Swollen macula: Top 5 PROFESSOR FARUQUE GHANCHI
AMD u DMO u RVO u CSR u CMO u
How do you identify swollen macula
Symptoms Minimum acuity Functioning acuity Contrast Glare Colour Distortion Central Field
Signs SWELLING u u Fluid u Exudates u Fibrosis Haemorrhage u Pigment change u
Optimum treatment •Screening First •Incipient •Symptoms Biological Disease Treatment •Service medical TESTS initiation Detection Initiation Design •Prodrome •Signs Contact •Diagnostic •Capacity Patient Delay Detection / Referral Service Delay Seeking healthcare Delay Patient Medical Practitioner Prior M, et al. Br J Ophthalmol 2013;0:1–5. doi:10.1136/bjophthalmol-2013-303813 Tailored/Individualised u Generic/ Population u Bradford Ophthalmology Research Network BORN for vision
AMD Dry Wet Drusen PED u u RPE changes nAMD u u Atrophy u CNV u u RAP Disciform scar u u CRA u IPCV
Drusen Types of Drusen – u u Soft, hard… but there is more! u Reticular drusen ? Risk for wet AMD
Serous PED Wet AMD - but no identifiable CNV u Conservative management u u Warn for new symptoms
Wet – neovascular AMD Retinal haemorrhage u u Deep intraretinal/ subretinal or subRPE u OCT outer retinal and RPE/Bruch’s changes
Fibrosis- end stage nAMD Scar in outer retina u Usually stable/ non progressive central scotoma u
AntiVEGF Very good outcomes with antiVEGF Local expereince u u injections u Both probably similar if Timely referral and treatment u u Outcome data collection AntiVEGF agents in clinical use in NHS u u Average 7 injections in first year LUCENTIS & EYLEA u 4+ in second year u u Treatment is indefinite
Not all AMD In practice look out for signs of nAMD u u OCT can help refine diagnosis Macular hole may be confusing u u Watzke’s sign with Volk lens on slitlamp
DMO Incidence of diabetes rising globally Diaabetic retinopathy is usually u u continuos –progressive condition Local diabetic population on the up u Background – preproliferative – u Screening programme helps early u proliferative stages diagnosis Maculopathy occurs at any stage u
DMO Definition u Cliniaclly significant macular oedema u u CSMO – clinical diagnosis Centre involving macular Oedema u u CiMO – OCT based u NICE guidance is based on this
Treatment of CiMO AntiVEGF Good results with AntiVEGF u u u Lucentis or Eylea u Improvement in vision 5-10 letters u If >400 micron (NICE) u Multiple injections and visits (monthly) in the first year u Ozurdex or Iluvien implant u Reduced number of injections in second u If unresponsive to antiVEGF and eye is year pseudophakic Steroid implants: Ozurdex /Iluvien u u Rescue treatment
RVO Epidemiology BRVO- natural history CRVO – natural history Spontaneous improvement 50- BRVO > CRVO Spontaneous improvement < 20% 60% Base line VA 6 /60 to 6/18 Prevalence: 6/12+ at one year 0.5–2.0% for BRVO Young age (<50) more favourable 20% worsen 0.1–0.2% for CRVO 20% still get severe issues (NV) 5 year incidence: Dehydration/ Inflammation 5% bilateral BRVO evident at 1.8% for BRVO 10% BILATERAL @ baseline presentation 0.2% for CRVO 5% get second eye involvement Most unilateral in 1 year 10% would get second eye involvement
CRVO treatment Risk factor assessment u Macular oedema u u Lucentis/ Eylea u Ozurdex injections Neovascular comlications u u Laser u Glaucoma Rx
BRVO treatment Risk factor assessment u Macular oedema u u Lmacular laser – if view is clear u Lucentis/ Eylea u Ozurdex injections Neovascular comlications u u Laser
CSR CSCR It was: u u Retinal/ RPE issue u Young man Now u u Central Serous Choroido(Retino)pathy u Leakey choroid u Any age
CSCR Types & management Acute Conservative u u Recurrent > 2 recurrences Individualised u u Persistent >4 months PDT, AntiVEGF, MR Antagonists u u Persistent with tracks (Chronic) PDT, AntiVEGF, MR Antagonists u u
CMO 1-19% u More with complicated surgery u Uveitis u Diabetic eye? u RVO u ERM u
CMO management Treat residual inflammation – steroid drops u Nonsteroidal anti-inflammatory drops u Oral Diamox u Steroids – periocular/ intraocular injections u u Oral?
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