All people with "diabetes mellitus" are at riskthose with Type I diabetes and those with Type II diabetes. The longer a person has diabetes, the higher their risk of developing some ocular problem. Between 40 and 45 percent of Americans diagnosed with diabetes have some stage of diabetic retinopathy. After 20 years of diabetes, nearly all patients with Type I diabetes and >60% of patients with Type II diabetes have some degree of retinopathy; however, these statistics were published in 2002 using data from four years earlier, limiting the usefulness of the research. The subjects would have been diagnosed with diabetes in the late 1970s, before modern fast acting insulin and home glucose testing.

Prior studies had also assumed a clear glycemic threshold between people at high and low risk of diabetic retinopathy.

However, it has been shown that the widely accepted WHO and American Diabetes Association diagnostic cutoff for diabetes of a fasting plasma glucose ≥ 7.0 mmol/l (126 mg/dl) does not accurately identify diabetic retinopathy among patients. The cohort study included a multi-ethnic, cross-sectional adult population sample in the US, as well as two cross-sectional adult populations in Australia. For the US-based component of the study, the sensitivity was 34.7% and specificity was 86.6%. For patients at similar risk to those in this study (15.8% had diabetic retinopathy), this leads to a positive predictive value of 32.7% and negative predictive value of 87.6%.

Published rates vary between trials, the proposed explanation being differences in study methods and reporting of prevalence rather than incidence values.

During pregnancy, diabetic retinopathy may also be a problem for women with diabetes.

It is recommended that all pregnant women with diabetes have dilated eye examinations each trimester to protect their vision.

People with Down's syndrome, who have extra chromosome 21 material, almost never acquire diabetic retinopathy. This protection appears to be due to the elevated levels of endostatin, an anti-angiogenic protein, derived from collagen XVIII. The collagen XVIII gene is located on chromosome 21.

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.

The two most common causes of retinopathy include diabetic retinopathy and retinopathy of prematurity. Diabetic retinopathy affects about 5 million people and retinopathy of prematurity affect about 50,000 premature infants each year worldwide. Hypertensive retinopathy is the next most common cause affecting anywhere from 3 to 14% of all non-diabetic adults.

Genetic mutations are rare causes of certain retinopathies and are usually X-linked including "NDP" family of genes causing Norrie Disease, FEVR, and Coats disease among others. There is emerging evidence that there may be a genetic predisposition in patients who develop retinopathy of prematurity and diabetic retinopathy. Trauma, especially to the head, and several diseases may cause Purtscher's retinopathy.

Purtscher's retinopathy was first characterized in 1910 and 1912 as a syndrome of sudden blindness after head trauma, with patches of hemorrhage and whitening of the retina in both eyes. Later, it was discovered to occur after other types of trauma, such as chest trauma, and is associated with several non-traumatic systemic diseases. Purtscher's retinopathy may also be associated with acute pancreatitis, vasculitis, embolization of such materials as fat and amniotic fluid, systemic lupus erythematosus, thrombotic thrombocytopenic purpura, and chronic renal failure. Purtscher's retinopathy may be caused by extensive fractures of the long bones.

In the UK, screening for diabetic retinopathy is part of the standard of care for people with diabetes. After one normal screening in people with diabetes, further screening is recommended every two years. Teleophthalmology has been employed in these programs.

Familial transmission is now recognized in a small proportion of people with MacTel type 2; however, the nature of any related genetic defect or defects remains elusive. The MacTel genetic study team hopes that exome analysis in the affected population and relatives may be more successful in identifying related variants.

CSR is a fluid detachment of macula layers from their supporting tissue. This allows choroidal fluid to leak beneath the retina. The buildup of fluid seems to occur because of small breaks in the retinal pigment epithelium.

CSR is sometimes called "idiopathic CSR" which means that its cause is unknown. Nevertheless, stress appears to play an important role. An oft-cited but potentially inaccurate conclusion is that persons in stressful occupations, such as airplane pilots, have a higher incidence of CSR.

