Sudden Visual Loss Flashcards
what 5 questions should you ask on presentation of sudden visual loss
headache? GCA
eye movements hurt? optic neuritis
light/flashes preceding visual loss? retinal detachment
like a curtain descending over vision? amaurosis fugax may precede permanent visual loss
poorly controlled DM?
what supplies the retina
CRA supplies the inner 2/3 and ciliary body the outer 1/3
presentation of CRAO
dramatic visual loss within seconds of occlusion
no pain
relative afferent pupillary defect occurs within seconds
describe the extent of vision loss in CRAO
in 90% acuity is finger counting or worse
CRAO fundoscopy
retina is pale and yellow due to oedema and there is a cherry red spot macula

causes of occlusion in CRAO
carotid artery disease or thrombo-embolic (clot, tumour, infective)
look for signs of atherosclerosis, heart valve disease, smoking etc
managment of CRAO
- if it presents within 24 hours the aim is to increase the retinal blood flow by reducing IOP by ocular massage
- vascular management is used to establish the source of the embolus (carotid doppler (US))
- risk factors must be managed and assessed

BRAO
retinal and visual changes relate only to the part of the retina supplied by the occluded artery

amaurosis fugax
transient CRAO
painless temporary loss of vision described to be like a curtain falling down. usually lasts around 5 minutes with full recovery
fundoscopy of Amaurosis Fugax
nothing abnormal seen usually
what can cause Amaurosis Fugax
can be due to the passage of emboli through the retinal arteries
a TIA causing Amaurosis Fugax is an early sign of internal carotid artery stenosis
management of Amaurosis Fugax
urgent referral to stroke clinic
aspirin
name some other causes of transient visual loss
migraine (visual loss usually followed by headache)
Always think of vascular causes such as platelet-fibrin/cholesterol micro-emboli from atherosclerotic plaques in the heart or carotid arteries
compare the appearance of veins and arteries on fundoscopy
veins appear thicker than arteries, which are pale inside due to muscle

CRVO
venous stasis - blood is going in but is not able to leave
describe the venous drainage of the eye
SOV drains into cavernous sinus via the superior orbital fissure

incidence of CRVO
increases with age
more common than CRAO
causes of CRVO
Blockage in veins cause by pressure from nearby artery or blood clot forming in the vein. This leads to bleeding and leakage of fluid from blood vessels.
virchow’s triad: stasis, hypercoagulability, hypertension
arteriosclerosis, hypertension, hyperviscosity
diabetes and polycythaemia
glaucoma
associated with heart disease, smoking etc
presentation of CRVO
if the whole central retinal vein is occluded there is blurring and visual loss, less sudden than CRAO.
it may be perceived as sudden by the patient but the mechanisms of visual loss are due to development of ischaemia and macular oedema
macular oedema in CRVO


describe the appearance of CRVO on fundoscopy
stormy sunset appearance - hyperaemia and haemorrhages

ischaemic CRVO
decreased perfusion, capillary closure and retinal hypoxia
marked RAPD
fundoscopy: cotton wool spots (infarcts), swollen optic nerve, macular oedema, risk of neovascularization (ischaemia leads to release of VEGF)
non-ischaemic CRVO
have better acuity and prognosis, but may progress to ischaemic forms, hence the need for follow up
managment of CRVO
monitor as complications may occur due to the formation of new vessels - laser photocoagulation treatment may be required
Anti-VEGFs
assess underlying risk factors eg hypertension, diabetes
anterior ischaemic optic neuropathy
occlusion of optic nerve head circulation
the optic nerve is damaged if the posterior ciliary arteries are blocked by inflammation or atheroma
2 types of AION
arteritic - due to inflammation (GCA)
non-arteritic - due to atherosclerosis
signs and symptoms of AION
sudden, profound visual loss
swollen pale optic disc is seen on fundoscopy

Vitreous Haemorrhage
haemorrhage often occurs into the vitreous cavity
bleeding can occur from new retinal vessels, retinal tears, retinal detachment or trauma
signs of Vitreous Haemorrhage
small extravasations of blood produce vitreous floaters (seen as small black dots or tiny ring like forms with clear centres)
large enough bleed may obscure vision and cause a loss of red reflex
what may be seen on fundoscopy of Vitreous Haemorrhage
haemorrhage

managment of Vitreous Haemorrhage
identify cause
a vitrectomy is done to remove the blood in the vitreous if the retina is torn/detached or the patient needs treatment of new vessels
optic neuritis
inflammation of the optic nerve
subacute unilateral loss of acuity occurs over hours or days
colour vision is affected more than acuity: red desaturation
pain on eye movement
swelling of optic disc

in optic neuritis will the pupillary defect be afferent or efferet
afferent
dyschromatopsia
ability to perceive colours is not fully normal
why does optic neuritis cause pain on eye movement
the sheath of the optic nerve is attached to the common tendinous ring where the rectus muscles of the eye attach

optic neuritis
what is the chief cause of registrable blindness in patients over 65
age related macular degeneration
cause of ARMD
unknown and multifactorial
risk factors include increasing age, smoking, positive family history, poor nutrition etc
pathophysiology of wet ARMD
abberant vessels grow from the choroid into the neuro-sensory retina and leak
this causes a build up of fluid/blood and eventually scarring

symptoms of wet ARMD
rapid central vision loss and distortion (metamorphopsia)

signs of wet ARMD
haemorrhage and exudate


wet ARMD
treatment of wet ARMD
injection of anti-VEGF into vitreous cavity