What is AMD?
AMD (Age-Related Macular Degeneration) is the leading cause of legal blindness in people aged 65 and over. But now, instead of neovascular AMD carrying a high risk of blindness, most people have the vision preserved or improved with treatment. This is due to breakthroughs in our understanding of the basic processes causing blindness. Blindness due to “neovascular”, or what has commonly been called “wet” macular degeneration, can be prevented in most patients through regular intravitreal injections of drugs like Lucentis and Eylea. In the future we hope to also be able to prevent the visual loss due to “dry” AMD.
AMD is best thought of as Accumulating Macular Damage. The disease causes cumulative retinal damage, rather than it being an ageing degenerative process.
The processes where the immune system prevents us being overrun by invading organisms can damage our own bodies as well. Our understanding of this disease has been revolutionized by the discovery that the majority of people with AMD lose vision because the retina is progressively damaged; by our own immune system as it fights off the bacteria and viruses, to which it is regularly exposed. To prevent loss of our own body’s cells, all cells have a protective coating which identifies them as “friend” not “foe.” This protective coating is similar to the paint on the Sydney Harbour Bridge, or the galvanising on corrugated iron that prevents the metal rusting. If the coating is not maintained, progressive rusting occurs so that the metal degrades with rust flakes, holes form and ultimately collapse occurs.
The retina is no different; but for the retina, the protective coating is called complement factor H and without it, retinal tissue is progressively damaged, causing accumulating piles of dead cells (called drusen) and thinning of the light detecting retinal tissue. People with the least effective complement factor H, will show extensive damage at a relatively young age (i.e.50-60s); versus those with more competent protection, where it may not show up until they are 90. The extent of tissue damage is thus the combination of the severity of the abnormality and age.
With diminishing numbers of light responsive tissue (the photoreceptors) and the interacting cells that keep them regenerated in their active state (the pigment cells), there is a progressive loss of the visual functional range. This slows the adjustment from bright light to dark, makes people susceptible to glare, requires a brighter light and magnification to read and eventually causes legal blindness.
Less photoreceptors mean the same as fewer pixels in a camera. Modern digital cameras are a useful analogy to our eye. Fewer light detecting cells (photoreceptors) means worse image quality. This is similar to the decreasing quality of an enlarged photo from a phone camera versus a full size professional one. The camera in a phone might take a reasonable photograph under good light and look ok when it is very small on the screen, but it will be very poor if taken under more extreme lighting conditions or when enlarged. A professional camera will cope with a much greater range of lighting, give better detail and will take photos at a faster rate.
In general, most people with AMD maintain good vision for a long time. Sometimes this phase is called “dry” (as in not wet) but as there are minimal visual effects, it is best thought of as early or minimal.
Early in the development of AMD, people notice that they need a brighter light to read, faces can be harder to recognise and they are more susceptible to glare or adjusting to dim lights (such as driving into an underground car park). In advanced AMD, abnormal blood vessels sprout under the retina causing distortion and blurred vision (neovascular or so called “wet” AMD). Prompt diagnosis is essential to optimise the vision by commencing treatment with an anti-VEGF drug.
In some cases, progressive difficulty reading can be due to areas of retinal atrophy (withering or “bald spots”) that have poor sensitivity around sharp central vison. This is usually referred to as “dry AMD” but that is a poor term. At the moment there is no treatment for this form of AMD, but some clinical trials are underway and you might be eligible for that.
It is important to know that AMD is due to an inherited susceptibility, for which there is no cure at the moment. Preventative measures help slow down deterioration, but do not cure the underlying disease.
In summary, the critical issues are:
- Natural antioxidants – lutein and zeaxanthin – derived from green and yellow vegetables are the most effective antioxidants. They also protect the macula by acting as a natural “sunblock” filter within the eye, by blocking potentially damaging blue light. It is critical that sufficient dietary intake is achieved, otherwise defective filtering results in long term retinal damage.
- Lutein: Best sources are green leafy vegetables (kale, spinach, broccoli, and romaine lettuce), corn, green peas and cabbage. (If you are unable to eat green leafy vegetables due to medication or other reasons, Blackmores Lutein-VisionTM and Lutein DefenceTM contain extracts from the green leafy vegetables. One tablet twice a day is best).
- Zeaxanthin: Yellow vegetables (yellow capsicum, mango, corn) and orange juice are excellent sources. The most concentrated source is goji berries. Egg yolks also have high concentrations of both Lutein and Zeaxanthin. Having six eggs per week has been shown to be beneficial to those with Macular Degeneration.
- Wear sunglasses and a hat. Remember that our eyes evolved to have colour vision in daylight and “black and white” vision at night. We now use our “B&W” system for long hours at daylight lighting levels with artificial lighting causing it to wear out.
What to do if you have been diagnosed with macular degeneration
Remember to regularly check the vision in each eye independently, particularly while reading. The Amsler grid chart is also very useful, but most people find that blurring or distortion of their reading vision is the first alarm.
You must report any changes (blurring, distortion of central shadow) promptly for an examination. Note: a cataract does not progress quickly, so any deterioration in your vision occurring over several weeks will not be a cataract or your glasses. It will be your eye changing quickly that is the problem. Early intervention is critical to prevent irreversible damage blinding you. Too many people go blind, assuming that the cataract has progressed or thinking that a scheduled appointment six weeks later would be “good enough”. Any deteriorating vision needs prompt assessment.
What will happen at your examination?
You will undergo standard preliminary examination (usually with a trained eye care technician such as an orthoptist) including distance and reading visual acuity, intraocular pressure and OCT examination. Your eyes will almost certainly be dilated with some drops, to enable a detailed examination of the macula and remaining retina.
If there is evidence of neovascular or “wet” AMD, prompt treatment with anti-VEGF drugs is essential and usually is performed on the day, to prevent further or irreversible visual deterioration. Regular reviews, initially four weekly, will then be arranged.
Treatment of wet or neovascular AMD
A class of drugs called anti-VEGF agents have revolutionised the management of neovascular or “wet” AMD. These drugs block the effect of an agent called Vascular Endothelial Growth Factor. This is a fertiliser produced by the body to grow new blood vessels. While this is an essential process while a baby is growing or if there is a wound that needs healing, some diseases trigger VEGF production as part of the disease process causing swelling, bleeding and scar tissue formation. In macular degeneration, an unknown trigger causes new blood vessels to grow, like sprouting mushrooms under the retina that push the retina upwards, causing distortion and blurring, ooze fluid and bleed. Injections into the eye cavity of an anti-VEGF drug such as Avastin, Lucentis or Eylea inactivate VEGF and suppress the neovascular complications. These injections are performed on a regular basis from 4 weeks through 3 monthly, depending on the disease activity. The injections are performed in the office with copious antiseptic and adequate local anaesthetic drops or gel. The injections are virtually pain-free and safe. The risk of an infection entering the eye is now 1 in 20,000 (recent review of results at Bascom Palmer Eye Centre) and rarely cause cataract formation.
Australia has a world leading patient awareness and government supported (PBS) strategy to manage macular degeneration. Such that both Lucentis and Eylea are on the PBS supported drug list, to minimise the out-of-pocket expenses to manage this disease. We have an outstanding public health awareness strategy, largely due to the efforts of the macula disease foundation encouraging much earlier referrals and prompt treatment, compared with most other countries.