CSR has also been associated with cortisol and corticosteroids. Persons with CSR have higher levels of cortisol. Cortisol is a hormone secreted by the adrenal cortex which allows the body to deal with stress, which may explain the CSR-stress association. There is extensive evidence to the effect that corticosteroids (e.g. cortisone), commonly used to treat inflammations, allergies, skin conditions and even certain eye conditions, can trigger CSR, aggravate it and cause relapses. In a study documented by Indian Journal of Pharmacology, a young male was using Prednisolone and began to display subretinal fluid indicative of CSR. With the discontinuation of the steroid drop the subretinal fluid resolved and did not show any sign of recurrence. Thus indicating the steroid was the probable cause of the CSR. A study of 60 persons with Cushing's syndrome found CSR in 3 (5%). Cushing's syndrome is characterized by very high cortisol levels. Certain sympathomimetic drugs have also been associated with causing the disease.

Evidence has also implicated helicobacter pylori (see gastritis) as playing a role. It would appear that the presence of the bacteria is well correlated with visual acuity and other retinal findings following an attack.

Evidence also shows that sufferers of MPGN type II kidney disease can develop retinal abnormalities including CSR caused by deposits of the same material that originally damaged the glomerular basement membrane in the kidneys.

Although a variety of complex classification schemes are described in the literature, there are essentially two forms of macular telangiectasia: type 1 and type 2. Type 1 is typically unilateral and occurs almost exclusively in males after the age of 40.

Type 2 is mostly bilateral, occurs equally in males and females.

Acute zonal occult outer retinopathy (AZOOR) is an inflammatory retinopathy in the category of white dot syndromes typified by acute loss of one or more zones of outer retinal function associated with photopsia, minimal funduscopic changes and abnormal electroretinography findings.

Risk factors for retinal detachment include severe myopia, retinal tears, trauma, family history, as well as complications from cataract surgery.

Retinal detachment can be mitigated in some cases when the warning signs are caught early. The most effective means of prevention and risk reduction is through education of the initial signs, and encouragement for people to seek ophthalmic medical attention if they have symptoms suggestive of a posterior vitreous detachment. Early examination allows detection of retinal tears which can be treated with laser or cryotherapy. This reduces the risk of retinal detachment in those who have tears from around 1:3 to 1:20. For this reason, the governing bodies in some sports require regular eye examination.

Trauma-related cases of retinal detachment can occur in high-impact sports or in high speed sports. Although some recommend avoiding activities that increase pressure in the eye, including diving and skydiving, there is little evidence to support this recommendation, especially in the general population. Nevertheless, ophthalmologists generally advise people with high degrees of myopia to try to avoid exposure to activities that have the potential for trauma, increase pressure on or within the eye itself, or include rapid acceleration and deceleration, such as bungee jumping or roller coaster rides.

Intraocular pressure spikes occur during any activity accompanied by the Valsalva maneuver, including weightlifting. An epidemiological study suggests that heavy manual lifting at work may be associated with increased risk of rhegmatogenous retinal detachment, but this relationship is not strong. In this study, obesity also appeared to increase the risk of retinal detachment. A high Body Mass Index (BMI) and elevated blood pressure have been identified as a risk factor in non-myopic individuals.

Genetic factors promoting local inflammation and photoreceptor degeneration may also be involved in the development of the disease.

Other risk factors include the following:

- Glaucoma

- AIDS

- Cataract surgery

- Diabetic retinopathy

- Eclampsia

- Family history of retinal detachment

- Homocysteinuria

- Malignant hypertension

- Metastatic cancer, which spreads to the eye (eye cancer)

- Retinoblastoma

- Severe myopia

- Smoking and passive smoking

- Stickler syndrome

- Von Hippel-Lindau disease

ROP prevalence varies, from 5–8% in developed countries with adequate neonatological facilities, to up to 30% in middle-income developing countries.

