Lecture 15: Vascular occlusions

Question 1

What type of vascular occlusions can you get?

Answer 1

BRVO
BRAO

CRVO
CRAO

Question 2

What is the most common type of RVO?
Where does it normally occur?
What is the likely cause?

Answer 2

branch retinal occlusion

Typically occurs at AV crossing

Venous compression by the artery may result in turbulent blood flow, endothelial damage, thrombosis and occlusion.
More likely when artery is sclerosed.

Question 3

What age does BRVO normally occur?
What are the risk factors?

Answer 3

mean: 60 years

systemic hypertension (50%)
diabetes mellitus
smoking
hyperlipidemia
cardiovascular disease
a history of glaucoma
short axial length
previous RVO in either eye
inflammatory conditions (e.g. sarcoidosis, Lyme disease).

Question 4

What quadrant do you usually get them in?
What are the symptoms of BRVO?

Answer 4

-Often superior temporal in presentation (~66% cases)

-May present with sudden onset, painless loss of vision;
-May be asymptomatic (usually if nasal branch)
-May result in sector field defect or central field defect (if macular branch, ~25% cases).

Question 5

What are the retinal signs of BRVO in the ACUTE stage?

Answer 5

-Haemorrhages (often flame shaped)
-Vessels dilated and tortuous distal to occlusion
-Retinal oedema (fluid leakage distal to occlusion)
-Cotton wool spots (sign of RNFL ischaemia)
-Signs follow distribution of vessel, usually respect horizontal raphe.

Question 6

What are the retinal signs of BRVO in the CHRONIC stage?

Answer 6

-Hard exudates
-Vascular sheathing (appear white)
-Macular pigment
-Collateral vessel formation (small and tortuous, may cross horizontal raphe to drain into unaffected quadrant)
-Retinal ischaemia occurs downstream to occlusion : VEGF upregulation : increased vessel permeability : macular oedema.

Question 7

What complications can you get of BRVO?

Answer 7

Macula: Chronic macular oedema (main cause visual loss), exudates, haemorrhage, epiretinal membrane.

Neovascularisation at disc or elsewhere

vitreous haemorrhage if large area of the retina is ischaemic.

Rarely, retinal detachments (rhegmatogenous, tractional)

Question 8

What is the cause of CRVO?
What are the mechanisms?
What are the risk factors?

Answer 8

Caused by thrombus formation where central retinal artery and vein leave the optic nerve head, often at lamina cribrosa.

Possible mechanisms:
Arteriosclerosis of CRA disturbing blood flow in vein.
Mechanical pressure in lamina cribrosa e.g. POAG
Vessel wall or blood changes.

Systemic hypertension, Diabetes mellitus, Open-angle glaucoma, Cardiovascular disease, Systemic inflammatory conditions.

Question 9

What are the signs and symptoms of ACUTE CRVO?

Answer 9

Variable sudden onset visual loss (better than 6/12 to worse than 6/60)
usually painless
RAPD may be present in affected eye
photophobia
Blood and Thunder” fundus
Retinal hemorrhages
dilated tortuous veins
cotton wool spots
macular oedema
unilateral optic disc oedema.

Question 10

What are the signs and symptoms of ischaemic CRVO?

What is the prevalence?

Answer 10

Prognosis worse than non ischaemic.
Severe visual loss
RAPD
Multiple intraretinal haemorrhages (dot, blot and flame)
cotton wool spots
optic disc swelling

20% of CRVO cases

Question 11

What are the signs of non-ischaemic CRVO?
What is the prevalence?

Answer 11

-Haemorrhage is superficial (flame).
-Presenting vision better than for ischaemic
-Fewer cotton wool spots seen

80%

Question 12

What complications can you get of CRVO?

Answer 12

Ischaemia causes VEGF upregulation, which can lead to:
-Persistent macular oedema
-New vessels at disc /elsewhere
- vitreous haemorrhage
-Neovascular glaucoma – red painful eye, risk of rapid visual loss

Question 13

How can the retina try to compensate for CRVO?

Answer 13

Optociliary shunt vessels can develop to divert retinal blood to choroidal circulation.

Question 14

What is the management of BRVO and CRVO?

Answer 14

Refer all cases to GP for investigation

seen by HES in 2-4 weeks:
-Macular oedema
-New vessel growth (retinal and anterior eye)
-Neovascular glaucoma

Neovascular glaucoma/rubeosis iridis – phone eye department for triage.

