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RB Y2 Ophthamology > Sudden Visual Loss > Flashcards

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

A
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
Q

anterior ischaemic optic neuropathy

A

occlusion of optic nerve head circulation

the optic nerve is damaged if the posterior ciliary arteries are blocked by inflammation or atheroma

26
Q

2 types of AION

A

arteritic - due to inflammation (GCA)

non-arteritic - due to atherosclerosis

27
Q

signs and symptoms of AION

A

sudden, profound visual loss

swollen pale optic disc is seen on fundoscopy

28
Q

Vitreous Haemorrhage

A

haemorrhage often occurs into the vitreous cavity

bleeding can occur from new retinal vessels, retinal tears, retinal detachment or trauma

29
Q

signs of Vitreous Haemorrhage

A

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
Q

what may be seen on fundoscopy of Vitreous Haemorrhage

A

haemorrhage

31
Q

managment of Vitreous Haemorrhage

A

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
Q

optic neuritis

A

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
Q

in optic neuritis will the pupillary defect be afferent or efferet

A

afferent

34
Q

dyschromatopsia

A

ability to perceive colours is not fully normal

35
Q

why does optic neuritis cause pain on eye movement

A

the sheath of the optic nerve is attached to the common tendinous ring where the rectus muscles of the eye attach

36
Q
A

optic neuritis

37
Q

what is the chief cause of registrable blindness in patients over 65

A

age related macular degeneration

38
Q

cause of ARMD

A

unknown and multifactorial

risk factors include increasing age, smoking, positive family history, poor nutrition etc

39
Q

pathophysiology of wet ARMD

A

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
Q

symptoms of wet ARMD

A

rapid central vision loss and distortion (metamorphopsia)

41
Q

signs of wet ARMD

A

haemorrhage and exudate

42
Q
A

wet ARMD

43
Q

treatment of wet ARMD

A

injection of anti-VEGF into vitreous cavity

RB Y2 Ophthamology (20 decks)

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