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

Age-related macular degeneration accounts for more than 54% of all vision loss in the white population in the USA. An estimated 8 million Americans are affected with early age-related macular degeneration, of whom over 1 million will develop advanced age-related macular degeneration within the next 5 years. In the UK, age-related macular degeneration is the cause of blindness in almost 42% of those who go blind aged 65–74 years, almost two-thirds of those aged 75–84 years, and almost three-quarters of those aged 85 years or older.

Macular degeneration is more likely to be found in Caucasians than in people of African descent.

No complications are encountered in most patients with lattice degeneration, although in young myopes, retinal detachment can occur. There are documented cases with macula-off retinal detachment in patients with asymptomatic lattice degeneration. Partial or complete vision loss almost always occurs in such cases. Currently there is no prevention or cure for lattice degeneration.

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.

This ocular pathology was first described by Iwanoff in 1865, and it has been shown to occur in about 7% of the population. It can occur more frequently in the older population with postmortem studies showing it in 2% of those aged 50 years and 20% in those aged 75 years.

Studies indicate drusen associated with AMD are similar in molecular composition to Beta-Amyloid (βA) plaques and deposits in other age-related diseases such as Alzheimer's disease and atherosclerosis. This suggests that similar pathways may be involved in the etiologies of AMD and other age-related diseases.

STGD1 is the most common form of inherited juvenile macular degeneration with a prevalence of approximately 1 in 10,000 births.

There is no good evidence for any preventive actions, since it appears this is a natural response to aging changes in the vitreous. Posterior vitreous detachment (PVD) has been estimated to occur in over 75 per cent of the population over age 65, that PVD is essentially a harmless condition (although with some disturbing symptoms), and that it does not normally threaten sight. However, since epiretinal membrane appears to be a protective response to PVD, where inflammation, exudative fluid, and scar tissue is formed, it is possible that NSAIDs may reduce the inflammation response. Usually there are flashing light experiences and the emergence of floaters in the eye that herald changes in the vitreous before the epiretinal membrane forms g

Optic disc drusen are found clinically in about 1% of the population but this increases to 3.4% in individuals with a family history of ODD. About two thirds to three quarters of clinical cases are bilateral. A necropsy study of 737 cases showed a 2.4% incidence with 2 out of 15 (13%) bilateral, perhaps indicating the insidious nature of many cases. An autosomal dominant inheritance pattern with incomplete penetrance and associated inherited dysplasia of the optic disc and its blood supply is suspected. Males and females are affected at equal rates. Caucasians are the most susceptible ethnic group. Certain conditions have been associated with disc drusen such as retinitis pigmentosa, angioid streaks, Usher syndrome, Noonan syndrome and Alagille syndrome. Optic disc drusen are not related to Bruch membrane drusen of the retina which have been associated with age-related macular degeneration.

Barrage laser is at times done prophylactically around a hole or tear associated with lattice degeneration in an eye at risk of developing a retinal detachment. It is not known if surgical interventions such as laser photocoagulation or cryotherapy is effective in preventing retinal detachment in patients with lattice degeneration or "asymptomatic" retinal detachment. Laser photocoagulation has been shown to reduce risks of retinal detachment in "symptomatic" lattice degeneration. There are documented cases wherein retina detached from areas which were otherwise healthy despite being treated previously with laser.

The long-term prognosis for patients with Stargardt disease is widely variable although the majority of people will progress to legal blindness.

Stargardt disease has no impact on general health and life expectancy is normal. Some patients, usually those with the late onset form, can maintain excellent visual acuities for extended periods, and are therefore able to perform tasks such as reading or driving.

