Patients with BRVO usually complain of sudden onset of blurred vision or a central visual field defect.

The eye examination findings of acute BRVO include superficial hemorrhages, retinal edema, and often cotton-wool spots in a sector of retina drained by the affected vein.The obstructed vein is dilated and tortuous.

The quadrant most commonly affected is the superotemporal (63%).

Retinal neovascularization occurs in 20% of cases within the first 6–12 months of occlusion and depends on the area of retinal nonperfusion. Neovascularization is more likely to occur if more than five disc diameters of nonperfusion are present and vitreous hemorrhage can ensue.

Patients with idiopathic macular telangiectasia type 1 are typically 40 years of age or older. They may have a coincident history of ischemic vascular diseases such as diabetes or hypertension, but these do not appear to be causative factors.

Macular telangiectasia type 2 usually present first between the ages of 50 and 60 years, with a mean age of 55–59 years. They may present with a wide range of visual impact, from totally asymptomatic to substantially impaired; in most cases however, patients retain functional acuity of 20/200 or better. Metamorphopsia may be a subjective complaint. Due to the development of paracentral scotomota (blind spots), reading ability is impaired early in the disease course. It might be even the first symptom of the disease.

The condition may remain stable for extended periods, sometimes interspersed with sudden decreases in vision. Patients’ loss of visual function is disproportionately worse than the impairment of their visual acuity, which is only mildly affected in many cases. In patients with MacTel, as compared with a reference population, there is a significantly higher prevalence of systemic conditions associated with vascular disease, including history of hypertension, history of diabetes, and history of coronary disease. MacTel does not cause total blindness, yet it commonly causes gradual loss of the central vision required for reading and driving.

The most common sign at presentation is leukocoria (abnormal white reflection of the retina). Symptoms typically begin as blurred vision, usually pronounced when one eye is closed (due to the unilateral nature of the disease). Often the unaffected eye will compensate for the loss of vision in the other eye; however, this results in some loss of depth perception and parallax. Deterioration of sight may begin in either the central or peripheral vision. Deterioration is likely to begin in the upper part of the vision field as this corresponds with the bottom of the eye where blood usually pools. Flashes of light, known as photopsia, and floaters are common symptoms. Persistent color patterns may also be perceived in the affected eye. Initially, these may be mistaken for psychological hallucinations, but are actually the result of both retinal detachment and foreign fluids mechanically interacting with the photoreceptors located on the retina.

One early warning sign of Coats' disease is yellow-eye in flash photography. Just as the red-eye effect is caused by a reflection off blood vessels in the back of a normal eye, an eye affected by Coats' will glow yellow in photographs as light reflects off cholesterol deposits. Children with yellow-eye in photographs are typically advised to immediately seek evaluation from an optometrist or ophthalmologist, who will assess and diagnose the condition and refer to a vitreo-retinal specialist.

Coats' disease itself is painless. Pain may occur if fluid is unable to drain from the eye properly, causing the internal pressure to swell, resulting in painful glaucoma.

Retinal hemorrhage is a disorder of the eye in which bleeding occurs into the light sensitive tissue on the back wall of the eye. A retinal hemorrhage can be caused by hypertension, retinal vein occlusion (a blockage of a retinal vein), or diabetes mellitus (which causes small fragile blood vessels to form, which are easily damaged). Retinal hemorrhages can also occur due to shaking, particularly in young infants (shaken baby syndrome) or from severe blows to the head.

Retinal hemorrhages that take place outside the macula can go undetected for many years, and may sometimes only be picked up when the eye is examined in detail by ophthalmoscopy, fundus photography, or a dilated fundus exam. However, some retinal hemorrhages can cause severe impairment of vision. They may occur in connection with posterior vitreous detachment or retinal detachment.

Many people often do not have symptoms until very late in their disease course. Patients often become symptomatic when there is irreversible damage. Symptoms are usually not painful and can include:

- Vitreous hemorrhage

- Floaters, or small objects that drift through the field of vision

- Decreased visual acuity

- "Curtain falling" over eyes

Branch retinal vein occlusion (BRVO) is a common retinal vascular disease of the elderly. It is caused by the occlusion of one of the branches of central retinal vein.