Question 15

What is the treatment for neovascularisation in BRVO/CRVO?

Answer 15

-Laser panretinal photocoagulation used to treat new vessels in iris / angle and for new retinal vessels.
-Likely to reduce hypoxia and VEGF production by reducing oxygen demand of photoreceptors and RPE.

Question 16

What is the treatment of neovascular glaucoma?

Answer 16

-aim is to keep eye pain free with topical steroids and atropine.
-If vision remains, IOP is controlled with anti-glaucoma drops and/or surgery.
-Anti-VEGF agents can cause regression of new vessels and reduced obstruction of angle.

Question 17

What is the treatment for macular oedema?

Answer 17

-Traditionally treated with laser
-ranibizumab or aflibercept
-Ozurdex, a dexamathasone (steroid) implant

Anti-VEGF is preferred in eyes with a previous history of glaucoma and younger patients who are phakic. Ozurdex may be a better choice in patients with recent cardiovascular events and in those who do not favour monthly injections

Question 18

What can cause a CRAO/BRAO?

What are the risk factors

Answer 18

-(CRAO) is most commonly caused by atherosclerosis, esp of carotid artery.
-Cardiac emboli are most common cause (aged <40 years)
-vascular inflammatory conditions e.g. giant cell arteritis, systemic lupus erythematosus.

hypertension, hyperlipidaemia, tobacco use, renal disease, atherosclerosis, Diabetes Mellitus, ischaemic heart disease, transient ischaemic attacks, strokes

Question 19

What is the presentation of CRAO/BRAO?

Answer 19

Sudden, severe, painless loss vision.
~90% px with CRAO have vision between counting fingers and light perception at presentation.
1-2% bilateral presentation.
Mean age early 60s.
May have history of amaurosis fugax (transient loss of vision lasting seconds-2 hours – vision returns to normal afterwards).
With branch occlusion, extent of visual loss will depend on location of occlusion.

Question 20

What are the signs of ACUTE CRAO/BRAO?

Answer 20

-Inner layers of the retina become oedematous and milky/opaque.
-Opacity greatest at macula where RNFL & RGC layers thickest.
-Fovea shows a ‘cherry red spot’ because fovea is nourished by underlying choroidal circulation, and because retina is thinnest here so underlying choroid seen.
Blood moves sluggishly in occluded vessels and blood flow may appear segmented (‘boxcarring’ or ‘cattle tracking’)

Question 21

What are the chronic signs of CRAO/BRAO?

Answer 21

Retinal opacification evident within 15 mins-2 hours. Resolves in 4- weeks. Ischaemic necrosis results.
Chronic appearance of attenuated retinal arterioles and optic nerve atrophy, RPE mottling.
Homogenous scar replaces inner retinal layers.

Question 22

What is a emboli?

How can it cause a CRAO/BRAO?

Answer 22

Glistening yellow cholesterol emboli often from atherosclerotic plaques in carotid artery, calcific emboli typically from cardiac valves

Emboli may dislodge after causing temporary visual loss (amaurosis fugax).
They may get trapped at a bifurcation and not obstruct flow.
May cause CRAO or BRAO.

Question 23

What is the management of BRAO/CRAO?

Answer 23

-Ask px to lie flat (raises pressure in ophthalmic artery)
-Ocular massage may help to dislodge the embolus – press on eye with heel of hand (10 sec on, 10 sec off for 5 mins).
-Can ask Px to breath into paper bag – increased CO2 levels will cause vasodilation.

EMERGANCY REFERRAL TO A&E

Question 24

What are px with CRAO/BRAO due to emboli at risk of?

Answer 24

stroke
heart attack

Question 25

What is the referral for arteritic CRAO/BRAO?

Answer 25

urgent due to temporal arteritis

Question 26

What is the opthalmological management of CRAO/BRAO?

Answer 26

1. By reducing IOP:
   Intravenous acetazolamide
   Anterior chamber paracentesis (inserting needle into the anterior chamber and withdrawing 0.1 to 0.2 ml aqueous fluid.
2. By causing vasodilation
   Finbrinolytic drugs may be used to break up the embolus, but most are cholesterol or calcium, which do not respond.
   In arteritic CRAO due to giant cell arteritis high dose systemic steroids prescribed to prevent fellow eye/other vessels from being affected.