The diagnosis of POHS is based on the clinical triad of multiple white, atrophic choroidal

scars, peripapillary pigment changes (dark spots around optic disc of the eye), and a maculopathy caused by choroidal neovascularization.

Completely distinct from POHS, acute ocular histoplasmosis may rarely occur in immunodeficiency.

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.

"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.

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.

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.

Signs and symptoms of macular degeneration include:

- Visual symptoms

- Distorted vision in the form of metamorphopsia, in which a grid of straight lines appears wavy and parts of the grid may appear blank: Patients often first notice this when looking at things like miniblinds in their home or telephone poles while driving. There may also be central scotomas, shadows or missing areas of vision

- Slow recovery of visual function after exposure to bright light (photostress test)

- Visual acuity drastically decreasing (two levels or more), e.g.: 20/20 to 20/80

- Blurred vision: Those with nonexudative macular degeneration may be asymptomatic or notice a gradual loss of central vision, whereas those with exudative macular degeneration often notice a rapid onset of vision loss (often caused by leakage and bleeding of abnormal blood vessels).

- Trouble discerning colors, specifically dark ones from dark ones and light ones from light ones

- A loss in contrast sensitivity

Macular degeneration by itself will not lead to total blindness. For that matter, only a very small number of people with visual impairment are totally blind. In almost all cases, some vision remains, mainly peripheral. Other complicating conditions may possibly lead to such an acute condition (severe stroke or trauma, untreated glaucoma, etc.), but few macular degeneration patients experience total visual loss.

The area of the macula comprises only about 2.1% of the retina, and the remaining 97.9% (the peripheral field) remains unaffected by the disease. Even though the macula provides such a small fraction of the visual field, almost half of the visual cortex is devoted to processing macular information.

The loss of central vision profoundly affects visual functioning. It is quite difficult, for example, to read without central vision. Pictures that attempt to depict the central visual loss of macular degeneration with a black spot do not really do justice to the devastating nature of the visual loss. This can be demonstrated by printing letters six inches high on a piece of paper and attempting to identify them while looking straight ahead and holding the paper slightly to the side. Most people find this difficult to do.

Presumed ocular histoplasmosis syndrome (POHS) is a syndrome affecting the eye, which is characterized by peripheral atrophic chorioretinal scars, atrophy or scarring adjacent to the optic disc and maculopathy.

The loss of vision in POHS is caused by choroidal neovascularization.

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.

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

Intermediate AMD is diagnosed by large drusen and/or any retinal pigment abnormalities. Intermediate AMD may cause some vision loss, however, like Early AMD, it is usually asymptomatic.

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.

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.

Optic nerve damage is progressive and insidious. Eventually 75% of patients will develop some peripheral field defects. These can include nasal step defects, enlarged blind spots, arcuate scotomas, sectoral field loss and altitudinal defects. Clinical symptoms correlate to visibility of the drusen. Central vision loss is a rare complication of bleeding from peripapillar choroidal neovascular membranes. Anterior ischemic optic neuropathy (AION) is a potential complication.

A macular hole is a small break in the macula, located in the center of the eye's light-sensitive tissue called the retina.

The first symptom of this disease is usually a slow loss of vision. Early signs of Retinitis include loss of night vision; making it harder to drive at night. Later signs of retinitis include loss of peripheral vision, leading to tunnel vision. In some cases, symptoms are experienced in only one of the eyes. Experiencing the vision of floaters, flashes, blurred vision and loss of side vision in just one of the eyes is an early indication of the onset of Retinitis.

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.

Putscher's retinopathy is a disease where part of the eye (retina) is damaged. Usually associated with severe head injuries, it may also occur with other types of trauma, such as long bone fractures, or with several non-traumatic systemic diseases. However, the exact cause of the disease is not well understood. There are no treatments specific for Purtscher's retinopathy, and the prognosis varies. The disease can threaten vision, sometimes causing temporary or permanent blindness.

It is named for the Austrian ophthalmologist, Othmar Purtscher (1852–1927), who detected it in 1910 and described it fully in 1912.

