Focal Ischaemic Retinal Disease

Focal Ischaemic Retinal Disease

·        Affects little vessels

·        Features:

o  Cotton wool spots:

§  Fluffy and off-white/yellow

§  Due to micro-infarction ® superficial area of necrosis and oedema

§  Axons are disrupted and become distended (cytoid bodies)

§  Resolve in 6 weeks

o  Hard exudates:

§  Discrete, brighter white, often around macula 

§  Plasma leaks from damaged capillaries (secondary to thickened basement membrane) in the outer plexiform layer (deeper in the retina) and forms proteinaceous lakes

§  Resolves over several months

o  Haemorrhage: usually arises from microemboli/thrombi damaging vessels

§  Flame: a small arteriole bursts into nerve fibre layer and spreads along nerve fibres

§  Dot: capillary bursts into outer plexiform layer

§  Blot: into the subretinal space

§  Roth‟s spots: central white infarct surrounded by haemorrhage

o  Microaneurysms:

§  Round or oval dilations of capillaries – look like lots of very little red dots

§  Central in diabetes, peripheral in central retinal vein occlusion

§  Due to reduced numbers of pericytes surrounding capillaries

o  Neovascularisation:

§  Response of the eye to vascular insufficiency, secondary to angiogenesis factors from ischaemia: proliferate around the margin of non-perfusion. Detect with fluorescein angiogram

§  Appears as fine lace work of new vessels.  They leak and bleed

§  Sites: 

·        Iris surface ® neovascular glaucoma, ectropion uvea

·        Pupillary membrane ® Posterior Synichiae

o   Vitreal Surface ® haemorrhage, pre-retinal fibrovascular membranes ® scarring ® retinal detachment

o   Easy to see if over optic disk (normally should only be large vessels)

·        Differentiating between Hypertensive and diabetic retinopathy:

Diabetic Retinopathy

·        Diabetes Mellitus

·        1/3 diabetes with > 30 years disease will loose some sight. Diabetics 25 times more likely to go blind

·        Risk related to duration Þ Type 1 (juvenile onset) more likely to cause damage

·        Retinal exam essential:

o   At diagnosis for maturity onset (may have had diabetes for 5 – 10 years)

o   After 5 years for juvenile onset and annually thereafter

o   Fluorescein angiography (injected in arm then photograph retina) to test for neovascularisation

·        Causes: Thickened basement membrane of retinal microcirculation ® leakage, oedema, nonperfusion and micro-aneurysms

·        Macular retinopathy: boggy, leaky macula ® blurred vision

·         Non-proliferative retinopathy (= Background Retinopathy): Progression: oedema (® blurred vision) ® microaneurysms ® hard exudates ® cotton wool spots ® small haemorrhages ® venous bleeding

·        Proliferative retinopathy:

o   Neovascularisation

o   Retinal detachment due to shrinkage of subsequent scars

o   Vitreous haemorrhage (can also be due to vitreous collapse tearing at retina or retinal venous occlusion – usually due to ­BP ® expanded artery ® compresses adjacent vein)

·        Treatment:

o   Regular checks

o   Blood sugar control

o   Treatment of vascular disease (eg ¯BP)

o   Laser treatment (photocoagulation): 2 – 3,000 burns (but NEVER on macula).  ¯O₂ demand ®

o   ¯neovascularisation.  Complications: ¯peripheral and night vision, macula oedema

o   Vitrectomy: if non-resolving vitreous haemorrhage or fibrovascular contraction of vitreous (which has risk of ® retraction of retina ® tear)

o   Retinal repair: reattach retina 

·        Diabetes can also cause: neovascular glaucoma (blocking flow past lens), more susceptible to damage from ­IOP, cataract, extraocular muscle palsy

Hypertensive Retinopathy 

·        Rarely causes visual loss.  Requires diastolic BP > 120 for many years

·        Stages:

o   Stage 0: no changes

o   Stage 1: „copper-wiring‟ of arterioles due to thickening of the walls due to medial thickening (very subjective)

o   Stage 2: Arteriovenous nipping  – thickened arterioles compressing underlying veins

o   Stage 3: Soft-exudates and/or flame haemorrhages (spread longitudinally along fibres)

o   Stage 4: Papilloedema plus the above

·        Bilateral and symmetric.  More cotton wool spots (nerve fibre hypoxia)

·        Retinopathy regresses if hypertension controlled (cf diabetes which doesn‟t)