Clinical Research Unit

• Kathleen Agorto, Clinical Research Orthoptist
• Dr Elisa Cornish, Medical Retina Specialist
• Thao Dinh, Clinical Research Orthoptist
• Associate Professor Samantha Fraser-Bell, Medical Retina Specialist
• Dr Anelisa Koh, Uveitis Fellow
  
• Emily Luu, Clinical Research Orthoptist
• Sharon McKenzie, Clinical Research Nurse
• Professor Matthew Simunovic, Vitreoretinal Surgeon
  
• Damian Stephens, Clinical Research Orthoptist
• Dr Richard Symes, Medical Retina Specialist
• Danijel Trifunovic, Clinical Research Unit Team Leader and Clinical Research Orthoptist
• Hong Vu, Clinical Research Orthoptist
  
• Maria Williams, Clinical Research Manager 
  
• Dr James Wong, Medical Retina Specialist
• Dr Sophia Zagora, Medical Retina Specialist

Wet AMD

Age-related macular degeneration damages the macula, which is the central part of the retina, the inner layer at the back of your eye. AMD causes more Australian adults to go blind every year than any other disease. This disease is characterised by drusen deposits, retinal pigment epithelium abnormalities, geographic atrophy and neovascular maculopathy. The advanced stages of the disease, which are associated with more severe vision loss, consist of either choroidal neovascularisation or geographic atrophy.

Wet AMD is a disease which affects fine, detailed central vision. Central vision is used for seeing detail in objects clearly and common daily tasks such as reading, driving and recognising people’s faces. In the wet form of macular degeneration, the damage to the eye is caused when abnormal blood vessels grow under the macula. These vessels can leak blood or fluid which then damages the macula and causes deterioration or loss of central vision. This can be quick and severe.

Wet AMD can be effectively treated and managed with administration of intravitreal (injected into the eye) anti-vascular endothelial growth factor (VEGF) agents. VEGF is a biological compound which is produced in the human eye, and is found at higher concentrations in diseases for which new blood vessels grow, such as wet macular degeneration. Anti-VEGF agents work by blocking VEGF in turn reducing the growth of abnormal vessels and cessation of leakage from the new vessel.

Dry AMD

Dry AMD clinically is characterised by the presence of drusen and/or geographic atrophy. Drusen can present in the form of hard or soft varieties. Hard drusen are round, discrete, yellow-white deposits. These are not necessarily limited to aging populations. Soft drusen have ill-defined borders and are usually larger than their hard counterparts. Soft drusen are age related and can be associated with the development of neovascularization, wet AMD. Drusen present at the macula will affect the central vision by causing metamorphopsia (straight lines to appear wavy), difficulty with reading and decreased contrast sensitivity.

The clinical features of geographic atrophy can be seen as defined areas of hypopigmentation or depigmentation due to absence or attenuation of retinal pigment epithelium. Large, usually not clearly seen choroidal vessels, can be more readily seen through atrophic patches. These patches can constrict a patient’s visual field and affecting the ability to read and navigate during activities of daily living.

As it currently stands, unlike wet AMD, there is no approved treatment for dry AMD. Further research into this is active and ongoing. Vitamin supplementation, dietary modification and smoking cessation are advised approaches to slow the progression of dry AMD.

The second most common macular disease after macular degeneration is diabetic macular oedema (DMO). This involves swelling of the macula which is secondary to damage to the macular blood vessels, something which commonly occurs in people with diabetes.

DMO is believed to occur in around 7% of people with diabetes. Given that diabetes affects 5-10% of Australians (in some Indigenous communities the rates are up to 50%), DMO is a common cause of loss of vision.

In the past, laser treatment was primarily used to treat DMO. However, this did not improve vision in most eyes, and many people continued to lose vision.

More recently, injections of specific medications into the eye have been developed to better control the swelling and damage. There are currently two main types of injections that are used to treat DMO:

• steroids
• vascular endothelial growth factor (VEGF) inhibitors.

VEGF inhibitors (such as Avastin, Lucentis or Eylea) were first developed to treat wet macular degeneration, however it is now evident that they are also effective treatments for DMO.

Idiopathic juxtafoveal macular telangiectasia (MacTel) is a condition of the retina about which little is known. It is a disorder of the blood vessels which supply the macula, the central part of the retina that lines the back of the eye and picks up the light like the film in a camera. The fovea in the center of the macula has no blood vessels at all because they would interfere with central vision.

MacTel refers to a curious, very poorly understood condition of the blood vessels around the fovea (juxtafoveal) which become dilated and incompetent, like varicose veins but on a much smaller scale. While MacTel does not usually cause total blindness, it commonly causes loss of the central vision, which is required for reading and driving vision, over a period of 10-20 years.

Clotting of blood in a retinal vein is a relatively common condition called retinal vein occlusion (RVO). When a retinal vein is occluded, blood returning from the retina that is drained by the vein is blocked, causing the retina to swell, a condition known as retinal oedema. If the retinal vein drains the macula, then macula oedema occurs which causes loss of vision.

Branch retinal vein occlusion

Branch retinal vein occlusion (BRVO) occurs when the obstruction is somewhere in one part the retinal branches. If the occluded vein does not drain the macula, then the patient may not even know it is there. If the macula is involved then vision is blurred and cannot be cleared with glasses.

Retinal vein occlusion often improves without treatment in the first three months, so usually no treatments are applied during that time.

After three months a fluorescein angiogram will be performed (unless the bleeding in the retina is so dense that it obscures what is going on). The angiogram will divide the occlusion into the non ischaemic and ischaemic types. For the non ischaemic types it will also show where the leakage which is causing the macular oedema is coming from.