Successfully reported this slideshow.
We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime.

Macular degeneration treatments - an update for orthoptists


Published on

This is a summary of current treatments for macular degeneration

Published in: Health & Medicine

Macular degeneration treatments - an update for orthoptists

  1. 1. Treatment of MacularDegenerationOrthoptic study day26thApril 2013
  2. 2. • What is macular degeneration?• Current treatments• Future developmentsAims
  3. 3. Basic retinal anatomy• Nerve layer (Neuro-retina)• Pigment layer (retinal pigment epithelium orRPE)• Blood vessel layer (choroid)
  4. 4. Nerve layer (Neuro-retina)• Rods and cones– Converts light energy into electrical impulses totransmit to the brain.– Most energy dependent of all tissue in body• Bipolar cells• Ganglion cells• Nerve fibre layer– 1.1 million nerve fibres per eye
  5. 5. Pigment layer• Recycles material from rods and cones– Recycling needed to maintain efficient function• Contains pigment to stop internal reflections– Prevents “glare” inside the eye– Melanin pigment• Single layer of cells
  6. 6. Blood vessel layer (choroid)• Supply oxygen and nutrients tophotoreceptors and RPE (outer retina)• Highest blood flow per unit area of any tissuein the body• Why vision goes just before you faint• Retina is always working very hard!
  7. 7. Is light bad for the eyes ?• Form of electromagnetic radiation• Look what happens with excess sunlight onthe skin• Eye is an optical system that exposes retinato radiation all the time• Light focused on the macula
  8. 8. What harm does light do to theretina?• Reacts with fat in cell membranes• Produces reactive oxygen (free radicals)• Damages the DNA in the cells• Repair mechanisms– Skin – repairs DNA all the time, new cells form– Brain – cannot create new cells as has to storememory– Retina – part of brain so cannot create new cells
  9. 9. How does retina protect itselffrom light?• Luteal (yellow) pigment at macular protectsagainst high energy blue light• Rods and cones have “outer segments”• Although a “non dividing system” these outersegment cell membranes are constantly shedthen recycled by the RPE to form new cellmembranes
  10. 10. How does macular degenerationstart?• Chronic damage to cells from high energy light– Damage to DNA (and cannot repair)• Recycling becomes less effective with age– Accumulation of “waste products” of metabolism• Toxins– Smoking• Genetic make up– Complement factor H
  11. 11. Demographics• AMD - most common cause of visual loss inpatients over 55 in Western world• Diabetic eye disease most common cause ofvisual loss in patients under 55 in Western world• Ageing population in UK – 20 million > age 50
  12. 12. Types of AMD• Dry– Most common form– Gradual loss of central vision– Not total blindness• Wet– 10-15% of AMD– Sudden loss of central vision– Not total blindness but often more severe central visualloss
  13. 13. Symptoms of AMD
  14. 14. Charles Bonnet syndrome• Brain make up its own images• Can be colours or shapes• Can be formed visual hallucinations
  15. 15. Optical coherence tomographyNormal anatomy
  16. 16. Dry AMD• Build up of waste products due to poorrecycling (Drusen)• Changes in melanin pigment in the RPE• Geographic atrophy
  17. 17. Dry AMDDrusen“Lumpy bumpy” RPE
  18. 18. Wet AMD• Abnormal blood vessels grow into retina fromchoroid and haemorrhage and leak• Vascular endothelial growth factor (VEGF)stimulates this blood vessel growth
  19. 19. Fundus fluorescein angiography• Dye injected into vein in arm• Abnormal blood vessels leak the dye• Choroidal neovascular membrane (CNV)
  20. 20. Visual loss with wet AMD• No treatment (natural history)– Loss of 5 lines of Snellen acuity in 2 years• Most of the loss of vision will take place withinthe first 6 months• Like a cut on the skin– First there is inflammation with swellingand haemorrhage– Then a scar forms (disciform scar)
