Supplements that include lutein and zeaxanthin may slow down the worsening of AMD. They have, however, not been shown to prevent the disease. There is not enough evidence to determine if statins have a role in preventing or slowing the progression of AMD. Antiangiogenic steroids such as anecortave acetate and triamcinolone acetonide have shown no evidence in preventing visual loss in people with neovascular AMD.

No medical or surgical treatment is available for this condition.

Macular edema sometimes occurs for a few days or weeks after cataract surgery, but most such cases can be successfully treated with NSAID or cortisone eye drops. Prophylactic use of Nonsteroidal anti-inflammatory drugs has been reported to reduce the risk of macular edema to some extent.

In 2010 the US FDA approved the use of Lucentis intravitreal injections for macular edema.

Iluvien, a sustained release intravitreal implant developed by Alimera Sciences, has been approved in Austria, Portugal and the U.K. for the treatment of vision impairment associated with chronic diabetic macular edema (DME) considered insufficiently responsive to available therapies. Additional EU country approvals are anticipated.

In 2013 Lucentis by intravitreal injection was approved by the National Institute for Health and Care Excellence in the UK for the treatment of macular edema caused by diabetes and/or retinal vein occlusion.

On July 29, 2014, Eylea (aflibercept), an intravitreal injection produced by Regeneron Pharmaceuticals Inc., was approved to treat DME in the United States.

In 2005, steroids were investigated for the treatment of macular edema due to retinal blood vessel blockage such as CRVO and BRVO.

Laser treatment of drusen has been studied. While it is possible to eliminate drusen with this treatment strategy, it has been shown that this fails to reduce the risk of developing the choroidal neovascularisation which causes the blindness associated with age-related macular degeneration.

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

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.

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.

Patients with optic disc drusen should be monitored periodically for ophthalmoscopy, Snellen acuity, contrast sensitivity, color vision, intraocular pressure and threshold visual fields. For those with visual field defects optical coherence tomography has been recommended for follow up of nerve fiber layer thickness. Associated conditions such as angioid streaks and retinitis pigmentosa should be screened for. Both the severity of optic disc drusen and the degree of intraocular pressure elevation have been associated with visual field loss. There is no widely accepted treatment for ODD, although some clinicians will prescribe eye drops designed to decrease the intra-ocular pressure and theoretically relieve mechanical stress on fibers of the optic disc. Rarely choroidal neovascular membranes may develop adjacent to the optic disc threatening bleeding and retinal scarring. Laser treatment or photodynamic therapy or other evolving therapies may prevent this complication.

To date, there is no known effective treatment for the non-proliferative form of macular telangiectasia type 2.

Treatment options are limited. No treatment has to date been shown to prevent progression. The variable course of progression of the disease makes it difficult to assess the efficacy of treatments. Retinal laser photocoagulation is not helpful. In fact, laser therapy may actually enhance vessel ectasia and promote intraretinal fibrosis in these individuals. It is hoped that a better understanding of the pathogenesis of the disease may lead to better treatments.

The use of vascular endothelial growth factor (VEGF) inhibitors, which have proven so successful in treating age-related macular degeneration, have not proven to be effective in non-proliferative MacTel type 2. Ranibizumab reduces the vascular leak seen on angiography, although microperimetry suggests that neural atrophy may still proceed in treated eyes.In proliferative stages (neovascularisation), treatment with Anti-VEGF can be helpful.

CNTF is believed to have neuroprotective properties and could thus be able to slow down the progression of MacTel type 2. It has been shown to be safe to use in MacTel patients in a phase 1 safety trial.

The most crucial aspect of managing patients with macular telangiectasia is recognition of the clinical signs. This condition is relatively uncommon: hence, many practitioners may not be familiar with or experienced in diagnosing the disorder. MacTel must be part of the differential in any case of idiopathic paramacular hemorrhage, vasculopathy, macular edema or focal pigment hypertrophy, especially in those patients without a history of retinopathy or contributory systemic disease.

