Age Related Macular Degeneration (ARMD)
Age related macular degeneration is the most common cause of severe visual loss in individuals over 50 years old. The incidence of this condition increases with increasing age.
The eye functions similarly to a camera. Images are focused by the cornea and lens onto the retina, which is analogous to the photographic film in a camera. The macular is a small area of the retina that enables fine detailed vision. It is this area that is affected in macular degeneration.
There are two main forms of macular degeneration:
- Atrophic (Dry) Macular Degeneration: This is the most common form of macular degeneration and is responsible for 90% of all cases. Generally it tends to be a slowly progressive disease with gradual damage of retinal structure due to the deposition of drusen in the deep retinal layers. This causes a decline in retinal pigment epithelial and then retinal photoreceptor function. Atrophy of the retinal structures may develop causing loss of visual acuity, colour vision, and contrast.
- Exudative (Wet) Macular Degeneration: This is a less common form of macular degeneration however usually causes more rapid and severe loss of vision due to bleeding from abnormal blood vessels under the macula. Untreated, this bleeding causes destruction of the delicate retinal structures and eventually scarring associated with severe and permanent visual loss.
Symptoms
Generally the symptoms are that of gradual impairment of vision with reduced definition and detail, reduced colour discrimination and contrast, and distortion of images (metamorphopsia). In the early stages, the time it takes to adapt to dark and bright light conditions may be prolonged. In the early stages of ‘wet’ macular degeneration these symptoms develop more rapidly, particularly distortion. This occurs due to elevation of the macula from fluid or blood. It is important to note that individuals who suffer from age related macular degeneration do not become completely blind although they may have significant visual impairment due to loss of central acuity. With treatment when indicated and possible and together with the aid of support services, patients usually retain sufficient vision to maintain their independence.
Risk factors
There are several factors known to be associated with an increased risk of developing macular degeneration. A family history of the disease and smoking are known risk factors.
There is much interest in issues relating to diet and AMD. There is some association between the incidence of macular degeneration in certain communities and eating a diet higher in processed foods and lower in fish and vegetables. A diet rich in omega 3 fatty acids (fish and nuts), vegetables rich in lutein (particularly dark green leaf and yellow vegetables), and deeply coloured fruits/ berries containing zeaxanthines may be beneficial as these food groups contain nutrients and naturally occurring antioxidants known to retard the progression of AMD. Some research has suggested that reducing the intake of margarine, in particular, is warranted however the collective evidence does not necessarily support this proposition. Given that there is strong evidence linking heart disease and atherosclerotic vascular disease with saturated fats in our diet, it is prudent to consider the recommendation to limit saturated fat intake in patients at risk of vascular and heart disease.
Ultraviolet and near blue light wavelengths from excessive sunlight exposure has also been implicated in causing macular degeneration but this has not confirmed in all research. However the use of sunglasses and hats is a good precaution to limit ocular exposure given the high levels of sunlight and UV light in Australia.
Treatment
Unfortunately, there is no treatment available currently for dry macula degeneration although there are several studies underway assessing the possibility of using a newly available laser modality to eliminate macular drusen and hopefully determine if this will improve retinal function. Maintaining a diet rich in lutein, zeaxanthines and omega 3 fatty acids may help prevent disease progression. Commercially available dietary supplements containing these agents and a variety of other trace elements following the recommendations of the AREDS trials may be beneficial in preventing a small percentage of severe disease progressing further, however, their use in mild disease is controversial.
Individuals who notice deterioration of vision or distortion should have their eyes checked by an ophthalmologist to determine if exudative macular degeneration is developing. Regular self testing using a modified Amsler Grid Chart is a very useful modality to monitor for early disease progression and any change in distortion should prompt early ophthalmic assessment. The ophthalmic examination will involve checking acuity, clinically examining the macula after papillary dilation with bi-microscopy, then performing optical coherence tomography (OCT) scans of the macula to assess in fine detail, the anatomy and pathological processes involving the macula. Subsequently, fluorescein angiography will be indicated to confirm the presence of blood vessel growth in the deeper retinal tissue causing either hemorrhage or leakage of fluid. In some cases of ‘wet’ macular degeneration, when indicated, prompt treatment with intravitreal injections of anti-vascular endothelial growth factor (anti-VEGF) agents such as Lucentis and Eylea (now available for authorised patients through the PBS after fluorescein angiographic confirmation) into the eye, may be useful in slowing and sometimes reversing visual loss in some patients and a number of important trials have confirmed the benefit of this treatment. These injections may have to be repeated regularly depending on the individual response for each patient.
Intra-vitreal injections are undertaken under topical and local anaesthesia using a sterile technique in the clinic’s treatment/procedure room. The technique involves firstly administering drops of topical anaesthetic after which the eye and eyelids are wiped with an antiseptic solution. A speculum is inserted to help keep the eyelids open and the eyelashes away from the sterile field. Local anaesthetic is injected under the conjunctiva at the site of the intravitreal injection near the corneal limbus. The intravitreal agent is then prepared and then injected into the eye. The eye is then irrigated to remove any residual antiseptic. Antibiotic ointment is applied and an eye pad placed until the patient reaches home. Antibiotic ointment is administered for 3 days post treatment. Attached is our post injection information sheet.
The main risks of treatment include intra-ocular infection (endophthalmitis) which is rare however is potentially blinding, lens damage causing cataract to develop, intravitreal haemorrhage, retinal detachment and elevated intra ocular pressure (usually temporary). Systemic risks include a slight increased chance of stroke and other thromboembolic events. Obviously these risks need to be weighed up individually against the potential benefits of treatment prior to proceeding.