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Eye Disease > Vascular Occlusions > Flashcards

Vascular Occlusions Flashcards

1
Q

What is the second most common retinal vascular disease?

A

RVO (retinal vein occlusions)

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2
Q

What is more common BRVO or CRVO?

A

BRVO

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3
Q

Why does a BRVO happen?

A

Venous compression by an artery which causes turbulent blood flow, endothelial damage and then thrombosis —> OCCLUSION

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4
Q

What is the main age occurrence of BRVOs?

A

60 years

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5
Q

What are some RF of BRVO?

A
  • Systemic HTN
  • DM
  • smoking
  • cardiovascular disease
  • glau history
  • previous RVO in either
  • inflammatory condition
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6
Q

What is a protective factor of BRVO ?

A

Vein crosses artery instead of artery crossing a vein

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7
Q

What are symptoms of BRVO?

A
  • Sudden painless loss of vision
  • Can be asymptomatic
  • If macula covered, sector field defect
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8
Q

Where are 66% of cases of BRVO on the retina ?

A

Superior temporal

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9
Q

In an acute stage of BRVO, what will you observe ?

A
  • Flame haemorrhages
  • dilated and tortuous veins
  • retinal oedema
  • CWS
  • normally respect the horizontal mid line
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10
Q

What signs may you see with a px who has chronic stage BRVO?

A
  • hard exudates
  • vascular sheathing (appearing white)
  • macula pigment
  • collateral vessel formation
  • retinal ischameia
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11
Q

What is collateral vessel formation?

A

Small, tortuous vessels that cross horizontal line to drain into unaffected quadrant

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12
Q

Where would retinal ischaemia occur in chronic BRVO?

A

Downstream to the occlusion

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13
Q

What does retinal ischaemia result due to BRVO?

A

Upregulation of VEGF + increased vessel permeability + macula oedema

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14
Q

Is this a chronic or acute stage BRVO?

A

Chronic (substantial amount of exudate)

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15
Q

What can you note that is similar in these two pictures in relation to the BVs?

A

Vascular sheathing (that white appearance)

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16
Q

What is the main cause of visual loss in BRVO?

A

Chronic macula oedema

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17
Q

What is an epiretinal membrane?

A

A membrane forming on the surface of the retina

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18
Q

What are six complications of BRVO?

A
  • Chronic macula oedema
  • Exudates
  • Haemorrhages
  • Epiretinal membrane
  • neovasc
  • RD (rare)
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19
Q

Why does neovasc occur?

A

Unregulation of VEGF

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20
Q

When would neovasc occur in BRVO?

A

ONLY if a large area of retina id ischameic

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21
Q

What type of RD will occur even though it is rare?

A

Tractional or rhegmatogenous

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22
Q

How long would it take macula oedema to resolve?

A

12 months in 40% if cases

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23
Q

What % of eyes will maintain a va <6/12?

A

50%

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24
Q

What % of eyes will have a va <6/60?

A

25%

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25
Q

Is neovasc glaucoma rare with BRVO?

A

Yes

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26
Q

After having BRVO in one eye, what %h have it in the other eye?

A

10%

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27
Q

Is retinal neovasc rare with BRVO?

A

YES

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28
Q

What causes CRVO?

A

Thrombus formation (blood clot) where the central artery and central vein leave the nerve head at the lamina cribosa

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29
Q

What are three possible mechanisms for CRVO?

A
  • Arteriosclerosis of CRA disturbing blood flow in vein
  • Mechanical pressure in lamina cribosa
  • Vessel wall or blood changes
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30
Q

Name some RF of CRVO

A
  • Systemic HTN
  • DM
  • OAG
  • cardiovascular disease
  • systemic inflammatory conditions
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31
Q

What is the acute presentation of CRVO? symptoms

A
  • sudden onset vision loss
  • painless
  • RAPD present
  • photos potentially
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32
Q

What is known to describe a CRVO?

A

BLOOD AND THUNDER

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33
Q

What signs would you see on a CRVO fundus?

A
  • Retinal haemorrhages
  • dilated tortuous veins
  • CWS
  • macula oedema
  • unilateral optic disc oedema
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34
Q

What are the two types of CRVOs?

A

Ishaemic and non-ischaemic

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35
Q

What % of CRVOs are ischaemic ?

A

20%

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36
Q

On Fluorescein angiography, what would you see with an ishaemic CRVO?