Macular degeneration is a condition affecting the tissues lying under the retina, while a macular hole involves damage from within the eye, at the junction between the vitreous and the retina itself. There is no relationship between the two diseases. Depending upon the degree of attachment or traction between the vitreous and the retina, there may be risk of developing a macular hole in the other eye. In those cases where the vitreous has already become separated from the retinal surface, there is very little chance of developing a macular hole in the other eye. On the other hand, when the vitreous remains adherent and pulling on the macular region in both eyes, then there may be a greater risk of developing a hole in the second eye. In very rare instances, trauma or other conditions lead to the development of a macular hole. In the vast majority of cases, however, macular holes develop spontaneously. As a result, there is no known way to prevent their development through any nutritional or chemical means, nor is there any way to know who is at risk for developing a hole prior to its appearance in one or both eyes.

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.

This condition is linked to the X chromosome.

- Siberian Husky - Night blindness by two to four years old.

- Samoyed - More severe disease than the Husky.

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.

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.

The vitreous (Latin for "glassy") humor is a gel which fills the eye behind the lens. Between it and the retina is the vitreous membrane. With age the vitreous humor changes, shrinking and developing pockets of liquefaction, similar to the way a gelatin dessert shrinks and detaches from the edge of a pan. At some stage the vitreous membrane may peel away from the retina. This is usually a sudden event, but it may also occur slowly over months.

Age and refractive error play a role in determining the onset of PVD in a healthy person. PVD is rare in emmetropic people under the age of 40 years, and increases with age to 86% in the 90s. Several studies have found a broad range of incidence of PVD, from 20% of autopsy cases to 57% in a more elderly population of patients (average age was 83.4 years).

People with myopia (nearsightedness) greater than 6 diopters are at higher risk of PVD at all ages.

Posterior vitreous detachment does not directly threaten vision. Even so, it is of increasing interest because the interaction between the vitreous body and the retina might play a decisive role in the development of major pathologic vitreoretinal conditions, such as epiretinal membrane.

PVD may also occur in cases of cataract surgery, within weeks or months of the surgery.

The vitreous membrane is more firmly attached to the retina anteriorly, at a structure called the vitreous base. The membrane does not normally detach from the vitreous base, although it can be detached with extreme trauma. However, the vitreous base may have an irregular posterior edge. When the edge is irregular, the forces of the vitreous membrane peeling off the retina can become concentrated at small posterior extensions of the vitreous base. Similarly, in some people with retinal lesions such as lattice retinal degeneration or chorio-retinal scars, the vitreous membrane may be abnormally adherent to the retina. If enough traction occurs the retina may tear at these points. If there are only small point tears, these can allow glial cells to enter the vitreous humor and proliferate to create a thin epiretinal membrane that distorts vision. In more severe cases, vitreous fluid may seep under the tear, separating the retina from the back of the eye, creating a retinal detachment. Trauma can be any form from a blunt force trauma to the face such as a boxer's punch or even in some cases has been known to be from extremely vigorous coughing or blowing of the nose.

A cone dystrophy is an inherited ocular disorder characterized by the loss of cone cells, the photoreceptors responsible for both central and color vision.

There is another retinal disease in Briards known as hereditary retinal dysplasia. These dogs are night blind from birth, and day vision varies. Puppies affected often have nystagmus. It is also known as lipid retinopathy.

Predisposing factors for Postoperative PVR are preoperative PVR, aphakia, high levels of vitreous proteins, duration of retinal detachment before corrective surgery, the size of the retinal hole or tear, intra-ocular inflammation, vitreous hemorrhage, and trauma to the eye. An equation to calculate the patient's risk for acquiring PVR is:

1 is added if the risk factor is present and 0 if the risk factor is absent. A patient is at a high risk for developing PVR is the PVR score is >6.33.

At least one type of autosomal dominant cone-rod dystrophy is caused by mutations in the guanylate cyclase 2D gene (GUCY2D) on chromosome 17.

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.

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.

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.

Coats' disease, (also known as exudative retinitis or retinal telangiectasis, sometimes spelled Coates' disease), is a rare congenital, nonhereditary eye disorder, causing full or partial blindness, characterized by abnormal development of blood vessels behind the retina. Coats' disease can also fall under glaucoma.

It can have a similar presentation to that of retinoblastoma.