Sudden Visual Loss Flashcards

1
Q

what 5 questions should you ask on presentation of sudden visual loss

A

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?

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2
Q

what supplies the retina

A

CRA supplies the inner 2/3 and ciliary body the outer 1/3

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3
Q

presentation of CRAO

A

dramatic visual loss within seconds of occlusion

no pain

relative afferent pupillary defect occurs within seconds

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4
Q

describe the extent of vision loss in CRAO

A

in 90% acuity is finger counting or worse

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5
Q

CRAO fundoscopy

A

retina is pale and yellow due to oedema and there is a cherry red spot macula

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6
Q

causes of occlusion in CRAO

A

carotid artery disease or thrombo-embolic (clot, tumour, infective)

look for signs of atherosclerosis, heart valve disease, smoking etc

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7
Q

managment of CRAO

A
  • 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
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8
Q

BRAO

A

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

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9
Q

amaurosis fugax

A

transient CRAO

painless temporary loss of vision described to be like a curtain falling down. usually lasts around 5 minutes with full recovery

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10
Q

fundoscopy of Amaurosis Fugax

A

nothing abnormal seen usually

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11
Q

what can cause Amaurosis Fugax

A

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

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12
Q

management of Amaurosis Fugax

A

urgent referral to stroke clinic

aspirin

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13
Q

name some other causes of transient visual loss

A

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

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14
Q

compare the appearance of veins and arteries on fundoscopy

A

veins appear thicker than arteries, which are pale inside due to muscle

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15
Q

CRVO

A

venous stasis - blood is going in but is not able to leave

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16
Q

describe the venous drainage of the eye

A

SOV drains into cavernous sinus via the superior orbital fissure

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17
Q

incidence of CRVO

A

increases with age

more common than CRAO

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18
Q

causes of CRVO

A

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

19
Q

presentation of CRVO

A

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

20
Q

macular oedema in CRVO

21
Q

describe the appearance of CRVO on fundoscopy

A

stormy sunset appearance - hyperaemia and haemorrhages

22
Q

ischaemic CRVO

A

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)

23
Q

non-ischaemic CRVO

A

have better acuity and prognosis, but may progress to ischaemic forms, hence the need for follow up

24
Q

managment of CRVO

A

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

25
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
26
2 types of AION
arteritic - due to inflammation (GCA) non-arteritic - due to atherosclerosis
27
signs and symptoms of AION
sudden, profound visual loss swollen pale optic disc is seen on fundoscopy
28
Vitreous Haemorrhage
haemorrhage often occurs into the vitreous cavity bleeding can occur from new retinal vessels, retinal tears, retinal detachment or trauma
29
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**
30
what may be seen on fundoscopy of Vitreous Haemorrhage
haemorrhage
31
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
32
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
33
in optic neuritis will the pupillary defect be afferent or efferet
afferent
34
dyschromatopsia
ability to perceive colours is not fully normal
35
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
36
optic neuritis
37
what is the chief cause of registrable blindness in patients over 65
age related macular degeneration
38
cause of ARMD
unknown and multifactorial risk factors include increasing age, smoking, positive family history, poor nutrition etc
39
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
40
symptoms of wet ARMD
rapid central vision loss and distortion (metamorphopsia)
41
signs of wet ARMD
haemorrhage and exudate
42
wet ARMD
43
treatment of wet ARMD
injection of anti-VEGF into vitreous cavity