Treatment options depend on the type and stage of MD. Whilst there is presently no cure, early detection is vital to save sight. The earlier you seek treatment, the more likely you are to have a better visual outcome compared to those who wait.
MD can cause many different symptoms. Diffculty with your vision should not be dismissed as part of 'getting older'. In its early stages MD may not be obvious to you but can be detected in with eye test before any visual symptoms occur. Early detection may allow you to take steps to slow the progression of MD.
Optical Coherence Tomography (OCT)
OCT is a standard investigation for the diagnosis and ongoing management of wet MD. It is a non-invasive imaging technique that uses light to produce very high resolution cross sectional images of the retinal layers. Repeated tests are usually necessary to monitor disease activity.
Fluorescein angiography (FA)
FA is sometimes used to investigate wet MD. It involves injecting fluorescein dye into a vein in the arm to image the blood circulation at the back of the eye. As the dye circulates through the choroidal and retinal blood vessels, a camera with a special filter is used to take a series of photographs over about 10 minutes. The dye highlights any abnormalities of or damage to the blood vessels.
Currently there are no medical treatments for dry MD. However, a considerable amount of research is being conducted to find a treatment.
There are a number of medical treatments available for wet MD. These treatments do not cure the disease but aim to stabilise vision and maintain the best vision for as long as possible. In some people, treatment can improve vision. Treatment options for wet MD should be discussed with an eye specialist.
In wet MD, blood vessels are prompted to grow under the retina by a protein called vascular endothelial growth factor (VEGF). These vessels can bleed, leak fluid and cause scarring under the retina leading to rapid vision loss that if left untreated becomes permanent. To slow or stop this process, various drugs that block VEGF (called anti-VEGFs) can be used.
These drugs consist of an antibody directed at VEGF. They are injected into the eye where they spread to the retina and block VEGF induced blood vessel growth. Anti-VEGF drugs have been proven effective in many clinical trials and maintain vision in the vast majority of patients with wet MD.
Treatment usually begins with monthly injections for 3 months. In order to maintain control of the disease, injections are usually required indefinitely. However, the interval between ongoing injections is determined on an individualised basis by the eye specialist in consultation with the patient.
Avastin was primarily developed, tested and approved to decrease new blood vessel growth associated with cancer. It is highly effective and used worldwide for treating wet MD. It is funded by PHARMAC, the NZ government agency that decides which medicines are subsidised for use in the community and public hospitals. However, it is not registered for the treatment of MD as it was not designed for use in the eye. Avastin is typically used as the initial treatment of wet MD in NZ.
Lucentis is very similar to Avastin. It is derived from the same parent molecule but is much smaller and has been pharmacologically altered to provide stronger binding to VEGF than Avastin. Lucentis was specifically formulated and registered for use in the eye. It costs significantly more than Avastin and its availability in the NZ public health service is restricted by PHARMAC.
Eylea is similar to Avastin and Lucentis but works slightly differently to them. It binds to VEGF significantly more strongly than both Avastin and Lucentis, and also binds placental growth factor (another factor involved in the development of abnormal blood vessels). It is longer acting and only needs to be injected every 2 to 3 months rather than monthly. It is registered for use in the eye but not funded by PHARMAC.
Photodynamic therapy (PDT)
This is a 2-step process combining a light-activated drug called Visudyne (verteporfin) with light from a cold laser directed onto the abnormal area of retina. Once activated, the drug causes the abnormal vessels to close off. PDT does not cause direct damage to the surrounding retina. Therefore, it can be used to treat new vessels that are under the centre of the macula (fovea).
Several treatments are needed to keep the leaking blood vessels closed and stop the progression of wet MD. Close follow up and monitoring is needed to determine if further treatment is required.
Unlike anti-VEGF drugs with which the vision is usually maintained, patients undergoing PDT continue to lose vision in the first 6 months. Their vision then stabilises so that the eye does not progress to severe vision loss.
PDT is now rarely used to treat ordinary wet MD. It is sometimes used in conjunction an anti-VEGF drug to treat a type of MD called polypoidal choroidal vasculopathy (PCV) as some of these cases do not settle completely with anti-VEGF treatment.
This treatment consists of a concentrated light beam of high-energy thermal light that is directed onto the retina to destroy and seal leaking blood vessels. It is not painful. The laser not only destroys the abnormal vessels but also destroys retina adjacent to them. Therefore, it may only be used for treating new vessels that are not under the central part of the macula.
Laser photocoagulation is only used for a small percentage of patients with wet MD. Close follow up is required as there is a 50% recurrence rate.
Nutrition and supplements
The Age Related Eye Disease Studies (AREDS I and II) are 2 major clinical trials that identified a specific formula of antioxidants including high dose zinc that significantly reduced the relative risk of progression of MD and delayed vision loss. The daily amounts of these are zinc 80 mg, copper 2 mg, vitamin E 400 IU, vitamin C 500 mg, lutein 10 mg and zeaxanthin 2 mg. More information is contained in MDNZ’s Nutrition and Supplements fact sheet. Any changes in diet or lifestyle should be undertaken in consultation with your doctor.