There is increasing evidence that ROP and blindness due to ROP are now public health problems in the middle income countries of Latin America, Eastern Europe and the more advanced economies in South East Asia and the Middle east region. In these countries ROP is often the most common cause of blindness in children. ROP is highly likely to become an increasing problem in India, China and other countries in Asia as these countries expand the provision of services for premature infants.

There is also evidence that the population of premature infants at risk of severe ROP varies depending on the level of neonatal intensive care being provided. In countries with high development indices and very low neonatal mortality rates (e.g. North America, western Europe), severe ROP is generally limited to extremely preterm infants i.e. those weighing less than 1 kg (2.2 lbs) at birth. At the other end of the development spectrum, countries with very low development indices and very high neonatal mortality rates (e.g. much of subSaharan Africa) ROP is rare as most premature babies do not have access to neonatal intensive care and so do not survive. Countries with moderate development indices are improving access to neonatal intensive care, and in these settings bigger, more mature babies are also at risk of severe ROP as neonatal care may be suboptimal i.e. those weighing 1.5–2 kg (3.3-4.4 lbs) at birth. These findings have two main implications: firstly, much can be done in countries with moderate development indices to improve neonatal care, to reduce the risk of severe ROP in bigger babies and increase survival of extremely preterm infants, and secondly, in these settings bigger more mature babies need to be included in ROP programs and examined regularly so as to detect those babies developing ROP requiring treatment.

In 2012, the World Health Organization published data on rates of preterm birth and the number of premature babies born in different regions of the world. This report contained three main findings:

- Premature birth has many different causes, and prevention is challenging,

- Prematurity is the most common cause of neonatal death in many countries, totaling as many as 1 million infants annually due to complications of preterm birth, and

- the number of preterm births is currently estimated to be 15 million, and increasing.

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 prognosis for CSR is generally excellent. Whilst immediate vision loss may be as poor as 20/200 in the affected eye, clinically over 90% of patients regain 20/30 vision or better within 6 months.

Once the fluid has resolved, by itself or through treatment, visual acuity should continue to improve and distortion should reduce as the eye heals. However, some visual abnormalities can remain even if visual acuity is measured at 20/20, and lasting problems include decreased night vision, reduced color discrimination, and localized distortion caused by scarring of the sub-retinal layers.

Complications include subretinal neovascularization and pigment epithelial detachment.

The disease can re-occur causing progressive vision loss. There is also a chronic form, titled as type II central serous retinopathy, which occurs in approximately 5% of cases. This exhibits diffuse rather than focalized abnormality of the pigment epithelium, producing a persistent subretinal fluid. The serous fluid in these cases tends to be shallow rather than dome shaped. Prognosis for this condition is less favorable and continued clinical consultation is advised.

ARN is associated with people who have latent herpes viruses that have been reactivated. The most common causes of the disease have been linked to VSV, HSV-1, HSV-2, and CMV respectively.

ARN cases have been reported in patients who have AIDS, are immunocompromised and in children. The disease is not limited to a specific gender. Most cases have been reported in young adults though children and the elderly can be affected.

Specific genetic markers in Caucasians in the United States have shown elevated risk for disease development (HLA-DQw7 and Bw62, DR4) as well as HLA-Aw33, B44, and DRw6 in the Japanese population.

Less common causes of vitreous hemorrhage make up 6.4–18% of cases, and include:

- Proliferative sickle cell retinopathy

- Macroaneurysm

- Age-related macular degeneration

- Terson syndrome

- Retinal neovascularization as a result of branch or central retinal vein occlusion

- Other – about 7 cases in 100,000 have no known cause attributed to them.

As one gets older, pockets of fluid can develop in the vitreous. When these pockets develop near the back of the eye, the vitreous can pull away from the retina and possibly tear it. Posterior vitreous detachment accounts for 3.7–11.7% of vitreous hemorrhage cases.

Several other diseases can result in retinopathy that can be confused with hypertensive retinopathy. These include diabetic retinopathy, retinopathy due to autoimmune disease, anemia, radiation retinopathy, and central retinal vein occlusion.