Those with ocular ischemic syndrome are typically between the ages of 50 and 80 (patients over 65) ; twice as many men as women are affected. More than 90% of those presenting with the condition have vision loss. Patients may report a dull, radiating ache over the eye and eyebrow. Those with ocular ischemic syndrome may also present with a history of other systemic diseases including arterial hypertension, diabetes mellitus, coronary artery disease, previous stroke, and hemodialysis.

The condition presents with visual loss secondary to hypoperfusion of the eye structures. The patient presents with intractable pain or ocular angina. On dilated examination, there may be blot retinal hemorrhages along with dilated and beaded retinal veins. The ocular perfusion pressure is decreased.

The corneal layers show edema and striae. There is mild anterior uveitis. A cherry-red spot may be seen in the macula, along with cotton-wool spots elsewhere, due to retinal nerve fiber layer hemorrhages. The retinal arteries may show spontaneous pulsations.

Retinal haemorrhages commonly occur in high attitude climbers, most likely due to the effects of systemic hypoxia on the eye. Risk is correlated with the maximum altitude reached, duration of exposure to high altitude conditions, and climb rate.

"Typical lattice" consists of sharply demarcated, spindle-shaped areas of retinal thinning, usually located between the equator of the retina and the posterior border of the vitreous base. This is more frequently located in the temporal half of the retina and is seen more superiorly than inferiorly.

"Atypical lattice" is characterised by radial lesions which appear continuous with the peripheral blood vessels. This type is typically seen in patients with Stickler syndrome.

Coats' usually affects only one eye (unilateral) and occurs predominantly in young males 1/100,000, with the onset of symptoms generally appearing in the first decade of life. Peak age of onset is between 6–8 years of age, but onset can range from 5 months to 71 years.

Coats' disease results in a gradual loss of vision. Blood leaks from the abnormal vessels into the back of the eye, leaving behind cholesterol deposits and damaging the retina. Coats' disease normally progresses slowly. At advanced stages, retinal detachment is likely to occur. Glaucoma, atrophy, and cataracts can also develop secondary to Coats' disease. In some cases, removal of the eye may be necessary (enucleation).

Macular edema occurs when fluid and protein deposits collect on or under the macula of the eye (a yellow central area of the retina) and causes it to thicken and swell (edema). The swelling may distort a person's central vision, because the macula holds tightly packed cones that provide sharp, clear, central vision to enable a person to see detail, form, and color that is directly in the centre of the field of view.

The most common cause found in adults is diabetic retinopathy. Abnormal blood vessels can form in the back of the eye of a person with diabetes. These new blood vessels are weaker and prone to breaking and causing hemorrhage. Diabetic retinopathy accounts for 31.5-54% of all cases of vitreous hemorrhage in adults in the United States.

Cystoid macular edema (CME) involves fluid accumulation in the outer plexiform layer secondary to abnormal perifoveal retinal capillary permeability. The edema is termed "cystoid" as it appears cystic; however, lacking an epithelial coating, it is not truly cystic. The cause for CME can be remembered with the mnemonic "DEPRIVEN" (diabetes, epinepherine, pars planitis, retinitis pigmentosa, Irvine-Gass syndrome, venous occlusion, E2-prostaglandin analogues, nicotinic acid/niacin).

Diabetic macular edema (DME) is similarly caused by leaking macular capillaries. DME is the most common cause of visual loss in both proliferative, and non-proliferative diabetic retinopathy.

A rhegmatogenous retinal detachment is commonly preceded by a posterior vitreous detachment which gives rise to these symptoms:

- flashes of light (photopsia) – very brief in the extreme peripheral (outside of center) part of vision

- a sudden dramatic increase in the number of floaters

- a ring of floaters or hairs just to the temporal (skull) side of the central vision

Although most posterior vitreous detachments do not progress to retinal detachments, those that do produce the following symptoms:

- a dense shadow that starts in the peripheral vision and slowly progresses towards the central vision

- the impression that a veil or curtain was drawn over the field of vision

- straight lines (scale, edge of the wall, road, etc.) that suddenly appear curved (positive Amsler grid test)

- central visual loss

In the event of an appearance of sudden flashes of light or floaters, an eye doctor needs to be consulted immediately. A shower of floaters or any loss of vision, too, is a medical emergency.