Treatment options for macular telangiectasia type 1 include laser photocoagulation, intra-vitreal injections of steroids, or anti-vascular endothelial growth factor (anti-VEGF) agents. Photocoagulation was recommended by Gass and remains to date the mainstay of treatment. It seems to be successful in causing resolution of exudation and VA improvement or stabilization in selected patients. Photocoagulation should be used sparingly to reduce the chance of producing a symptomatic paracentral scotoma and metamorphopsia. Small burns (100–200 μm) of moderate intensity in a grid-pattern and on multiple occasions, if necessary, are recommended. It is unnecessary to destroy every dilated capillary, and, particularly during the initial session of photocoagulation, those on the edge of the capillary-free zone should be avoided.

Intravitreal injections of triamcinolone acetonide (IVTA) which have proved to be beneficial in the treatment of macular edema by their anti-inflammatory effect, their downregulation of VEGF production, and stabilization of the blood retinal barrier were reported anecdotally in the management of macular telangiectasia type 1. In two case reports, IVTA of 4 mg allowed a transitory reduction of retinal edema, with variable or no increase in VA. As expected with all IVTA injections, the edema recurred within 3–6 months, and no permanent improvement could be shown.14,15 In general, the effect of IVTA is short-lived and complications, mainly increased intraocular pressure and cataract, limit its use.

Indocyanine green angiography-guided laser photocoagulation directed at the leaky microaneurysms and vessels combined with sub-Tenon’s capsule injection of triamcinolone acetonide has also been reported in a limited number of patients with macular telangiectasia type 1 with improvement or stabilization of vision after a mean follow-up of 10 months.16 Further studies are needed to assess the efficacy of this treatment modality.

Recently, intravitreal injections of anti-VEGF agents, namely bevacizumab, a humanized monoclonal antibody targeted against pro-angiogenic, circulatory VEGF, and ranibizumab, a FDA-approved monoclonal antibody fragment that targets all VEGF-A isoforms, have shown improved visual outcome and reduced leakage in macular edema form diabetes and retinal venous occlusions. In one reported patient with macular telangiectasia type 1, a single intravitreal bevacizumab injection resulted in a marked increase in VA from 20/50 to 20/20, with significant and sustained decrease in both leakage on FA and cystoid macular edema on OCT up to 12 months. It is likely that patients with macular telangiectasia type 1 with pronounced macular edema from leaky telangiectasis may benefit functionally and morphologically from intravitreal anti-VEGF injections, but this warrants further studies.

Today, laser photocoagulation remains mostly effective, but the optimal treatment of macular telangiectasia type 1 is questioned, and larger series comparing different treatment modalities seem warranted. The rarity of the disease however, makes it difficult to assess in a controlled randomized manner.

However, these treatment modalities should be considered only in cases of marked and rapid vision loss secondary to macular edema or CNV. Otherwise, a conservative approach is recommended, since many of these patients will stabilize without intervention.

Surgeons can remove or peel the membrane through the sclera and improve vision by 2 or more Snellen lines. Usually the vitreous is replaced at the same time with clear (BSS) fluid, in a vitrectomy. Surgery is not usually recommended unless the distortions are severe enough to interfere with daily living, since there are the usual hazards of surgery, infections, and a possibility of retinal detachment. More common complications are high intraocular pressure, bleeding in the eye, and cataracts, which are the most frequent complication of vitrectomy surgery. Many patients will develop a cataract within the first few years after surgery. In fact, the visual distortions and diplopia created by cataracts may sometimes be confused with epiretinal membrane.

N-Acetylcarnosine drops have been investigated as a medical treatment for cataracts. The drops are believed to work by reducing oxidation and glycation damage in the lens, particularly reducing crystallin crosslinking. Some benefit has been shown in small manufacturer sponsored randomized controlled trials but further independent corroboration is still required.