A

Fluorescein not permeating to Large areas of retinal capillaries —> this is causing the ischaemia due to lack of blood supply
(In the pic right is a normal eye)

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37
Q

What are signs if an ischaemic CRVO?

A
  • Severe vision loss
  • RAPD
  • Multiple intraretinal haemorrhages
  • CWS
  • optic disc swelling
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38
Q

In Relation to FA, what classifies an ischaemic CRVO?

A

Area of non-perfusion (where the Fluorescein fails to get to) is greater than 10 DD

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39
Q

What % of CRVO does non-ishaemic CRVO account for?

A

80%

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40
Q

Where are the haemorrhages + what type of haemorrhages are common with CRVO?

A

Superficial flame

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41
Q

What is different in non-ischaemic CRVO compared to ishaemic?

A
  • superficial flame haemorrhages
  • va is better
  • fewer CWS
42
Q

What is different in non-ischaemic CRVO compared to ishaemic?

A
  • superficial flame haemorrhages
  • va is better
  • fewer CWS
43
Q

What are complications of CRVO?

A
  • ishaemia
  • upregulation of VEGF
44
Q

What can an up regulation of VEGF lead to in CRVO?

A
  1. Macula oedema
  2. NVD
  3. NVE
  4. Vitreous haemorrhage
  5. Neovasc glaucoma
45
Q

In chronic compensation cases of CRVO, what do we tend to see in relation to the haemorrhages?

A

A re absorbtion (flame first , then dot and blot )

46
Q

What can develop to divert retinal blood to choroidal circulation ?

A

Optociliary shunt vessels

47
Q

What is a DD of chronic compensation after CRVO?

A

Diabetic retinopathy as you are left with deeper dot and blot haemorrhages

48
Q

In non-ishaemic CRVO what % of eyes does macula oedema resolve?

A

30%

49
Q

Is neovasc glaucoma rare in non-ishaemic CRVO ?

A

Yes

50
Q

What can a poor VA caused by CRVO mean?

A

Poorer VA prognosis

51
Q

True or false:
80% of eyes with VA <6/60 at presentation of CRVO will no improve over time

A

True :(

52
Q

What % of eyes with Visio <6/60 will develop rubeosis iridis?

A

44%- they need to be followed up by an ophthalmologist

53
Q

What are two that must be considered when managing CRVO or BRVO?

A

1) managing underlying cause
2) ophthalmic implications such as macula oedema, NVE, neovasc glaucoma

54
Q

What must you do in ALL cases of CRVO and BRVO?

A

Refer to GP for investigation AND Refer to be seen by an ophthalmologist within 2-4weeks of presentation

But look at local referral schemes

55
Q

If px has neovasc glaucoma, what should you do?

A

Phone eye department for triage

56
Q

What is the treatment for NVE?

A

Laser pan-retinal photocoagulation

57
Q

What does Laser pan-retinal photocoagulation Do?

A

Reduce hypoxia and VEGF production by reducing O2 demand of photoreceptors and RPE

58
Q

What is neovasc glaucoma caused by?

A

New vessels on iris or angle which blocks drainage

59
Q

What is the aim when treating neovasc glaucoma if eye is blind?

A

Keep eye pain free with topical steroids and atropine

60
Q

What is treatment when Treating neovasc glaucoma if there is vision?

A

Control IOPs with anti-glaucoma drops. Or/amd surgery

61
Q

What referral is required for undiagnosed neovasc glaucoma?

A

UGRENT (if pressure is >40mmHg then is an emergency)

62
Q

What is commonly used to treat macula oedema in CRVO which causing vision loss?

A

Anti-VEGF (Lucentis or Eyelea) or dexamethasone (steroid)

63
Q

Which types of px is Anti-VEGF preferred in?

A

Previous history of glaucoma, younger px who are phakic

64
Q

Which types of px would you want to use a steroid to treat macula oedema?

A

Recent cardiovascular events + px who do not favour monthly injections

65
Q

What is the main cause of CRAO?

A

Embolus from atherosclerosis (like plaque that breaks off) and lodges in a narrow part of CRA

66
Q

What are some RF of CRAO?

A
  • HTN
  • DM
  • tobacco use
  • renal disease
  • atherosclerosis
  • TIA
  • GCA
  • Lupus
67
Q

What is a px at risk of if they have CRAO or BRAO?

