannot be fully corrected optically with glasses. Partial correction often improves the binocular vision considerably though. In the young (under 50 years of age), these cells occasionally pull free and disintegrate on their own; but in the majority of sufferers (over 60 years of age) the condition is permanent. The underlying photoreceptor cells, rod cells and cone cells, are usually not damaged unless the membrane becomes quite thick and hard; so usually there is no macular degeneration.