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

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.

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.

Purtscher's retinopathy can lead to loss of vision, and recovery of vision may occur very little. However, vision recovery does occur in some cases, and reports have varied on the long-term prognosis.

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.

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.

Diabetic retinopathy, also known as diabetic eye disease, is a medical condition in which damage occurs to the retina due to diabetes and is a leading cause of blindness.

It affects up to 80 percent of people who have had diabetes for 20 years or more. At least 90% of new cases could be reduced if there were proper treatment and monitoring of the eyes. The longer a person has diabetes, the higher his or her chances of developing diabetic retinopathy. Each year in the United States, diabetic retinopathy accounts for 12% of all new cases of blindness. It is also the leading cause of blindness for people aged 20 to 64 years.

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.

This condition is often associated with diabetes in advanced proliferative diabetic retinopathy. Other conditions causing rubeosis iridis include central retinal vein occlusion, ocular ischemic syndrome, and chronic retinal detachment.

Macular telangiectasia type 1 must be differentiated from secondary telangiectasis caused by retinal vascular diseases such as retinal venous occlusions, diabetic retinopathy, radiation retinopathy, sickle cell maculopathy, inflammatory retinopathy/Irvine–Gass syndrome, ocular ischemic syndrome/carotid artery obstruction, hypertensive retinopathy, polycythemia vera retinopathy, and localized retinal capillary hemangioma. In addition, Macular telangiectasia type 1 should be clearly differentiated from dilated perifoveal capillaries with evidence of vitreous cellular infiltration secondary to acquired inflammatory disease or tapetoretinal dystrophy. Less commonly, macular telangiectasis has been described in association with fascioscapulohumeral muscular dystrophy, incontinentia pigmenti, and familial exudative vitreoretinopathy with posterior pole involvement.

Macular telangiectasia type 2 is commonly under-diagnosed. The findings may appear very similar to diabetic retinopathy, and many cases ave been incorrectly ascribed to diabetic retinopathy or age-related macular degeneration. Recognition of this condition can save an affected patient from unnecessarily undergoing extensive medical testing and/or treatment. MacTel should be considered in cases of mild paramacular dot and blot hemorrhages and in cases of macular and paramacular RPE hyperplasia where no other cause can be identified.

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.

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.

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.

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.

Rubeosis iridis, also called neovascularization of the iris (NVI), is a medical condition of the iris of the eye in which new abnormal blood vessels (formed by neovascularization) are found on the surface of the iris.

Chloroquine retinopathy, also known as Bull's eye maculopathy, is a retinopathy (damage of the retina) caused by the drugs chloroquine or hydroxychloroquine, which are sometimes used in the treatment of autoimmune disorders such as rheumatoid arthritis and systemic lupus erythematosus. This eye toxicity limits long-term use of the drugs.

Most patients with hypertensive retinopathy have no symptoms. However, some may report decreased or blurred vision, and headaches.

Most common:

- Floaters

- Blurred vision

Intermediate uveitis normally only affects one eye. Less common is the presence of pain and photophobia.

Inflammation in the back of the eye is commonly characterized by:

- Floaters

- Blurred vision

- Photopsia or seeing flashing lights

Signs of damage to the retina caused by hypertension include:

- Arteriolar changes, such as generalized arteriolar narrowing, focal arteriolar narrowing, arteriovenous nicking, changes in the arteriolar wall (arteriosclerosis) and abnormalities at points where arterioles and venules cross. Manifestations of these changes include "Copper wire arterioles" where the central light reflex occupies most of the width of the arteriole and "Silver wire arterioles" where the central light reflex occupies all of the width of the arteriole, and "arterio-venular (AV) nicking" or "AV nipping", due to venous constriction and banking.

- advanced retinopathy lesions, such as microaneurysms, blot hemorrhages and/or flame hemorrhages, ischemic changes (e.g. "cotton wool spots"), hard exudates and in severe cases swelling of the optic disc (optic disc edema), a ring of exudates around the retina called a "macular star" and visual acuity loss, typically due to macular involvement.

Mild signs of hypertensive retinopathy can be seen quite frequently in normal people (3–14% of adult individuals aged ≥40 years), even without hypertension. Hypertensive retinopathy is commonly considered a diagnostic feature of a hypertensive emergency although it is not invariably present.

This type of retinoschisis is very common with a prevalence of up to 7 percent in normal persons. Its cause is unknown. It can easily be confused with retinal detachment by the non-expert observer and in difficult cases even the expert may have difficulty differentiating the two. Such differentiation is important since retinal detachment almost always requires treatment while retinoschisis never itself requires treatment and leads to retinal detachment (and hence to visual loss) only occasionally. Unfortunately one still sees cases of uncomplicated retinoschisis treated by laser retinopexy or cryopexy in an attempt to stop its progression towards the macula. Such treatments are not only ineffective but unnecessarily risk complications. There is no documented case in the literature of degenerative retinoschisis itself (as opposed to the occasional situation of retinal detachment complicating retinoschisis) in which the splitting of the retina has progressed through the fovea. There is no clinical utility in differentiating between typical and reticular retinoschisis. Degenerative retinoschisis is not known to be a genetically inherited condition.

There is always vision loss in the region of the schisis as the sensory retina is separated from the ganglion layer. But like the loss is in the periphery, it goes unnoticed. It is the very rare schisis that encroaches on the macula where retinopexy is then properly used.

Retinoschisis is an eye disease characterized by the abnormal splitting of the retina's neurosensory layers, usually in the outer plexiform layer. Most common forms are asymptomatic, some rarer forms result in a loss of vision in the corresponding visual field.

Some discrepancy exists as to whether acute zonal occult outer retinopathy (AZOOR) is actually considered a white dot syndrome. However, AZOOR may definitely be related to other diseases included in the white dot syndrome group. AZOOR occurs in young to middle age adults and may eventually progress to retinal cell death. Symptoms include acute visual field loss and photopsias. Suspected causes for AZOOR include autoimmune, viral, and fungal.

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.

The risk of toxicity is low for individuals without complicating conditions during the first 5 years of treatment using less than 6.5 mg/kg/day of hydroxychloroquine or 3 mg/kg/day of chloroquine, and/or cumulative doses of less than 1000 gram and 460 gram (total dose), respectively. Some physicians suggest that lean body weight is more accurate when calculating daily dosage.

Most patients are routinely given 400 mg of hydroxychloroquine daily (or 250 mg chloroquine). This dose is considered acceptable.

The earliest signs of toxicity include bilateral paracentral visual field changes (best detected with a red test object) and a subtle granular depigmentation of the paracentral RPE.

With continued drug exposure, there is progressive development of a bilateral atrophic bull's-eye maculopathy and paracentral scotomata, which may in severe cases ultimately spread over the entire fundus, causing widespread retinal atrophy and visual loss.