Central retinal arterial/vein occlusion Flashcards

1
Q

Define central retinal vein occlusion.

A

Interruption of the normal venous drainage from the retinal tissue. Either the central vein or one of its branches can become occluded.

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2
Q

How common is CRVO?

A

< 1% global prevalence but increases with age

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3
Q

What is the pathophysiology of CRVO?

A
  • Thrombus formation
  • Usually at arteriovenous crossings
  • Atherosclerosis in retinal arteries causes compression on the retinal veins causing occlusion OR vascular inflammatory vein disease causes vein occlusion.
  • This causes increased venous pressure, intra-retinal haemorrhage, oedema and eventually ischaemia
  • Local factors such as VEGF may be released causing neovascularisation
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4
Q

What are the risk factors for CRVO?

A

Stroke risk factors:
Atherosclerosis
Systemic hypertension
Diabetes mellitus
Hyperlipidaemia
Smoking hx
CVD
Glaucoma
HIgh BMI
Increased serum alpha 2 globulin
Short axial length
Age >65yrs

Other: protein C resistance, factor V leiden, hypercoagulable state, protein S deficiency, antithrombin III deficiency, hyperhomocysteinaemia, vasculitis.

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5
Q

What are the clinical features of CRVO?

A
  • Sudden painless unilateral vision loss
  • CVD risk factors
  • Floaters (if vitreous haemorrhage due to neovascularisation)

O/E:

  • Macular oedema
  • Vitreous haemorrhage
  • Reduced acuity
  • RAPD or low visual acuity (ischaemic CRVO)
  • Rule out novascularisation with slit lamp testing
  • Intra-retinal haemorrhages and thickening
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6
Q

What investigations would you do in CRVO?

A

Clincial diagnosis - if not confirmed then:

Fluorescein angiogram - gives info on complications of CRVO and when planning treatment
Optical coherence tomography (OCT)- shows macular oedema in more detail

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7
Q

What are the complications of CRVO?

A
  • retinal ischaemia
  • macular oedema
  • neovascularisation
  • loss of vision
  • vitreous haemorrhage
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8
Q

What is the management of CRVO?

A

Depends on location and complications. Different management options include:

  • Observation + management of underlying risk factors - CVD, vasculitis, or hypercoagulability
  • VEGF inhibitors intravitreally
  • Intravitreal corticosteroids
  • Panretinal photocoagulation (PRP)
  • Control intraocular pressure
  • Pars plana vitrectomy
  • Grid laser photocoagulation
  • Scatter laser photocoagulation
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9
Q

What is the prognosis with CRVO?

A

Non-ischaemic CRVO has a better prognosis
1% per year will develop RVO in the opposite eye

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10
Q

Describe the differences between CRAO and CRVO.

A
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11
Q

Define CRAO.

A

Blockage of the central retinal artery or one of it’s branches

Should be considered in all cases of sudden, painless loss of vision. However, it is relatively uncommon, and usually affects the elderly.

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12
Q

What is shown?

A

Central retinal vein occlusion - flame haemorrhages

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13
Q

How common is CRAO?

A

Rare
Mean age of diagnosis 60-65yrs

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14
Q

What are the risk factors for CRAO?

A
  • Carotid artery sclerosis - MOST COMMON; up to 70% affected have CAS
  • Cardiogenic embolism e.g. IE, AF, rheumatic heart disease, valvular disease
  • Small artery disease
  • Vascular disease e.g. radiation injury, carotid artery dissection
  • Haematologic disease e.g. SCD, antiphospholipid, leukaemia
  • Inflammatory disease e.g. GCA, SLE, PAN
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15
Q

What are the clinical features of CRAO?

A
  • Acute painless profound loss of vision
  • May be preceded by transient monocular blindness
  • RAPD
  • Other: headache of GCA, stroke/TIA neurology post-carotid artery stenosis
    O/E:
  • Ischaemic retinal whitening
  • “Cherry red spot” in macula
  • Retinal emboli
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16
Q

Describe RAPD.

A

Swinging light test shows a non-reactive pupil - affected pupil dilates when light is swung on it.

Dilation - sympathetic via superior cervical ganglion and spinal cord
Constriction - parasympathetic - ciliary ganglion and Edinger Westphal nucleus of CN3 (optic nerve).

17
Q

What is the origin of the retinal artery ?

A

Internal carotid artery –>
Ophthalmic artery –>
Central retinal artery

18
Q

How do you diagnose central retinal artery occlusion?

A

Clinical diagnosis - if still uncertain…

Fluorescein angiography - shows slowed or absent filling with normal filling of the choroid; if choroid affected consider GCA
ESR, CRP - exclude GCA

Other:
Carotid artery imaging
US temporal artery
Cardiac evaluation
Coagulation screen

19
Q

What is the prognosis with CRAO?

A

In most cases apparently normal perfusion is restored within hours or days but visual acuity may not improve
Pigmentary changes may develop after many weeks

20
Q

What is the management of CRAO?

A

No treatment has been shown to be effective but may try:

  • Paracentesis
  • Ocular massage - may dislodge the embolus
  • Intraocular hypotensive agents - mannitol, acetazolamide
  • Intraarterial thrombolytic therapy
  • Vasodilators - isosorbide dinitrate

Other:

  • Corticosteroids - effectiveif cause is GCA
21
Q

What are the complications of CRAO?

A

Neovascularisation - may involve the retina or iris and anterior chamber angle
Neovascular glaucoma
Vitreous haemorrhage - rare

22
Q

What is shown?

A

Central retinal artery occlusion with pale retina

23
Q

What is the diagnosis?

A

Branch retinal vein occlusion