In most patients, optic disc drusen are an incidental finding. It is important to differentiate them from other conditions that present with optic disc elevation, especially papilledema, which could imply raised intracranial pressure or tumors. True papilledema may present with exudates or cotton-wool spots, unlike ODD. The optic disc margins are characteristically irregular in ODD but not blurred as there is no swelling of the retinal nerve fibers. Spontaneous venous pulsations are present in about 80 percent of patients with ODD, but absent in cases of true disc edema. Other causes of disc elevation clinicians must exclude may be: hyaloid traction, epipapillary glial tissue, myelinated nerve fibres, scleral infiltration, vitreopapillary traction and high hyperopia. Disorders associated with disc elevation include: Alagille syndrome, Down syndrome, Kenny-Caffey syndrome, Leber Hereditary Optic Neuropathy and linear nevus sebaceous syndrome.

If the vitreous is firmly attached to the retina when it pulls away, it can tear the retina and create a macular hole. Also, once the vitreous has pulled away from the surface of the retina, some of the fibers can remain on the retinal surface and can contract. This increases tension on the retina and can lead to a macular hole. In either case, the fluid that has replaced the shrunken vitreous can then seep through the hole onto the macula, blurring and distorting central vision.

The causes of macular edema are numerous and different causes may be inter-related.

- It is commonly associated with diabetes. Chronic or uncontrolled diabetes type 2 can affect peripheral blood vessels including those of the retina which may leak fluid, blood and occasionally fats into the retina causing it to swell.

- Age-related macular degeneration may cause macular edema. As individuals age there may be a natural deterioration in the macula which can lead to the depositing of drusen under the retina sometimes with the formation of abnormal blood vessels.

- Replacement of the lens as treatment for cataract can cause pseudophakic macular edema. (‘pseudophakia’ means ‘replacement lens’) also known as Irvine-Gass syndrome The surgery involved sometimes irritates the retina (and other parts of the eye) causing the capillaries in the retina to dilate and leak fluid into the retina. Less common today with modern lens replacement techniques.

- Chronic uveitis and intermediate uveitis can be a cause.

- Blockage of a vein in the retina can cause engorgement of the other retinal veins causing them to leak fluid under or into the retina. The blockage may be caused, among other things, by atherosclerosis, high blood pressure and glaucoma.

- A number of drugs can cause changes in the retina that can lead to macular edema. The effect of each drug is variable and some drugs have a lesser role in causation. The principal medication known to affect the retina are:- latanoprost, epinephrine, rosiglitazone, timolol and thiazolidinediones among others.

- A few congenital diseases are known to be associated with macular edema for example retinitis pigmentosa and retinoschisis.

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.

Retinal detachment is a disorder of the eye in which the retina separates from the layer underneath. Symptoms include an increase in the number of floaters, flashes of light, and worsening of the outer part of the visual field. This may be described as a curtain over part of the field of vision. In about 7% of cases both eyes are affected. Without treatment permanent loss of vision may occur.

The mechanism most commonly involves a break in the retina that then allows the fluid in the eye to get behind the retina. A break in the retina can occur from a posterior vitreous detachment, injury to the eye, or inflammation of the eye. Other risk factors include being short sighted and previous cataract surgery. Retinal detachments also rarely occur due to a choroidal tumor. Diagnosis is by either looking at the back of the eye with an ophthalmoscope or by ultrasound.

In those with a retinal tear, efforts to prevent it becoming a detachment include cryotherapy using a cold probe or photocoagulation using a laser. Treatment of retinal detachment should be carried out in a timely manner. This may include scleral buckling where silicone is sutured to the outside of the eye, pneumatic retinopexy where gas is injected into the eye, or vitrectomy where the vitreous is partly removed and replaced with either gas or oil.

Retinal detachments affect between 0.6 and 1.8 people per 10,000 per year. About 0.3% of people are affected at some point in their life. It is most common in people who are in their 60s or 70s. Males are more often affected than females. The long term outcomes depend on the duration of the detachment and whether the macula was detached. If treated before the macula detaches outcomes are generally good.

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

Vitreous hemorrhage is the extravasation, or leakage, of blood into the areas in and around the vitreous humor of the eye. The vitreous humor is the clear gel that fills the space between the lens and the retina of the eye. A variety of conditions can result in blood leaking into the vitreous humor, which can cause impaired vision, floaters, and photopsia.