medical retina (see DM) Flashcards
5 findings on fundoscopy of non-proliferative retinopathy
- microaneurysms;
- exudate;
- dot haemorrhages;
- blot haemorrhages;
- cotton wool spots
how does exudate form (diabetic retinopathy)
internal-retinal lipid deposits due to plasma leakage/oedema from microaneurysms or capillaries
how do cotton wool spots form (retinopathy)
axoplasmic debris from nerve-fibre infarcts - i.e. debris from death of nerve fibres
what is branch retinal vein occlusion
occlusion of a branch of the retinal vein as it is crossed by a retinal arteriole
what is central retinal vein occlusion (CRVO)
occlusion of vein in optic nerve as it runs alongside the central retinal artery
severe/ischaemic CRVO presentation
acute onset - often at night and noticed upon waking; PAINLESS loss of vision; visual acuity between 6/60-hand motions only at 1m
severe CRVO retinal signson fundoscopy (5)
- severe intraretinal haemorrhages;
- engorged retinal veins;
- disc swelling;
- macular oedema;
- cotton wool spots
what clinical test will be +ve in severe CRVO
RAPD -> indicates severe loss of afferent visual input
3 complications of CRVO
rubeotic glaucoma; macular oedema; retinal neovascularisation
all are treatable
5 risk factors for CRVO
- age;
- HTN;
- arteriosclerosis;
- hyperlipidaemia;
- pro-thrombotic conditions
is the other eye at risk in CRVO
yes - the fellow eye may develop a retinal vein occlusion in 10% of people within 2-4yrs -> prevention by treating risk factors
mild/non-ischaemic CRVO presentation
acute onset - often at night and noticed upon waking; PAINLESS loss of vision; visual acuity between 6/12-6/36
will RAPD be +ve in mild CRVO
no -> maintained afferent visual input
what changes occur to capillaries in CRVO and what does it lead to
damage to retinal capillary walls -> VEGF released -> leakage of plasma into the retina (macular oedema)
macular oedema treatment
anti-VGEF intravitreal injection
what does peripheral retinal ischaemia lead to (VGEF)
production of VGEF ->diffuses though the eye and stimulates growth of new blood vessels (rubeosis) on the iris and in the drainage angle -> can lead to angle closure glaucoma
how can rubeosis be treated
panretinal photocoagulation (PRP) - destroys ischemic retina, minimizes the eye’s oxygen demand, and reduces the amount of VEGF being released
branch retinal vein occlusion (BRVO) presentation
acute onset - often at night and noticed upon waking; PAINLESS loss of vision; visual acuity between 6/9-hand movementd at 1m
may be asymptomatic if fovea not affected
BRVO retinal signs (4)
- intraretinal haemorrhages in area of affected vein branch only;
- engorged branch retinal vein;
- macular oedema;
- cotton wool spots
is RAPD +ve in BRVO
no - smaller area of retina involved than CRVO
BRVO complications (3)
macular oedema; retinal neovascularisation; vitreous haemorrhage
what is hypertensive retinopathy
damage to the retina due to HTN
what can lowgrade hypertensionlead to
accelerated ateriosclerosis
retinal signs of hypertensive retinopathy (4)
thickened arteriole wall; “silver wiring” - increased central light reflex; narrowed/straightened arterioles; AV nipping - thickened arteriole constricts the venule
what is geographical atrophy
chronic progressive degeneration of the macula - loss of patches of choroid/ retinal pigment epithelium/ retina in an irregular shape
what is amaurosis fugax
“fleeting blindness” - transient and sudden monocular blindness (like a curtain coming down)
what can cause amaurosis fugax (2)
- carotid atheroma leading to emboli (fibrin-platelet/cholesterol);
- cardiac valve emboli (calcific) - rarer
what assessment must be done post amaurosis fugax
stroke risk assessment - TIA clinic for carotid scan, ECG, anti-platelet
what is the life expectancy for pts w CRAO
5.5 years
retinal presentation of CRAO (4)
- pale retina/whitening - due to infarcted swollen inner 2/3 retina supplied by the CRA;
- “cherry red spot” - fovea -> no inner retinal covering fovea centre and photorecptors supplied by choroidal circulation;
- retinal artery narrowing;
- emboli may be present;
- boxcarring (segmental blood flow)
4 causes of CRAO
- carotic atheroma - 90% of CRAOs are embolic in nature;
- calcified aortic valve lesions (emboli - rare);
- GCA (must rule this out!);
- traumatic vessel wall damage
how can an embolus in the CRA attempt to be disloged
by lowering IOP -> aids the perfusion pressure gradient (usually ineffective)
GCA symptoms (8)
- headache;
- temporal/scalp tenderness;
- jaw claudication;
- systemic symptoms (fever, lethargy malaise);
- transient vision loss;
- permanent ischaemic optic neuropathy;
- retinal artery occlusion;
- temproal artery thickening/tender/pulseless
3 tests for GCA
- BLOODS (raised ESR, CRP, platelets);
- carotid ultrasound;
- temporal atery biopsy
is retinal artery occlusion an emergency?
yes - immediated systemic evaluation and referral to TIA service required
what may patients who have CRAO concurrently present with
silent ischaemic stroke
5 risk factors for retinal artery occlusive disease
- older age (>70%);
- diabetes mellitus;
- arterial hypertension;
- ischaemic heart disease;
- smoking
CRAO vs BRAO presentation
CRAO - Loss of vision over entire field;
BRAO - hemi field defect (or may even have 6/6 vision if cilioretinal artery sparing)
what vessels are usually involvedin BRAO
temporal retinal vessels
BRAO treatment
does not usually require treatment unless perifoveolar vessels are threatened
CRAO/BRAO investigations
- FBC for anaemia, polycythemia, platelet disorders etc. ;
- ESR/CRP for inflammatory ateritis;
- fribrinogen levels, anti-APPL, aPTT, serum protein coagulopathies;
- cholesterol, triglycerides, lipids for atherosclerotic disease;
- echo/ECG for valve disease or AF;
- blood cultures - bacterial endo/septic emboli
2 managements fro RAO in emergency care
- ocular massage - disloges the embolus to a point further down the arterial circulation and improves retinal perfusion;
- anterior chamber paracentesis - if visual loss has been present <24hrs, slit-lamp removal of 0.1-0.4mL of aqueous humour to decrease IOP -> allows greater perfusion and embolus to be pushed further down the vascular tree
medical therapy for CRAO
treatment is directed towards lowering IOP, increasinf retinal perfusion and increasing oxygen delivery to hypoxic tissues
- timolol (start early);
- acetazolamide + mannitol;
- carbogen therapy (5%CO2, 95% O2) -> CO2 dilated retinal arterioles and O2 increases oxygen deliveryto ischaemic tissues;
- hyperbaric oxygen therapy (if initiated within 2-12hrs)