Femtosecond laser mode-locking, used during cataract surgery, was originally used to cut accurate and predictable flaps in LASIK surgery, and has been introduced to cataract surgery. The incision at the junction of the sclera and cornea and the hole in capsule during capsulorhexis, traditionally made with a handheld blade, needle, and forceps, are dependent on skill and experience of the surgeon. Sophisticated three-dimensional images of the eyes can be used to guide lasers to make these incisions. can also then break up the cataract as in phacoemulsification.

Stem cells have been used in a clinical trial for lens regeneration in twelve children under the age of two with cataracts present at birth. The children were followed for six months, so it is unknown what the long-term results will be, and it is unknown if this procedure would work in adults.

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.

Cryotherapy (freezing) or laser photocoagulation are occasionally used alone to wall off a small area of retinal detachment so that the detachment does not spread.

The treatment method used depends on the cause of the hemorrhage. In most cases, the patient is advised to rest with the head elevated 30–45°, and sometimes to put patches over the eyes to limit movement prior to treatment in order to allow the blood to settle. The patient is also advised to avoid taking medications that cause blood thinning (such as aspirin or similar medications).

The goal of the treatment is to fix the cause of the hemorrhage as quickly as possible. Retinal tears are closed by Laser treatment or cryotherapy, and detached retinas are reattached surgically.

Even after treatment, it can take months for the body to clear all of the blood from the vitreous. In cases of vitreous hemorrhage due to detached retina,long-standing vitreous hemorrhage with a duration of more than 2–3 months, or cases associated with rubeosis iridis or glaucoma, a vitrectomy may be necessary to remove the standing blood in the vitreous.

Optic pits themselves do not need to be treated. However, patients should follow up with their eye care professional annually or even sooner if the patient notices any visual loss whatsoever. Treatment of PVD or serous retinal detachment will be necessary if either develops in a patient with an optic pit.

CNV is conventionally treated with intravitreal injections of angiogenesis inhibitors (also known as "anti-VEGF" drugs) to control neovascularization and reduce the area of fluid below the retinal pigment epithelium. Angiogenesis inhibitors include pegaptanib, ranibizumab and bevacizumab (known by a variety of trade names, such as Macugen, Avastin or Lucentis). These inhibitors slow or stop the formation of new blood vessels (angiogenesis), typically by binding to or deactivating the transmission of vascular endothelial growth factor ('VEGF'), a signal protein produced by cells to stimulate formation of new blood vessels. The effectiveness of angiogenesis inhibitors has been shown to significantly improve visual prognosis with CNV, the recurrence rate for these neovascular areas remains high.

CNV may also be treated with photodynamic therapy coupled with a photosensitive drug such as verteporfin (Visudyne). The drug is given intravenously. It is then activated in the eye by a laser light. The drug destroys the new blood vessels, and prevents any new vessels forming by forming thrombi.

Telemedicine programs are available that allow primary care clinics to take images using specially designed retinal imaging equipment which can then be shared electronically with specialists at other locations for review. In 2009, Community Health Center, Inc. implemented a telemedicine retinal screening program for low-income patients with diabetes as part of those patients annual visits at the Federally Qualified Health Center.

Currently, there is no treatment for the disease. However, ophthalmologists recommend wearing sunglasses and hats outdoors and blue-light blocking glasses when exposed to artificial light sources, such as screens and lights. Tobacco smoke and second-hand smoke should be avoided. Animal studies also show that high doses of vitamin A can be detrimental by building up more lipofuscin toxin. Dietary non-supplemental vitamin A intake may not further the disease progression.

Clinical trials are being conducted with promising early results. The trials may one day lead to treatments that might halt, and possibly even reverse, the effects of Stargardt disease using stem cell therapy, gene therapy, or pharmacotherapy.

The Argus retinal prosthesis, an electronic retinal implant, was successfully fitted to a 67-year-old woman in Italy at the Careggi Hospital in 2016. The patient had a very advanced stage of Stargardt’s disease, and a total absence of peripheral and central visual fields.

Retinoschisis involving the central part of the retina secondary to an optic disc pit was erroneously considered to be a serous retinal detachment until correctly described by Lincoff as retinoschisis. Significant visual loss may occur and following a period of observation for spontaneous resolution, treatment with temporal peripapillary laser photocoagulation followed by vitrectomy and gas injection followed by face-down positioning is very effective in treating this condition.

