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.

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.

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.

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.

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.

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.

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.

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.

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.

Vitrectomy is the common way to treat a macular hole. It is done by placing a gas bubble in the vitreous of the eye which helps flatten macular hole and holds it in place as the eye heals. The gas bubble slowly shrinks on its own. Treatment is also done using ocriplasmin.

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.

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

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.

Treatment modalities currently under clinical investigation include cell therapy, gene therapy and oral therapies.

Regarding cell therapy, Advanced Cell Technology, now called Ocata Therapeutics, has completed Phase I/II multicenter clinical trial using retinal cells derived from human embryonic stem cells (hESCs) to treat patients with Stargardt. After treating and collecting data on 18 patients, Advanced Cell was given approval to test its stem cell therapy on patients with 20/100 vision. In October 2014, the results of the Phase I/II clinical trial were published in "the Lancet".

Research at the preclinical (animal) stage include a new compound that can remove lipofuscin from retinal pigment epithelial cells.

Careful eye examination by an ophthalmologist or optometrist is critical for diagnosing symptomatic VMA. Imaging technologies such as optical coherence tomography (OCT) have significantly improved the accuracy of diagnosing symptomatic VMA.

A new FDA approved drug was released on the market late 2013. Jetrea (Brand name) or Ocriplasmin (Generic name) is the first drug of its kind used to treat vitreomacular adhension.

Mechanism of Action: Ocriplasmin is a truncated human plasmin with proteolytic activity against protein components of the vitreous body and vitreretinal interface. It dissolves the protein matrix responsible for the vitreomacular adhesion.

Adverse drug reactions: Decreased vision, potential for lens sublaxation, dyschromatopsia (yellow vision), eye pain, floaters, blurred vision.

New Drug comparison Rating gave Jetea a 5 indicating an important advance.

Previously, no recommended treatment was available for the patient with mild symptomatic VMA. In symptomatic VMA patients with more significant vision loss, the standard of care is pars plana vitrectomy (PPV), which involves surgically removing the vitreous from the eye, thereby surgically releasing the symptomatic VMA. In other words, vitrectomy induces PVD to release the traction/adhesion on the retina. An estimated 850,000 vitrectomy procedures are performed globally on an annual basis with 250,000 in the United States alone.

A standard PPV procedure can lead to serious complications including small-gauge PPV. Complications can include retinal detachment, retinal tears, endophthalmitis, and postoperative cataract formation. Additionally, PPV may result in incomplete separation, and it may potentially leave a nidus for vasoactive and vasoproliferative substances, or it may induce development of fibrovascular membranes. As with any invasive surgical procedure, PPV introduces trauma to the vitreous and surrounding tissue.

There are data showing that nonsurgical induction of PVD using ocriplasmin (a recombinant protease with activity against fibronectin and laminin) can offer the benefits of successful PVD while eliminating the risks associated with a surgical procedure, i.e. vitrectomy. Pharmacologic vitreolysis is an improvement over invasive surgery as it induces complete separation, creates a more physiologic state of the vitreomacular interface, prevents the development of fibrovascular membranes, is less traumatic to the vitreous, and is potentially prophylactic. As of 2012, ThromboGenics is still developing the ocriplasmin biological agent. Ocriplasmin is approved recently under the name Jetrea for use in the United States by the FDA.view.

An experimental test of injections of perfluoropropane (CF) on 15 symptomatic eyes of 14 patients showed that vitreomacular traction resolved in 6 eyes within 1 month and resolved in 3 more eyes within 6 months.

Though there is no treatment for Cone dystrophy, certain supplements may help in delaying the progression of the disease.

The beta-carotenoids, lutein and zeaxanthin, have been evidenced to reduce the risk of developing age related macular degeneration (AMD), and may therefore provide similar benefits to Cone dystrophy sufferers.

Consuming omega-3 fatty acids (docosahexaenoic acid and eicosapentaenoic acid) has been correlated with a reduced progression of early AMD, and in conjunction with low glycemic index foods, with reduced progression of advanced AMD, and may therefore delay the progression of cone dystrophy.

Optic pits occur equally between men and women. They are seen in roughly 1 in 10,000 eyes, and approximately 85% of optic pits are found to be unilateral (i.e. in only one eye of any affected individual). About 70% are found on the temporal side (or lateral one-half) of the optic disc. Another 20% are found centrally, while the remaining pits are located either superiorly (in the upper one-half), inferiorly (in the lower one-half), or nasally (in the medial one-half towards the nose).

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.

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.