  21. 21. Injection treatments for wet AMD• Developed from cancer research• Vascular endothelial growth factor– Produced by the retina– Stimulates formation of abnormal, leaky bloodvessels• Anti-VEGF– Lucentis, Avastin, Eylea– Blocks VEFG molecule therefore stops leakagefrom the blood vessels
  22. 22. Judah Folkman MD• Prof of Paediatric Surgery at Harvard• 17 Honorary degrees• His lab discovered angiogenesis molecules thatstimulate blood vessel formation to allow tumourgrowth• Anti-angiogenesis drugs inhibit tumour growth• AntiVEGF treatment has developed from hisstudies
  23. 23. Landmark Marina and Anchorstudies• Lucentis injected every month for 2 years• Average improvement of vision 10 letters• Maintained vision in most patients• If frequency of injections less than everymonth reduced effect noted• Most UK practice is now 3 loading injectionover 3 months then as needed injections
  24. 24. Source: HORIZON data. Genentech.Treated-Initial (n=388) Untreated (n=33)ETDRSLetters-20-15-10-50510153 6 9 12 15 18 21 24HORIZON StudyHORIZON Study+5.1-6.7+2.0-6.924MonthInitial baselineMarina/Anchor StudiesMarina/Anchor Studies+10.2-3.2
  25. 25. Average number of injections andcosts• 8 injections in the first year• 6 injections in the second year• Each injection costs £1,750 to the NHS– £750 for Lucentis• The first 2 years cost the NHS £24,000• Average life expectancy from diagnosis– 10 years
  26. 26. Costs – Avastin vs. Lucentis
  27. 27. INJECTING
  28. 28. First nurse-delivered injectionsservice in UK, 2008• Peter Simcock, Brian Kingett, Nicola Mann• 7,000 injections to date
  29. 29. Problems with injections• Does not address fundamental cause of wetAMD• Multiple injections for elderly patients• VEGF may be needed to help improvecirculation– Avoid if high risk of or recent stroke or heartattack• Risk of injection itself– Infection of eye (endophthalmitis) 1 in 1,000
  30. 30. How to reduce frequency ofinjections• Radiation damages proliferating cells– Endothelial cells (forming the abnormal bloodvessels– Inflammatory cells (causing damage to tissue)– Fibroblasts (causing scar tissue formation)• Internal beam – Merlot study• External beam – Intrepid study
  31. 31. MERLOT – first “portfolio study”in WEEU, 2010• Finished recruiting, results awaited• Vitrectomy + beta irradiation from strontiumsource
  32. 32. Intrepid study• Similar to MERLOT but external beamirradiation• X rays delivered via contact lens• IRay system from Oraya theraputics Inc• Reduced injection rate by one third in study• Await “real world” results
  33. 33. Eylea• Anti-VEGF treatment• Aflibercept• May be more powerful than Lucentis• Less frequent injection?• Good for patients that have responded poorlyto Lucentis
  34. 34. What about dry AMD?• Main treatment remains low visual aids• Stem cell treatment• Neuro-protection• Intraocular telescopes– VIP IOL– Implantable miniature telescope– ARGUS II (digital camera in glassescommunicates with retinal chip)
  35. 35. What about diet and AMD ?• Eat fresh fruit, dark green leaved vegetables• Vitamins supplements only if severe
  36. 36. Vitamins and AMD• Antioxidant treatments to “mop up” freeradicals• AREDS (Age related eye disease study)– Vit C 500mg, E 400IU, Beta carotene 15mg andzinc 80mg– Decreased risk of progression of AMD withsubgroup analysis only• AREDS 2 study (ongoing)– Investigating the benefits of lutein, zeaxanthin andomega 3 fatty acid supplementation
  37. 37. Other macular degenerations• Epiretinal membrane / Cellophane maculopathy– Scar tissue on surface of macula– Surgical treatment with vitrectomy and peel• Vitreomacular traction– Surgical treatment with vitrectomy– New medical treatment with Ocriplasmin (Jetrea)• Macular holes– (Phaco)Vitrectomy with gas and limited posturing– ? Jetrea in small holes
  38. 38. Epiretinal membrane
  39. 39. Vitreomacular traction
  40. 40. Macular holes