Common symptoms of vitreous hemorrhage include:

- Blurry vision

- Floaters- faint cobweb-like apparitions floating through the field of vision

- Reddish tint to vision

- Photopsia – brief flashes of light in the peripheral vision

Small vitreous hemorrhage often manifests itself as "floaters". A moderate case will often result in dark streaks in the vision, while dense vitreous hemorrhage can significantly inhibit vision.

Vitreous hemorrhage is diagnosed by identifying symptoms, examining the eye, and performing tests to identify cause. Some common tests include:

- Examination of the eye with a microscope

- Pupil dilation and examination

- An ultrasound examination may be used if the doctor does not have a clear view of the back of the eye

- Blood tests to check for specific causes such as diabetes

- A CT scan to check for injury around the eye

- Referral to a retinal specialist

Macular telangiectasia describes two distinct retinal diseases affecting the macula of the eye, macular telangiectasia type 1 and macular telangiectasia type 2.

Macular telangiectasia (MacTel) type 1 is a very rare disease, typically unilateral and usually affecting male patients. MacTel type 2 is more frequent than type 1 and generally affects both eyes (bilateral). It usually affects both sexes equally. Both types of MacTel should not be confused with Age-related macular degeneration (AMD), from which it can be distinguished by symptoms, clinical features, pathogenesis, and disease management. However, both AMD and MacTel eventually lead to (photoreceptor) atrophy and thus loss of central vision.

The etiology of both types of MacTel is still unknown and no treatment has been found to be effective to prevent further progression. Because lost photoreceptors cannot be recovered, early diagnosis and treatment appear to be essential to prevent loss of visual function. Several centers are currently trying to find new diagnostics and treatments to understand the causes and biochemical reactions in order to halt or counteract the adverse effects.

Contemporary research has shown that MacTel type 2 is likely a neurodegenerative disease with secondary changes of the blood vessels of the macula. Although MacTel type 2 has been previously regarded as a rare disease, it is in fact probably much more common than previously thought. The very subtle nature of the early findings in MacTel mean the diagnoses are often missed by optometrists and general ophthalmologists. Due to increased research activity since 2005, many new insights have been gained into this condition since its first description by Dr. J. Donald Gass in 1982.

Diabetic retinopathy often has no early warning signs. Even macular edema, which can cause rapid vision loss, may not have any warning signs for some time. In general, however, a person with macular edema is likely to have blurred vision, making it hard to do things like read or drive. In some cases, the vision will get better or worse during the day.

In the first stage which is called non-proliferative diabetic retinopathy (NPDR) there are no symptoms, the signs are not visible to the eye and patients will have 20/20 vision. The only way to detect NPDR is by fundus photography, in which microaneurysms (microscopic blood-filled bulges in the artery walls) can be seen. If there is reduced vision, fluorescein angiography can be done to see the back of the eye. Narrowing or blocked retinal blood vessels can be seen clearly and this is called retinal ischemia (lack of blood flow).

Macular edema in which blood vessels leak their contents into the macular region can occur at any stage of NPDR. The symptoms of macular edema are blurred vision and darkened or distorted images that are not the same in both eyes. Ten percent (10%) of diabetic patients will have vision loss related to macular edema. Optical Coherence Tomography can show the areas of

retinal thickening (due to fluid accumulation) of macular edema.

In the second stage, abnormal new blood vessels (neovascularisation) form at the back of the eye as part of "proliferative diabetic retinopathy" (PDR); these can burst and bleed (vitreous hemorrhage) and blur the vision, because these new blood vessels are fragile. The first time this bleeding occurs, it may not be very severe. In most cases, it will leave just a few specks of blood, or spots floating in a person's visual field, though the spots often go away after a few hours.

These spots are often followed within a few days or weeks by a much greater leakage of blood, which blurs the vision. In extreme cases, a person may only be able to tell light from dark in that eye. It may take the blood anywhere from a few days to months or even years to clear from the inside of the eye, and in some cases the blood will not clear. These types of large hemorrhages tend to happen more than once, often during sleep.

