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Opthalmology > Sudden Vision Loss > Flashcards

Sudden Vision Loss Flashcards

1
Q

What are some important history taking points for an acute loss of vision

A 
pain
sudden/gradual
intermitternt/constatn? 
flashes/floaters
unilateral/bilateral
total loss? blurred? (can you see light) 
central/side vision 
colour/loss
PMH - ocular specifically
FHx of eye diseae
cardiovascular health
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2
Q

what should always be examined in patients that come in with acute loss of vision

A 
acuity
visual fields
pupil reactions
fundoscopy 
bloods - CV risk factors, inflammatory markers
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3
Q

What are causes of acute loss of vision

A 
acute corneal disease
Giant cell arteritis 
anterior chamber haemorrhage 
vitreous haemorrhage 
optic neuritis/ischaemic optic neuropathy 
branch retinal vein occlusion
central retinal vein occlusion
central retinal artery occlusion
branch retinal artery occlusion 
retinal detachment 
macular haemorrhgae 
bitemporal hemianopia 
optic nerve compression via papilloedeme 
migraine 
CVA
acute angle closure glaucoma 
anterior uveitis
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4
Q

What are causes of painful loss of vision

A 
Giant cell arteritis 
Migraine 
optic neuritis
acute angle closure glaucoma 
anterior uveitis
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5
Q

what does acute corneal disease make the cornea look like

A

cloudy

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6
Q

when is acute corneal disease not painful

A

when infected by HSV

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7
Q

what age group is most affected by giant cell arteritis

A

> 50

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8
Q

what blood test is most indicative of giant cell arteritis, and what values are you looking for

A

ESR, >50

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9
Q

what are some symptoms of giant cell arteritis

A 
scalp tenderness - particulary over pterygoid
visual obscurations 
jaw claudication (pain on chewing) 
weight loss
decreased appetite
proximal myopathy )dif
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10
Q

How should you investigate suspected giant cell arteritis

A

urgent ESR + CRP

refer to opthal

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11
Q

how do you treat giant cell arteritis

A

IV steroids 80mg/day

followed by discharge + oral pred 12-18 months (following histology)

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12
Q

if untreated what is the prognosis of giant cell arteritis

A

can go blind in a few hours

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13
Q

What must be done before giving someone long term steroids for giant cell arteritis

A

histology sample must be taken from the superficial temporal artery to confirm diagnosis

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14
Q

what can you see histologically that would confirm giant cell arteritis

A

tunica media thickening
smaller lumen size
commonly giant cells found (hence the name)

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15
Q

what are some features of Temporal Arteritis

A

> 60, acute visual loss (usually central), pain on chewing/combing hair nad when moving eyes red eye, raised ESR

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16
Q

what should always be done if optic neuritis is suspected

A

baseline MRI (rule out MS)

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17
Q

what is optic neuritis associated with and what percentage risk is there

A

MS - 50% lifetime risk, in 15-25% of MS patients optic neuritis is the first presentation

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18
Q

how do you treat optic neuritis

A

if MRI normal - symptomatic relief with IV steroids (methylprednisolone) if required - speeds recovery but doesnt recover any more vision than it would usually

If 2+ demylelinated lesions seen on MRI then MS is high risk and neurology referral is required for assessment for inteferon-1a or 1b

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19
Q

whats the pathology of optic neuritis

A

inflammatory demyelination of the optic nerve

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20
Q

optic neuritis prognosis

A

most regain normal vision in 6 months

if it returns, risk of MS is higher

21
Q

what is more common, venous occlusion or retinal artery occlusion, and which is worse

A

venous, aterial is usually worse

22
Q

what are features of a branch retinal vein occlusion

A

ventral visual loss - usually on waking
fundoscopy: cotton wool spots + haemorrhages in 1 quadrant of the eye
commonly raised BP and irregularity in routine bloods

23
Q

what is the treatment for branch retinal vein occlusion

A

if mild - watch and wait (50% get better with no treatment)

otherwise: if neovascularisation is present, panretinal photocoagulation may be offered

macular laser therapy is offered if the macula is ‘waterlogged’

Anti-VEGF drugs or a dexamethasone implant may be injected into the eye

24
Q

what are examples of some anti-VEGF drugs

A

Ranibizumab( Lucentis)
Aflibercept ( Eylea)
Bevacizumab (Avastin)