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.

Stages 1 and 2 do not lead to blindness. However, they can progress to the more severe stages. Threshold disease is defined as disease that has a 50% likelihood of progressing to retinal detachment. Threshold disease is considered to be present when stage 3 ROP is present in either zone I or zone II, with at least 5 continuous or 8 total clock hours of disease, and the presence of "plus" disease. Progression to stage 4 (partial retinal detachment), or to stage 5 (total retinal detachment), will result in substantial or total loss of vision for the infant.

- Refractive errors (most common)

- Squint

- Amblyopia

- Retinal detachment and blindness

- Glaucoma

The incidence of retinal detachment in otherwise normal eyes is around 5 new cases in 100,000 persons per year. Detachment is more frequent in middle-aged or elderly populations, with rates of around 20 in 100,000 per year. The lifetime risk in normal individuals is about 1 in 300. Asymptomatic retinal breaks are present in about 6% of eyes in both clinical and autopsy studies.

- Retinal detachment is more common in people with severe myopia (above 5–6 diopters), in whom the retina is more thinly stretched. In such patients, lifetime risk rises to 1 in 20. About two-thirds of cases of retinal detachment occur in myopics. Myopic retinal detachment patients tend to be younger than non-myopic ones.

- Retinal detachment is more frequent after surgery for cataracts. The estimated long-term prevalence of retinal detachment after cataract surgery is in the range of 5 to 16 per 1000 cataract operations, but is much higher in patients who are highly myopic, with a prevalence of up to 7% being reported in one study. One study found that the probability of experiencing retinal detachment within 10 years of cataract surgery may be about 5 times higher than in the absence of treatment.

- Tractional retinal detachments can also occur in patients with proliferative diabetic retinopathy or those with proliferative retinopathy of sickle cell disease. In proliferative retinopathy, abnormal blood vessels (neovascularization) grow within the retina and extend into the vitreous. In advanced disease, the vessels can pull the retina away from the back wall of the eye, leading to tractional retinal detachment.

Although retinal detachment usually occurs in just one eye, there is a 15% chance of it developing in the other eye, and this risk increases to 25–30% in patients who have had a retinal detachment and cataracts extracted from both eyes.

There is an association between the grade of retinopathy and mortality. In a classic study in 1939 Keith and colleagues described the prognosis of people with differing severity of retinopathy. They showed 70% of those with grade 1 retinopathy were alive after 3 years whereas only 6% of those with grade 4 survived.The most widely used modern classification system bears their name. The role of retinopathy grading in risk stratification is debated, but it has been proposed that individuals with signs of hypertensive retinopathy signs, especially retinal hemorrhages, microaneurysms and cotton-wool spots, should be assessed carefully.

This may be present in conditions causing traction on the retina especially at the macula. This may occur in:

a) The vitreomacular traction syndrome; b) Proliferative diabetic retinopathy with vitreoretinal traction; c) Atypical cases of impending macular hole.

DUSN may be caused by a helminthic infection with Toxocara canis, Baylisascaris procyonis, or Ancylostoma caninum. The characteristic lesions are believed to result from a single nematode migrating within the subretinal space. Although previously thought to be endemic in some areas, that belief was likely due to under awareness. DUSN has been diagnosed in patients in many countries and climates including America, Brazil, China and India.

In a study done published by the British Journal of Ophthalmology, the cases of ARN/BARN reported in 2001-2002 in the UK, Varicella Zoster Virus was the most common culprit for the disease and presented mostly in men than in women.

Researchers have also looked at two cases of ARN in patients who have been diagnosed with an immunodeficiency virus. The disease presented itself more so in the outer retina until it progressed far enough to then affect the inner retina. The patients were not so responsive to the antiviral agents given to them through an IV, acyclovir specifically. The cases progressed to retinal detachment. The patients tested positive for the herpes virus. Researchers are now wondering if this type of ARN is specific to those who have the immunodeficiency virus.