ARMD
Also cal ed senile macular degeneration
Bilateral disease of persons over 50 years of age
Leading cause of blindness in developed countries in a population of
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above 65 years of ageETIOPATHOGENESIS
risk factors are heredity,nutrition, smoking, hypertension, exposure to
sun light,hyperopia, blue eyes and cataract particularly nuclear opacity.
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The disease is most prevalent in Caucasians.CLINICAL TYPES
1 Non exudative
2 Exudative
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1.Non-exudative or atrophic ARMD
It is also cal ed dry or geographic ARMD
SYMPTOMS-
Mild to moderate gradual loss of vision.
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Patients may complain of Distorted vision and difficulty inreading due to Central shadowing
SIGNS- can be described as 3 stages
EARLY STAGE ? characterized by macular drusens,focal
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hyperpigmentation,pale area of retinal pigment atrophyINTERMEDIATE STAGE- show sharply circumscribed
circular areas of RPE ATROPHY , loss of chorio
capil aries,macular drusens
ADVANCED STAGE- enlargement of atrophic areas
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within which the larger choroidal vessels may becomevisible and pre existing drusen disappear(geographical
atrophy)
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Non exudative ARMD? 2.EXUDATIVE- also cal ed wet or neovascular ARMD.
? Associated with comparatively rapidly progressive marked loss of
vision
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? TYPICAL LESIONS? drusen with retinal pigment epithelial detachment- dome shaped
elevation
? Choroidal neovascularisation proliferating in sub RPE space-(type
1) , subretinal space( type 2)
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? Haemorrhagic pigment epithelial detachment(PED)-dark elevatedmount
? Haemorraghic detachment of neurosensory retina
? Disciform sub-retinal scarring
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Exudative ARMD
DIAGNOSIS
Examination of macula by slitlamp biomicroscopy with +90D/+78D non contact lens or mainster
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contact lensFundus fluorescein angiography and indocyanine green angiography help in detecting choroidal
neovascularization (CNV) in relation to foveal avascular zone. CNV may be classical or occult:
Classical CNVM -lacy hyperfluorescence with progressive leakage
Occult CNVM- stippled hyperfluorescence(type 1) or as late leakage of undetermined source(type2)
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Optical coherence tomography (OCT) reveals subretinal fluid, intraretinal thickening, choroidalneovascularization and haemorrhages in exudative ARMD
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FFA showing leakage and lacyOCT picture of CNVM
pattern in CNVM
TREATMENT
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Treatment of non exudative ARMDDietary supplements and antioxidants
Smoking cessation
Amsler grid used regularly al ows the patients to detect new or
progressive metamorphopsia prompting them to seek ophthalmic
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advice.Refraction with increased near add may be helpful in early cases
Low vision aid may be needed in advanced cases of geographical
atrophy.
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Treatment modalities available for exudative (neovascular)ARMD :
Intravitreal anti-VEGF therapy has become the treatment of first
choice for al CNV lesions. Anti-VEGFs are injected intravitreal y.
These include: Bevacizumab (Avastin), dose: 1.25 mg, or
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Ranibizumab (Lucentis), dose: 0.5 mg/0.05 ml, orPegaptanib (Macugen), dose: 0.3 mg in 90 ml
Anti-VEGF improve the vision in 30?40% of cases and stabilize the
vision in rest of the cases
repeated injections are required at an interval of 1?3 months
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Although anti-VEGF therapy is the preferred strategy for the treatment of CNV,
some patients may choose not to undergo an intravitreal procedure
Other options include PDT, TPT, argon laser photocoagulation
Photodynamic therapy (PDT) is the treatment of choice after anti-VEGF
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injections for subfoveal and juxtafoveal classic CNVMTranspupillary thermotherapy (TTT) with a diode laser (810 nm) may be
considered for subfoveal occult CNVM. PDT is definitely better than TTT but is
very expensive.
Double frequency and YAG 532 nm photocoagulation may be used for
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extrafoveal choroidal neovascular membrane (CNVM)Surgical treatment. Submacular surgery to remove CNVM and macular
translocation surgery are being evaluated.
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