On funduscopic exam, a doctor will see cotton wool spots, flame hemorrhages (similar lesions are also caused by the alpha-toxin of "Clostridium novyi"), and dot-blot hemorrhages.

Retinopathy is any damage to the retina of the eyes, which may cause vision impairment. Retinopathy often refers to retinal vascular disease, or damage to the retina caused by abnormal blood flow. Age-related macular degeneration is technically included under the umbrella term retinopathy but is often discussed as a separate entity. Retinopathy, or retinal vascular disease, can be broadly categorized into proliferative and non-proliferative types. Frequently, retinopathy is an ocular manifestation of systemic disease as seen in diabetes or hypertension. Diabetes is the most common cause of retinopathy in the U.S. as of 2008. Diabetic retinopathy is the leading cause of blindness in working-aged people. It accounts for about 5% of blindness worldwide and is designated a priority eye disease by the World Health Organization.

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.

Lattice degeneration is a disease of the human eye wherein the peripheral retina becomes atrophic in a lattice pattern and may develop tears, breaks, or holes, which may further progress to retinal detachment. It is an important cause of retinal detachment in young myopic individuals. The cause is unknown, but pathology reveals inadequate blood flow resulting in ischemia and fibrosis.

Lattice degeneration occurs in approximately 6–8% of the general population and in approximately 30% of phakic retinal detachments. Similar lesions are seen in patients with Ehlers-Danlos syndrome, Marfan syndrome, and Stickler syndrome, all of which are associated with an increased risk of retinal detachment. Risk of developing lattice degeneration in one eye is also increased if lattice degeneration is already present in the other eye.

Central retinal artery occlusions cause sudden, acute, and painless loss of vision in one eye. Fundoscopic exam will show a red lesion, called a "cherry red spot," with surrounding pale retina (the pale color is caused by ischemia of the retina).

When this occurs there is a characteristic pattern of symptoms:

- Flashes of light (photopsia)

- A sudden dramatic increase in the number of floaters

- A ring of floaters or hairs just to the temporal side of the central vision

As a posterior vitreous detachment proceeds, adherent vitreous membrane may pull on the retina. While there are no pain fibers in the retina, vitreous traction may stimulate the retina, with resultant flashes that can look like a perfect circle.

If a retinal vessel is torn, the leakage of blood into the vitreous cavity is often perceived as a "shower" of floaters. Retinal vessels may tear in association with a retinal tear, or occasionally without the retina being torn.

Berlin's edema (commotio retinae) is a common condition caused by blunt injury to the eye. It is characterized by decreased vision in the injured eye a few hours after the injury. Under examination the retina appears opaque and white in colour in the periphery but the blood vessels are normally seen along with "cherry red spot" in the foveal reigion.This whitening is indicative of cell damage, which occurs in the retinal pigment epithelium and outer segment layer of photoreceptors. Damage to the outer segment often results in photoreceptor death through uncertain mechanisms. Usually there is no leakage of fluid and therefore it is not considered a true edema. The choroidal fluorescence in fluorescent angiography is absent. Visual acuity ranges from 20/20 to 20/400.

The prognosis is excellent except in case of complications of choroidal rupture, hemorrhage or pigment epithelial damage, but damage to the macula will result in poorer recovery. The outcome can be worsened in the case of retinal detachment, atrophy or hyperplasia. Visual field defects can occur. In late cases cystoid macular edema sometimes develops which can further lead to macular destruction.

Commotio retinae is usually self limiting and there is no treatment as such. It usually resolves in 3–4 weeks without any complications and sequelae.

If carotid occlusive disease results in ophthalmic artery occlusion, general ocular ischemia may result in retinal neovascularization, rubeosis iridis, cells and flare, iris necrosis, and cataract. The condition leads to neovascularization in various eye tissues due to the ischemia. The eye pressure may become high due to associated neovascular glaucoma. An ischemic optic neuropathy may eventually occur.

The risk of retinal detachment is greatest in the first 6 weeks following a vitreous detachment, but can occur over 3 months after the event.

The risk of retinal tears and detachment associated with vitreous detachment is higher in patients with myopic retinal degeneration, lattice degeneration, and a familial or personal history of previous retinal tears/detachment.