Age-related macular degeneration (AMD) causes vision loss by damaging the retina, a paper-thin tissue lining the back of the eye that detects fine details and colors. At its center lies the macula which detects these details and colors.

Wet AMD occurs when abnormal blood vessels form and leak fluid beneath the retina. An eye care provider can diagnose it using fundus fluorescein angiography as a diagnostic test for wet AMD.

Treatment for Dry AMD

The dry form of AMD occurs when light-sensing cells in the macula begin to break down over time, eventually leading to its thinning and blurred vision. Although scientists don’t fully understand why this happens, 8 out of 10 people with AMD experience it at some point. Over time, contrast detection may become impaired so objects appear blurry even under bright lighting conditions; but early stages can often be delayed with regular visits to an ophthalmologist and by taking certain dietary supplements.

An important diet recommendation for AMD prevention includes eating plenty of Omega 3 fish such as salmon and trout, along with vegetables high in Lutein such as spinach, kale and broccoli. Supplementing with Vitamin C and Zeaxanthin has also proven successful at slowing the progression of AMD; an AREDS formula was even designed specifically to deliver this combination of nutrients as an oral medication and has shown to slow vision decline for people suffering both dry and wet AMD.

Studies suggest that metformin, a widely prescribed diabetes medication, could reduce the risk of AMD in those living with diabetes; however, more research needs to be completed in order to confirm this finding.

Anti-VEGF agents provide another experimental therapy option for wet AMD. This molecule works by stopping the formation of new blood vessels, which cause wet AMD. Therapy typically involves administering an injection directly into the eye. Some patients may require fluorescein angiography as a measure to evaluate treatment efficacy – injecting special dye into arm veins before photographing retina as dye passes through, which allows ophthalmologist to spot leaky blood vessels, retinal edema or subretinal fluid which cause loss of central vision; then cauterizing abnormal blood vessels in order to stop leakage of fluid into vision loss thereby restoring vision loss in those affected.

Treatment for Atrophic AMD

Age-related macular degeneration (AMD) is a progressive eye disease that over time leads to permanent loss of central vision. The condition begins with protein deposits called drusen that form under the retinal pigment epithelium layer of the macula and eventually progresses as far as detaching all central vision altogether. RPE cells in the macula play an invaluable role in supporting light-sensitive photoreceptor cells by providing metabolic nourishment to these photoreceptor cells. Over time, oxidative stress, accumulation of lipofuscin and inflammation of the RPE contributes to its degradation and irreversible macular atrophy. Progression of dry macular degeneration is typically gradual and there is no effective treatment other than supplementation with antioxidative micronutrients and verteporfin photodynamic therapy for severe cases that do not respond to pharmaceutical interventions.

Recent research published in Ophthalmology revealed that treated wet AMD eyes appear to have greater macular atrophy than their untreated counterparts; however, they still maintain an even symmetry between both eyes. Researchers concluded this difference wasn’t caused by early onset atrophy but rather slower rate of atrophy in treated eyes than untreated.

While atrophic AMD cannot be reversed, its progression can be significantly slowed with anti-VEGF injections. These drugs work to stop abnormal new blood vessel growth in the eye that leads to wet AMD (neovascularization). Anti-VEGF injections are administered via series of intravitreal injections given monthly with local anesthetic eye drops used prior to each session in order to numb any potential discomfort before injecting any medication directly into the eye.

Patients diagnosed with wet-form macular degeneration can be easily identified using International Classification of Diseases, 9th Revision (ICD)-9 or ICD-10 codes from medical records or electronic health record systems. VEHSS uses these codes to identify individuals with self-reported diagnoses of AMD; data obtained through National Health Interview Survey and the NHIS are also utilized by this system to ascertain self-reported AMD diagnoses.

Treatment for Vascular AMD

Though the exact cause and pathogenesis of wet AMD remain enigmatic, recent clinical studies have demonstrated that anti-vascular endothelial growth factor (anti-VEGF) medications like ranibizumab, bevacizumab and brolucizumab may improve vision by reducing vision loss and slowing disease progression. By inhibiting the action of VEGF these anti-VEGF medicines reduce new blood vessel growth that leads to choroidal neovascularization – the central retinal bleeds responsible for severe visual loss caused by wet AMD.

Researchers conducted a large, multicenter trial comparing bevacizumab and ranibizumab, and discovered they both performed similarly in terms of improving vision for those with neovascular wet AMD. These results confirmed the findings from other trials as well as being in line with NICE guidance on this condition (NG82).

These treatments may be costly for those requiring regular injections, but have shown significant promise in terms of maintaining vision over time. As of now, these are the mainstay treatment for neovascular wet AMD in most industrialized countries; however, their current limitations require further study in order to maximize visual outcomes, reduce treatment burden and limit geographic atrophy.

Gene therapy for retinal diseases, a one-time procedure to deliver therapeutic proteins directly into the eye, has already produced improved visual outcomes in wet AMD patients. The technique known as AAV-mediated Gene Delivery will soon be expanded to treat other monogenic blinding disorders.

JAMA Ophthalmology recently reported in their journal that some eyes with wet neovascular AMD can maintain good vision even years after discontinuing anti-VEGF therapy. Researchers found that 6.4% of participants in one study could stop monthly injections while still attaining functional vision acuity scores of at least 68 letters (Snellen 20/40 or better) using an as-needed injection regime; both groups achieved comparable vision outcomes at five years.

Treatment for Exudative AMD

10-15% of patients with dry AMD will progress to what’s known as wet or exudative age-related macular degeneration (AMD). This occurs when abnormally growing blood vessels begin leaking fluid underneath the retina. If left untreated, leakage could lead to subretinal hemorrhage or retinal detachments which in turn could result in serious vision loss or even blindness if untreated – wet AMD may be less common but results in faster and more severe vision loss than dry AMD.

Wet AMD is caused by abnormal growth of blood vessels between layers of cells in the retina known as choroidal neovascularization (CNV), leading to severe vision loss from AMD. CNV often begins as small bleeding spots in the macula but can quickly progress and cover larger parts or all of the retina.

CNV in the retina is caused by abnormally elevated levels of vascular endothelial growth factor (VEGF), a protein which promotes abnormal blood vessel formation that leaks fluid and blood into the eye, leading to central vision loss as well as macular edema or retinal detachment.

Wet AMD involves new blood vessels appearing as thin segments on an OCT scan as thin segments of choroid with or without fluid leaks, detectable as early as eight months before any visual loss symptoms appear. Early detection is crucial; recent research indicates that ORL thickness on OCT images can accurately predict if an eye will eventually develop wet AMD.

Treatment for wet AMD typically entails monthly injections of anti-VEGF medications like Bevacizumab, Ranibizumab or Pegaptanib to block new blood vessel growth under your retina that could bleed under it and compromise vision. These injections should be given into the vitreous gel within your eye for best results.

Research continues to look for ways to enhance the efficacy of anti-VEGF drugs, with one approach being the use of AAV (adeno-associated virus) gene therapy as one possible strategy. This method has already proven successful in treating monogenic blinding diseases such as LCA2.