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Chapter 17 Acquired Macular Disorders Age-related macular degeneration 334 Polypoidal choroidal vasculopathy 341 Age-related macular hole 342 Central serous retinopathy 344 Cystoid macular oedema 345 Macular epiretinal membrane 347 Degenerative myopia 348 Angioid streaks FINAL 350 Choroidal folds 351 NOT Hypotony maculopathy - 351 Vitreomacular traction syndrome ELSEVIER 352 Solar maculopathy OF 352 Idiopathic choroidal neovascularization 352 CONTENT PROPERTY SAMPLE 334 Acquired Macular Disorders Age-related macular degeneration Drusen 1. Histopathology (Fig. 17.1) • Discrete deposits of the abnormal material located between the basal lamina of the RPE and the inner collagenous layer of Bruch membrane. • Thickening of Bruch membrane Fig. 17.2 Hard drusen compounded by excessive production of basement mem- brane deposit by the RPE. a FINAL Atrophy and depigmentation NOT - RPE ELSEVIER OF Bruch membrane Drusen Thickening CONTENTb Fig. 17.1 Histopathology of drusen 2. Signs – yellow sub-RPEPROPERTY excrescences distributed symmetricallySAMPLE at both posterior poles. a. Small hard drusen – less than half a vein width in diameter with discrete margins (Fig. 17.2). b. Large soft drusen – vein width or more in diameter with indistinct margins (Fig. 17.3a). Fig. 17.3 (a) Soft drusen; (b) FA c. Calcifi ed drusen – may be hard or soft (Fig. 17.4). Age-related macular degeneration 335 a Fig. 17.4 Calcifi ed drusen b 3. FA a. Hyperfl uorescence – window defect due to atrophy of the overlying RPE and late staining (see FINAL Fig. 17.3b). b. Hypofl uorescence – of hydrophobic NOT (high lipid content) drusen. - 4. Drusen and AMD – features ELSEVIER associated with an increased risk of subsequent visual loss include largeOF soft and/or confl uent drusen, and Fig. 17.5 (a) Confl uent soft drusen with RPE changes; (b) FA focal RPE hyperpigmentation (Fig.CONTENT 17.5), particularly if the other eye has AMD. 3. Signs in chronological order: 5. Prophylactic treatment – high-dose PROPERTY • Focal hyperpigmentation or multivitamins and antioxidants can atrophy of the RPE associated decrease the risk ofSAMPLE progression of with drusen. AMD in eyes with the following high • Sharply circumscribed, areas of risk characteristics: visual loss in the RPE atrophy associated with contralateral eye from pre-existing dry variable loss of the choriocapil- or wet AMD, and confl uent soft drusen laris (Fig. 17.6). even in the absence of visual loss. • Enlargement of the atrophic areas (Fig. 17.7). Atrophic (dry) age-related 4. FA – hyperfl uorescence due to an macular degeneration RPE window defect (Fig. 17.8). 5. Treatment – not possible. 1. Pathogenesis – slowly progressive atrophy of the photoreceptors, RPE, and choriocapillaris. 2. Presentation – gradual impairment of vision over months or years. 336 Acquired Macular Disorders a Fig. 17.6 Dry AMD b FINAL NOT - ELSEVIER OF Fig. 17.9 (a) PED; (b) ICG Fig. 17.7 Geographic atrophy CONTENT a PROPERTY b SAMPLE Fig. 17.8 Window defect in dry AMD Age-related macular degeneration 337 Retinal pigment epithelial 6. FA – well demarcated oval area of detachment hyperfl uorescence which increases in density but not in size (Fig. 17.11). 1. Pathogenesis – reduction of 7. Course – may follow one of the hydraulic conductivity of the following patterns: thickened Bruch membrane impeding a. Spontaneous resolution – without movement of fl uid from the RPE residua. towards the choroid. b. Geographic atrophy – following 2. Presentation – metamorphopsia and spontaneous resolution. impairment of central vision. c. Detachment of the sensory retina. 3. Signs – circumscribed, dome-shaped d. RPE tear formation. elevation at the posterior pole (Fig. 17.9a). Retinal pigment epithelial tear 4. ICG – oval hypofl uorescence with a faint ring of surrounding hyperfl uores- 1. Pathogenesis – tearing of the RPE at cence (Fig. 17.9b). the junction of attached and 5. OCT – separation of the RPE from detached RPE due to tangential Bruch membrane (Fig. 17.10). stress – mayFINAL be spontaneous, or more commonly, follows laser photocoagulation, PDT or anti-VEGF therapyNOT of CNV. - ELSEVIER2. Presentation – sudden worsening of central vision. OF 3. Signs – crescent shaped RPE dehiscence with a retracted and folded fl ap (Fig. 17.12a). CONTENT4. FA – relative hypofl uorescence over Fig. 17.10 OCT of PED the fl ap with adjacent hyperfl uores- cence due to the exposed choriocap- PROPERTY illaris (Fig. 17.12b–d). SAMPLE a b Fig. 17.11 FA of PED 338 Acquired Macular Disorders a b c d e f g h Fig. 17.12 RPE tear 5. OCT – loss of the normal dome- shaped profi le of the RPE in the FINAL PED, with hyper-refl ectivity adjacent to the folded RPE (Fig. 17.12e–h). NOT 6. Prognosis – poor for subfoveal tears. - ELSEVIER Neovascular (wet) age-related macular degeneration OF Pathogenesis Fig. 17.13 CNV in wet AMD • CNV originating from the choriocapil-CONTENT laris grows through defects in Bruch membrane (Fig. 17.13). Fluorescein angiography • Initial visual loss isPROPERTY caused by 1. Classic CNV leakage from CNV underSAMPLE the sensory • Well-defi ned membrane which fi lls retina and under the RPE. with dye in a ‘lacy’ pattern during • This is followed by bleeding from the very early phase of dye transit CNV. (Fig. 17.14b), fl uoresces brightly • Permanent visual loss is caused by during peak dye transit (Fig. subretinal (disciform) scarring. 