Risk factors such as UVB exposure and smoking can be addressed. Although no means of preventing cataracts has been scientifically proven, wearing sunglasses that counteract ultraviolet light may slow their development. While adequate intake of antioxidants (such as vitamins A, C, and E) has been thought to protect against the risk of cataracts, clinical trials have shown no benefit from supplements; though evidence is mixed, but weakly positive, for a potential protective effect of the nutrients lutein and zeaxanthin. Statin use is somewhat associated with a lower risk of nuclear sclerotic cataracts.

Several options exist for the treatment of BRVO. These treatments aim for the two of the most significant complications of BRVO, namely macular edema and neovascularization.

- Systemic treatment with oral Aspirin, subcutaneous Heparin, or intravenous thrombolysis have not been shown to be effective treatments for CRVO and for BRVO no reliable clinical trial has been published.

- Laser treatment of the macular area to reduce macular edema is indicated in patients who have 20/40 or worse vision and did not spontaneously improve for at least 3 months (to permit the maximum spontaneous resolution) after the development of the vein occlusion. It is typically administered with the argon laser and is focused on edematous retina within the arcades drained by the obstructed vein and avoiding the foveal avascular zone. Leaking microvascular abnormalities may be treated directly, but prominent collateral vessels should be avoided.

- The second indication of laser treatment is in case of neovascularization. Retinal photocoagulation is applied to the involved retina to cover the entire involved segment, extending from the arcade out to the periphery. Ischemia alone is not an indication for treatment provided that follow-up could be maintained.

- Preservative-free, nondispersive Triamcinolone acetonide in 1 or 4 mg dosage may be injected into the vitreous to treat macular edema but has complications including elevated intraocular pressure and development of cataract. Triamcinolone injection is shown to have similar effect on visual acuity when compared with standard care (Laser therapy), However, the rates of elevated intraocular pressure and cataract formation is much higher with the triamcinolone injection, especially the higher dosage. Intravitreal injection of Dexamethasone implant (Ozurdex; 700,350 μg) is being studied, its effect may last for 180 days. The injection may be repeated however with less pronounced effect. Although the implant was designed to cause less complications, pressure rise and cataract formation is noted with this treatment too.

- Anti-VEGF drugs such as Bevacizumab (Avastin; 1.25 -2.5 mg in 0.05ml) and Ranibizumab (lucentis) injections are being used and investigated. Intravitreal anti-VEGFs have a low incidence of adverse side effects compared with intravitreal corticosteroids, but are currently short acting requiring frequent injections. Anti-VEGF injection may be used for macular edema or neovascularization. The mechanism of action and duration of anti-VEGF effect on macular edema is currently unknown. The intraocular levels of VEGF are increased in eyes with macular edema secondary to BRVO and the elevated VEGF levels are correlated to the degree and severity of the areas of capillary nonperfusion and macular edema.

- Surgery is employed occasionally for longstanding vitreous hemorrhage and other serious complications such as epiretinal membrane and retinal detachment.

- Arteriovenous sheathotomy has been reported in small, uncontrolled series of patients with BRVO. BRVO typically occurs at arteriovenous crossings, where the artery and vein share a common adventitial sheath. In arteriovenous sheathotomy an incision is made in the adventitial sheath adjacent to the arteriovenous crossing and is extended along the membrane that holds the blood vessels in position to the point where they cross, the overlying artery is then separated from the vein.

There are good results from multiple doses of intravitreal injections of anti-VEGF drugs such as bevacizumab. A 2017 systematic review update found moderate evidence that aflibercept may have advantages in improving visual outcomes over bevacizumab and ranibizumab, after one year. Present recommended treatment for diabetic macular edema is Modified Grid laser photocoagulation combined with multiple injections of anti-VEGF drugs.

Usually being asymptomatic, drusen are typically found during routine eye exams where the pupils have been dilated.