Level 4, 187 Macquarie Street
Sydney NSW 2000
Phone: 02 9247 9972
Fax: 02 9232 3086
Email: patientservices@eyeassociates.com.au

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The eye is like a camera. Light rays pass through the cornea, the lens and the vitreous to focus on the retina. The cornea is the window at the very front of your eye. The lens is behind the coloured part of your eye (iris). Cloudiness of the lens is called cataract. The vitreous is a jelly-like substance that gives the eyeball its shape and also helps to keep the retina in place. Finally, the retina is the tissue at the back of the eye that picks up the light like the film of a camera and transmits it to the brain via the optic nerve. The central part of the retina, which does the straight ahead vision which is necessary for reading and driving, is called the macula.



From the age of 60 years old, and sometimes even earlier, most people develop signs of degeneration of their maculas, just as they do in other parts of the body (e.g. wrinkles of your skin). The degeneration is seen as tiny crystals of debris under the macula which are called ‘drusen’. Drusen do not usually affect the vision; most eyes with drusen actually never lose vision. Early macular degeneration is so common however, that the small proportion of people who develop advanced degeneration make up the vast majority of people who are ‘legally blind’ in Australia and other western countries.


Some eyes with early AMD may progress through ‘intermediate’, to ‘advanced’ AMD. Intermediate AMD refers to eyes with more extensive drusen than early AMD. Vision is still normal in these eyes, or only slightly impaired.
Advanced AMD is the process that may destroy central vision. It may be either ‘dry’ or ‘wet’.

adv_amdDry AMD occurs when areas of the macula overlying drusen gradually thin out. Eventually holes form in the macula, which are referred to as areas of ‘atrophy’. If these atrophic areas involve the very centre of the macula then the central vision is lost. Fortunately, dry AMD progresses very slowly over many years, although the loss of central vision when it finally occurs may appear sudden.

Wet AMD occurs when an abnormal blood vessel grows into the degenerating macula. Destruction of the central vision may occur relatively quickly, over a few weeks to months, due to bleeding and scarring.

Even if it involves both eyes, AMD never causes total blindness because patients keep their peripheral vision, which is usually enough for them to get about with, especially in their own homes. Many people with advanced AMD in both eyes remain independent.


Anyone above the age of 60 may be developing AMD. AMD tends to run in families, so people with a family history (parents/brothers/sisters) of loss of reading vision which cannot be corrected by glasses may have an increased risk of developing the condition.



The biggest modifiable risk factor for AMD is smoking. Quitting smoking reduces the risk of developing the disease by up to five times. Wearing sunglasses outdoors may also reduce the risk of AMD.


There has been a lot of interest in dietary prevention of AMD recently, particularly in Australia for some reason. In general, the role of diet has been somewhat overstated. Nevertheless, it does appear that a diet rich in zeaxanthin and lutein, two types of vitamin A that are found in high levels in the macula where they function as antioxidants, is mildly protective. Such foods include leafy greens (spinach, broccoli, brussel sprouts etc.) and brightly coloured vegetables (corn and capsicum). It is recommended to eat one cup of these at least three times a week.

Eating fish occasionally is also protective. Since AMD is also weakly associated with cardiovascular disease, it makes sense to eat a low fat diet, but the recent rumors that certain types of fat were better or worse than others appear to have been based on a misunderstanding of the scientific evidence. It may be true that people who eat butter have a lower risk of developing AMD, but this may be because they have shorter life spans because of an increased risk of cardiovascular disease.


The only form of advanced AMD that is treatable is the wet form. Since current treatments of wet AMD work better the earlier they are applied, it is important to detect it as soon as possible after it starts. Elderly people should not accept loss of vision as an inevitable part of ageing. There is always a reason for it and this must be established sooner rather than later. The cardinal early symptom of wet AMD is distortion of straight lines. Elderly people at risk should test for this once a week as they read the paper. A tiled surface such as a bathroom floor provides a good pattern for testing. Your eye doctor may give you an ‘Amsler Grid‘ for this. Remember to test each eye individually with your reading glasses on.


Ophthalmologists (eye doctors) can assess your eyes to look for any signs of AMD and to ensure your eyes are healthy. You will need a referral to be seen by an Ophthalmologist; your GP, optometrist or specialist can provide this.

On arrival at your ophthalmologist’s rooms, you will first be seen by an Orthoptist. The orthoptist will take a history, assess your vision, check your eye pressure, and instill dilation drops to enlarge the pupil, which takes at least another 30 minutes. This will cause your vision to go blurry and be light sensitive for several hours after the consultation. It is advised to not drive for approximately two hours after the drops have been instilled and it is also recommended to bring a pair of sunglasses to wear.

During your consultation, you may be advised to undergo a fluorescein angiogram. This test involves fluorescein dye, which is injected into the arm causing the dye to travel through the blood vessels to the eye where photos are taken for further assessment. There may be side effects, which will be explained thoroughly at the time. A fluorescein angiogram is essential for diagnosing and planning the treatment of wet AMD.



As well as the advice concerning diet as described above, patients with AMD may also benefit from vitamin supplementation. Once again the benefit of this is somewhat overstated, and there are more people taking vitamin supplementation unnecessarily than people who actually need it. However, it was demonstrated by the Age Related Eye Disease Study (AREDS) that supplementation with high doses of beta carotene, vitamins D, E and zinc (all taken together) reduces the risk of developing advanced AMD in the second eye of people who have lost vision in their first eye by around 20%. A product containing this formulation (apart from the beta carotene, which causes lung cancer in smokers) is available in Australia called ‘Macuvision’,but there are many other brands available. Tablets containing lutein are also available. The AREDS2 study showed that lutein supplementation may be beneficial, but only in 20% of people who have the lowest intake of leafy greens.