17.14c), and then leaks into the Clinical features subretinal space and around the CNV within 1–2 min. 1. Presentation – metamorphopsia, • Late staining of fi brous tissue positive scotoma, and blurring of within the CNV (Fig. 17.14d). central vision. • Classic CNV is classifi ed 2. Signs – serous retinal elevation, according to its relation to the foveal thickening, CMO, subretinal centre of FAZ as extrafoveal, haemorrhage, and hard exudate subfoveal, and juxtafoveal. formation (Fig. 17.14a). Age-related macular degeneration 339 • CNV can be further subdivided Course into wholly classic and predomi- The course of untreated CNV is often nantly classic in which 50% or relentless and the prognosis very poor less of the lesion has a classic due to the following complications. component. 1. Haemorrhagic PED 2. Occult CNV – poorly defi ned with • Initially, the blood is confi ned to less precise features on the early the sub-RPE space and appears as frames (Fig. 17.15b) and gives rise a dark elevated mound (Fig. 17.16). to late, diffuse or multifocal leakage • The blood may then break into the (Fig. 17.15c,d). subretinal space and assumes a 3. Fibrovascular PED – combination of more diffuse outline and a lighter CNV and PED in which the CNV red colour (Fig. 17.17). fl uoresces brighter (hot spot) than 2. Vitreous haemorrhage – when the detachment; in other cases, the subretinal blood breaks through into CNV may be obscured by blood or the vitreous cavity; rare. turbid fl uid. 3. Subretinal (disciform) scarring – causes permanent loss of central vision (Fig.FINAL 17.18). NOT - a ELSEVIERb OF CONTENT PROPERTY SAMPLE c d Fig. 17.14 FA of classic subfoveal CNV 340 Acquired Macular Disorders a b c d FINAL NOT - ELSEVIER OF Fig. 17.15 FA of occult CNV CONTENT PROPERTY SAMPLE Fig. 17.16 Sub-RPE haemorrhage Fig. 17.17 Subretinal haemorrhage Polypoidal choroidal vasculopathy 341 Retinal angiomatous proliferation 1. Defi nition – uncommon type of wet AMD in which neovascularization originates from the retinal vascula- ture and not the choriocapillaris. 2. Signs • Intraretinal and subretinal neovascularization often accompa- nied by haemorrhage and oedema. • CNV associated with fi brovascular Fig. 17.18 Disciform scar PED and retinochoroidal anasto- moses. 3. FA – similar to purely occult or 4. Massive subretinal exudation – due minimally classic CNV. to chronic leakage from CNV 4. ICG – hot FINALspot in mid or late frames. (Fig. 17.19). 5. Treatment – PDT with adjunctive intravitreal triamcinolone. NOT - ELSEVIERPolypoidal choroidal OF vasculopathy 1. Defi nition – bilateral, choroidal CONTENTvascular disease in which the inner choroidal vessels consist of a dilated network with multiple terminal PROPERTY aneurysmal protuberances that have a polypoidal confi guration. SAMPLE 2. Signs a. Exudative – multiple PED, serous Fig. 17.19 Massive exudation RD, and lipid deposits (Fig. 17.20a). b. Haemorrhagic – haemorrhagic PED Treatment and subretinal haemorrhage (Fig. 17.21a). 1. Photodynamic therapy (PDT) – for 3. ICG – polypoidal dilatations beneath subfoveal, predominantly classic CNV the RPE that fi ll slowly and then leak not larger than 5400 µm in eyes with intensely (Figs 17.20b & 17.21b). a visual acuity of 6/60 or better. 4. Course 2. Anti-vascular endothelium growth • Spontaneous resolution in 50%. factor (anti-VEGF) agents – • In the remainder occasional intravitreal bevacizumab (Avastin), repeated bleeding and leakage, ranibizumab (Lucentis) and pegap- resulting in macular damage and tanib (Macugen) are used to treat visual loss. any type of CNV. 5. Treatment – PDT. 342 Acquired Macular Disorders a a b b FINAL NOT - ELSEVIER OF Fig. 17.20 (a) Exudative polypoidal; Fig. 17.21 (a) Haemorrhagic polypoi- (b) ICG dal; (b) ICG CONTENT Age-related macular hole • Stage 2 (early hole) – full- PROPERTY thickness defect, less than 1. Pathogenesis – abnormal vitreo- SAMPLE 300 µm in diameter with or without foveolar attachment, with resultant an overlying pseudo-operculum. antero-posterior and tangential • Stage 3 (established hole) – full- traction. thickness defect more than 2. Presentation – in old age. 400 µm in diameter with an 3. Staging (Fig. 17.22) attached posterior vitreous face • Stage 1a (impending) – fl at umbo, with or without an overlying yellow foveolar spot 100–200 µm pseudo-operculum. in diameter with loss of the • Stage 4 – round defect more than foveolar refl ex. 400 µm in diameter surrounded • Stage 1b (occult) – yellow ring with by a cuff of subretinal fl uid and a bridging interface of vitreous tiny yellowish deposits within its cortex. crater, and completely detached vitreous cortex (Fig.

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