A

Life-threatening cardiovascular/cerebrovascular incident

68
Q

Why is CRAO and BROA so serious?

A

They have these emboli floating around their blood which can get jammed anywhere in the body, INCLUDING THE BRAIN

69
Q

What is the presentation of someone with CRAO or BRAO?

A

-SUDDEN painless loss of vision
-May have a history of amaurosis fugax
-Mean age of 60 yrs

70
Q

In 90% of cases what vision would someone with CRAO or BRAO have ?

A

Counting Fingers (CF) or Light Perception(LP)

71
Q

What is amaurosis fugax?

A

Transient loss of vision lasting 2 seconds- 2 hours

72
Q

What would the fundus look like with someone with an acute BRAO and CRAO?

A
  • Oedematous, milky opaque Retina
  • Cherry red spot
  • Segmented BV
73
Q

Why would an opacity be greatest where the macula is?

A

The NFL and retinal ganglion cell layer is thickest here

74
Q

Why is there a cherry red spot?

A

Fovea blood supply is the choroidal circulation + retina is thinnest here

75
Q

Why are segmented bV seen?

A

Blood is moving sluggishly

76
Q

What would someone with a chronic BRAO OR CRAO fundus look like?

A
  • retinal opacification
  • attenuated retinal arterioles
  • optic nerve atrophy
  • RPE mottling
  • homogeneous scar
77
Q

What does retinal opacification that has resolved 4 weeks result in?

A

Ischaemic necrosis

78
Q

Where has a glistening yellow cholesterol emboli come from?

A

Atherosclerotic plaques from the carotid artery

79
Q

Where has calcific emboli come from? And how do they look?

A

Cardiac valves + non-glistening platelet

80
Q

Where ate Calcific emboli more commonly found?

A

At the optic disc

81
Q

What is the name of the glistening yellow cholesterol emboli?

A

Hollenhorst plaque i

82
Q

Can emboli dislodge?

A

Yes, if so a px would have experience amaurosis fugax

83
Q

If an embolus is trapped does that necessarily mean there is no blood flowing?

A

No- it may just reduce blood flow
REQUIRES URGENT REFERRAL

84
Q

What is the management for a px with retinal emboli or history of transient painless vision loss?

A

Urgent referral for cardiovascular assessment

85
Q

What is the outcome of CRAO or BRAO?

A

Severe vision loss

86
Q

If there is any spontaneous recovery in vision, when would that be?

A

In the first 7 days

87
Q

What is the outcome of a BRAO or CRAO if a px has a cilioretinal artery ?

A

80% will return with a VA of 6/7.5 or better

88
Q

What is a long term complication of CRAO or BRAO?

A

Retinal or anterior eye neovasc

89
Q

What is management of CRAO or BRAO?

A

SAME DAY EMERGENCY

90
Q

In practice what can you do/advise if they have a CRAO or BRAO?

A
  • ask px to lie flat
  • ocular massage
  • ask px to breathe into a paper bag

KEY THING TO DO IS GET THEM TO HOSPITAL

91
Q

What does lying flat do?

A

Raises pressure on ophthalmic artery

92
Q

How is an ocular massage carried out?

A

Press on the eye with heel of hand, 10 seconds on 10 seconds off for 5 mins

93
Q

What does breathing into a paper bag do?

A

Increase co2 levels which can cause vasodilation

94
Q

What is the window for vision improvement?

A

4 hours

95
Q

What are px who have BRAO and CRAO at risk of ?

A

Heart attack or stroke therefore urgent referral for a medical assessment even if window for vision restoration has passed

96
Q

Is the visual outcome worse or better for someone with A-AION which has caused arteritic CRAO/BRAO?

A

WORSE!- URGENT referral

97
Q

How does an ophthalmologist aim to increase perfusion?

A

Reduce IOPs or causing vasodilation

98
Q

What are some ways IOP is reduced for CRAO and BRAO treatment?

A
  • intravenous acetazolamide
  • anterior chamber paracentesis
99
Q

What is anterior chamber paracentesis?

A

Insert a needle into AC and withdraw some of the aqueous to reduce pressure

100
Q

Which drugs will be used to try to break up the embolus?

A

Fibrinolytic drugs

101
Q

How is arteritic CRAO due to GCA treated? And why?

A

High dose systemic steroids to prevent the other eye or other vessels being affected

Eye Disease (48 decks)

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