Apart from the preventative measures already outlined, there are no treatments for dry AMD. In particular, there is nothing that can be done to repair the areas of atrophy once they become established. One day it may be possible to do this with transplants or stem cell therapy, but so far attempts at such treatment have failed dismally, even in animal models. Clinical trials are currently in progress of agents designed to slow the enlargement of areas of atrophy.


wet_amdThe treatment of AMD depends on what is found by the fluorescein angiogram. The technical term for the abnormal blood vessels is ‘choroidal neovascularisation’ or ‘CNV’ (‘choroidal’ because they come from the choroid, which is the name for the region under the retina that contains an important part of the retinal blood supply; ‘neo’ = new, ‘vascular’ = blood vessel). The following are the main points that are looked for during the angiogram:

  • Location: is the CNV under or away from the centre of the macula?
  • Type: ‘classic’ – well defined – or ‘occult’ -poorly defined
  • Size: small or large



In around 2005 a major breakthrough occurred in the field of treatment for macular degeneration in which agents directed towards “Vascular Endothelial Growth Factor” were found to be extremely effective to treat wet AMD. Vascular endothelial growth factor (VEGF) is a protein or factor that is thought to induce the growth of abnormal blood vessels in wet AMD. Lucentis or Avastin are treatments of consistent antibodies against VEGF. Lucentis was the agent that was tested in clinical trials. The studies showed that after monthly injections for 2 years the vision in 80% of patients with wet AMD stabilised and in 50% the vision actually improved. Anti VEGF injections need to be given in eyes with recent loss of vision. If there is long standing loss of vision, even if there is bleeding or swelling, the treatments are less effective and may be of no use at all. Lucentis was the proven agent. Avastin is a related agent that is produced for the treatment of bowel cancer. The drug company that made Avastin did not believe that it would be helpful for the treatment of wet AMD, however it turns out that it appears to be just as effective as Lucentis. However this has not been specifically tested for use inside the eye and so whilst it is much cheaper, Lucentis remains the preferred agent; Lucentis has been approved and will be reimbursed by the Australian Government for patients with wet AMD. Avastin is generally used in patients with macular disease who do not have AMD or are under the age of 55 years for which the government does not subsidise the treatment. More recently another VEGF inhibitor, Eylea, has been made available for the treatment of wet AMD and is reimbursed by the government.

Other treatments for wet AMD include ‘Cold’ and ‘Hot’ laser as set out below, but 90% of patients with wet AMD now are treated with intravitreal drug therapy.



The traditional form of laser treatment of CNV uses a hot laser to cauterise the abnormal vessel. Your eye doctor will put an anaesthetic eye drop in your eye, then insert a contact lens which will keep the eye still and stop you blinking. A tiny beam of concentrated light (one fifth of a millimeter in diameter) is then used to destroy the abnormal blood vessel. The treatment is usually not painful, although it does dazzle the vision so you may not see anything from the treated eye for up to a couple of hours later (you should still be able to see with the other eye).

You must try to keep your eyes still during the treatment. Your eye doctor may ask you to look directly at the red aiming beam at the start of the procedure in order to determine precisely where your reading centre is, but after that you should not look at the aiming beam because an accidental burn to the reading centre may destroy your central vision permanently. It is best to ignore what is going on in the eye being treated by keeping your other eye open and staring straight ahead. All this sounds difficult but it usually turns out to be easier than the patient expects.

Sometimes laser treatment itself can damage the central vision, particularly when the CNV is not under the centre of the macula but is very close to it. However, even when the side effects are taken into account, hot laser treatment halves the risk of continued loss of vision. In other words you can still lose vision after laser treatment, it is just less likely. It is not uncommon to meet patients who complain that their vision was normal until they had laser treatment then it got worse. Some are convinced that the laser treatment damaged the vision. More often in fact the vision was going to get worse anyway (that is why they had the treatment in the first place) and the laser treatment did not stop it.

Even if the treatment is successful in the first instance, CNV will return in 50% of cases after hot laser. Your eye will be checked with another angiogram around three weeks after treatment, then after six weeks, then three monthly for at least two years. If you notice progressive loss of vision, or recurrence of the distortion, you must return to see your eye doctor within one week.


Photodynamic therapy (PDT) was developed to treat CNV beneath the centre of the macula (fovea) without damaging central vision the way that hot laser does. PDT uses a light sensitive dye, (verteporfin), which binds to abnormal blood vessels but washes out of normal vessels. Verteporfin is infused into a vein in your arm over 10 minutes, then you are moved to the laser. Your doctor will insert a contact lens to keep the eye open, then shine a red light on the CNV that only damages what the verteporfin is bound to. In this way the CNV can be shut down without damaging the overlying central macula. This type of laser is much easier to tolerate than hot laser. When you leave you will hardly be aware that anything has been done to your eye.

Photodynamic therapy is certainly better than no treatment in selected cases, but it is far from perfect. It works best for small vessels, which are mostly of the ‘classic’ type on angiography. In these eyes it improves the chance of keeping vision at the current level from 1:3 (untreated) to 2:3. Therefore 1:3 patients will continue to lose vision even if they have PDT. Vision will improve in some patients after PDT, but unfortunately this is not common. There is also a small risk of around 1:50 that PDT will actually destroy the central vision, so that what is likely to happen over the ensuing months happens in the week after treatment.