Vascular Occlusions Flashcards
Outline the causes, epidemiology and presentation of Central Retinal Artery Occlusion.
Causes:
Obstruction of central retinal artery by:
A) Embolus (more common) [carotid artery and heart disease]
- Cholesterol crystals from
carotid arteries
- Platelet-fibrin emboli
arising from large vessel
stenosis
- Calcific emboli arising from
carotid valve stenosis
B) Thrombus
- Blood clot
- Stenosis of carotid artery
Epidemiology:
Onset mid-sixties
Male to female ratio 2:1
Rare (incidence 1.9 in 100,000 in U.S.)
Presentation:
Sudden painless profound loss of vision
May be preceded by transient loss of vision
- Amaurosis Fugax
Explain Amaurosis Fugax.
Transient obscuration of retinal artery by embolus (transient ischaemic attack [TIA]) < 24 hours Sudden monocular loss of vision Painless “Like blind coming down” Clears slowly in reverse direction Repetitive
Optometric Management:
Refer to G.P. urgently after excluding giant cell
arteritis
What are the risk factors for CRAO?
Systemic hypertension Diabetes mellitus Hyperlipidemia Carotid artery disease Coronary artery disease TIA/CVA Giant cell arteritis Tobacco smoking
What are the early and late signs of CRAO?
Early:
Symptoms: Visual acuity usually CF to LP
[Exceptions cilio-retinal artery
(25%)]
Signs: Pale oedematous retina especially at the posterior pole Cherry red spot at macula - Macula blood supply from choroid via posterior ciliary arteries - Surrounding retina pale in comparison - Macula is thinner - transparency Arterial attenuation Segmentation Emboli may be seen RAPD
Late:
Optic Disc Atrophy
Arterial attenuation and segmentation
VA normally remains markedly reduced despite treatment
Outline the optometric management of CRAO.
Measure visual acuity
Check pupils
Urgent referral to Eye Casualty
(If < 12 hours old)
First Aid - aim to dislodge embolus
- Ocular digital massage
- Breathe into paper bag
- Increase CO2 levels
Reduce IOP:
- Anterior chamber paracentesis
- Intravenous acetazolamide and ocular massage
Dilation of arteries:
- Ocular massage
- Retrobulbar vasodilator drugs
- Inhalation of carbogen
Lysing of embolus/thrombus
Systemic anticoagulants
Explain Branch Retinal Artery Occlusion.
Occur in seventh decade
Results from embolus
90% temporal retinal
arteries
Sudden painless loss of
vision
Hemifield or sector loss
of vision
Superior Altitudinal VF loss
Prognosis good
(74% - V/A 6/12 + VF
defect)
Outline the general cause, epidemiology and presentation of Central Retinal Vein Occlusion.
Cause:
Obstruction of central retinal vein below lamina
cribosa
Epidemiology:
More commonly affect older people in their midsixties, but can also occur in younger patients
Male to female ratio equal 5.2 in 1,000
Presentation:
Sudden painless loss of vision
Variable deficit
May go unnoticed
Outline the systemic and ocular causes of CRVO.
Systemic: Systemic hypertension Diabetes Arteriosclerosis Hyperviscosity syndromes Oral contraceptive pill
Ocular:
Raised IOP > 30mmHG
What are the general signs of CRVO?
Blood and thunder
Flame-shaped
haemorrhages in all 4
quadrants
Disc oedema
Venous dilation
Multiple cotton wool
spots
RAPD likely
Compare the signs of non-ischaemic and ischaemic CRVO.
Non-ischaemic: VA is better than 6/60 RAPD is not marked Less haemorrhages No/few cotton wool spots 20% become ischaemic
Ischaemic: Visual acuity < 6/60 less Marked RAPD Extensive haemorrhages in 4 quadrants Disc swelling Venous tortuosity Cotton wool spots Risk of developing retinal and iris neovascularisation
Name and explain a CRVO complication.
Neovascular Glaucoma
“100 day” glaucoma Retinal hypoxia Angiogenesis substance released New vessels develop in angle Fibrovascular membrane develops across trabecular meshwork
Early intervention
required
Intractable and
devastating
Outline the Optometric Management of CRVO.
Normal IOP:
Refer to Ophthalmologist within 2
weeks
AND
Refer to G.P. for full cardiovascular
investigation
If IOP > 30mmHG:
Refer to ophthalmologist within 24
hours
AND
Refer to G.P. for full cardiovascular
investigation
Outline the Opthalmological Management of CRVO.
Fluorescein angiogram
- Ischaemic or non-ischaemic?
New vessels:
- Pan-retinal photocoagulation
- Intra-vitreal anti-VEGF?
Macula oedema
- Intravitreal steroids
eg triamcinolone acetonide, or
dexamethasone bigradeable
implant - Intravitreal anti-VEGF (eg
Lucentis)
Investigation and treatment
of underlying cause
Explain Branch Retinal Vein Occlusion.
Hemi field visual loss
Obstructed vein dilated and
tortuous
Retinal oedema
Scattered superficial and deep
retinal haemorrhages,
- respect the horizontal midline,
confined to one quadrant
Causes – systemic
cardiovascular
Outline the Optometric Management of BRVO.
Measure visual acuity
Fundus examination
- Dilated BIO
Pupil reactions
Visual field
Refer to GP cardiovascular investigation
Ophthalmological referral
Outline the Opthalmological Management of BRVO
Fluorescein angiogram
Grid laser coagulation if
macula oedema
persistent
Retinal
neovascularisation rarer
in BRVO
Prognosis good if treated
VA ≥6/12
But 25% will have VA <6/60
Define Anterior Ischaemic Optic
Neuropathy and its Epidemiology
Name the two types of AION
Ischaemia of anterior optic nerve head
Occlusion of the posterior ciliary arteries
Epidemiology
Almost exclusively after the age of 50 years
Incidence 18 per 100,000 after 50 years
Woman > men (2:1 ratio)
Two types:
Arteritic (A-AION)
Non-arteritic (NA-AION)
Explain A-AION
5 - 10% of cases
Older patients than NA-AION
- Typically 7 to 8th decades
Profound loss of vision
- NLP, LP or HM
Pale oedematous optic nerve
head
Splinter haemorrhages
RAPD
Associated with temporal arteritis
NB Risk of visual loss in other
eye, myocardial infarction,
renal failure, aortic aneurysm
Outline the Optometric Management of A-AION
Investigation
VA, Pupils, Colour vision, VFs,
IOP
Dilated fundus examination?
Management
Emergency referral to casualty
Contact ophthalmologist
Outline the Opthalmological Management of A-AION
Investigation:
Blood tests
Temporal artery biopsy
Scans (Doppler, MRI)
Management:
Aspirin, treatment of
cardiovascular problem
If arteritic, high doses of
systemic steroids for years
What is Temporal Arteritis?
Giant cell arteritis (GCA)
Inflammation of medium and large
arteries
Symptoms
Headache
- normally constant
- gradual onset to a diffuse severe
aching
- superficial scalp tenderness -
temporal
- worse at night and in the cold
General malaise, weight loss, jaw
claudication, amaurosis fugax
Polymyalgia rheumatica
Explain NA-AION
90 - 95% of cases
Presentation: Sudden loss of vision Mild to severe Usually on waking Vision loss either static or progressive 20% lose vision in other eye within 5 years “At risk” disc Associated with hypertension, diabetes
Signs: Oedematous optic nerve head - Diffuse or segmental - Hyperaemic or pale Visual field loss - Usually altitudinal Contralateral eye - Small disc - Small or absent cup - Subsequent optic atrophy 33% left with near normal V/A