25
Q

what are some risk factors for retinal vein occlusion

A 
hypertension
diabetes
high cholesterol 
smoking 
older age 
glaucoma 
inflammatory disease of the eye
26
Q

what is the prognosis of retinal vein occlusion

A 
mild = good 
extensive = not good, risk of proliferative retinopathy
27
Q

what are features of central retinal vein occlusion

A 
affects all vision (not just central) 
variable acuity
RAPD present if severe
haemorrhages in all quadrants (this varies)
swollen nerve - cant see margins 
filated tortuous veins 
cotton wool spots
28
Q

what is a roth spot

A

a haemorrhage inside a cotton wool spot

29
Q

what is the prognosis of central retinal vein occlusion

A

only 10-20% of severe patients recover some vision

30
Q

how do you treat central retinal vein occlusion

A

if neovascularisation is present, panretinal photocoagulation may be offered

macular laser therapy is offered if the macula is ‘waterlogged’

Anti-VEGF drugs or a dexamethasone implant may be injected into the eye

treat immediately as waiting is less effective than branch occlusions

31
Q

what is a severe complication of central retinal vein occlusion

A

rubeotic glaucoma - neovascularisation involving the iris causing a blockage of the drainage angle

32
Q

What is the treatment of rubeotic glaucoma

A

panretinal photocoagulopathy

33
Q

What sign means there is high risk of rubeotic glaucoma developing in central retinal vein occlusion

A

RAPD present

34
Q

what are some features of a central retinal artery occlusion

A

low acuity to no light perception
afferent pupil defect (decreased constriction when waced with light)
RAPD
carotid bruits
fundoscopy: retinal odema, cherry red spot in macula, retinal arteriole emboli

35
Q

what investigations should be done for central retinal artery occlusion

A 
BP
Fundoscopy
carotid USS and doppler neck
standard bloods
ESR
cardiac echo
36
Q

what treatments for retinal artery occlusion can be done in primary care

A

rebreathe into paper bag to increased carbon dioxide and dilate vesssels to move emboli into periphery

ocular massage

37
Q

what treatments for central retinal artery occlusion can be done in secondary care

A 
IV Carbonic anhydrase inhibitor (acetazolamide/diamox) 
or paracentesis (needle to drop IOP)
38
Q

What is the urgency of central retinal artery occlusion

A

12 hours until retina dies so refer to eye casualty immediately - 90 mins until ischemia starts

39
Q

what are some features of branch retinal artery occlusion

A 
RAPD
carotid bruits
hypertensive retinopathy 
fields defects  
acuity is 6/5 to count fingers
40
Q

how do you manage branch retinal artery occlusion

A 
BP
Fundoscopy
carotid USS and doppler neck
standard bloods
ESR
cardiac echo 
IV Carbonic anhydrase inhibitor (acetazolamide/diamox) 
or paracentesis (needle to drop IOP)
41
Q

what are some features of retinal detachment/vitreous haemorrhage

A 
floaters and flashes with field loss
acuity may be lost unless macula stays attached 
RAPD - only if detached enough
abnormal red reflex  
shadows in visual fields
42
Q

what is the pathology of retinal detachment

A

vitreous liquifies and detaches from retina, normally its ok but sometimes the retina comes with it and tears, fluid then gets into the tear and separates the retina from the underlying layers causing further detachment and ischaemia

43
Q

what is a risk factor for retinal detachment

A

myopia (short sightedness)

44
Q

what is the treatment for retinal detachment/vitreous haemorrhage

A

if there is a tear - laser treatment

detachment - surgery/close breaks and oppose both surfaces

45
Q

when should you aim to treat by in retinal detachment

A

before the foeva detaches as this causes significant blindness risk

46
Q

what are some features of vitreous haemorrhage

A

blurring of fundoscopy/vision due to bleeding into vitreous

47
Q

what are some features of macular haemorrhage

A

acute visual lose with a +ve scotoma, variable acuity, NO RAPD, visual fields should be good, fundoscopy reveals minor/major correlates with acuity

48
Q

what causes bitemporal hemianopia

A

pituitary tumour (bitemporal superior quadrantinopia) /growth in superior aspect of rafkes pouch (bitempora inferior quadrantinopia)

49
Q

if vitreous haemorrhage is seen what scan should be performed and why

A

Ultrasound B scan to rule out any retinal detachment

Opthalmology (16 decks)

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