Vascular Occlusions Flashcards

1
Q

Outline the causes, epidemiology and presentation of Central Retinal Artery Occlusion.

A

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

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2
Q

Explain Amaurosis Fugax.

A
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

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3
Q

What are the risk factors for CRAO?

A
Systemic hypertension
Diabetes mellitus
Hyperlipidemia
Carotid artery disease
Coronary artery disease
TIA/CVA
Giant cell arteritis
Tobacco smoking
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4
Q

What are the early and late signs of CRAO?

A

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

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5
Q

Outline the optometric management of CRAO.

A

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

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6
Q

Explain Branch Retinal Artery Occlusion.

A

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)

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7
Q

Outline the general cause, epidemiology and presentation of Central Retinal Vein Occlusion.

A

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

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8
Q

Outline the systemic and ocular causes of CRVO.

A
Systemic:
Systemic hypertension
Diabetes
Arteriosclerosis
Hyperviscosity
syndromes
Oral contraceptive pill

Ocular:
Raised IOP > 30mmHG

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9
Q

What are the general signs of CRVO?

A

Blood and thunder

Flame-shaped
haemorrhages in all 4
quadrants

Disc oedema

Venous dilation

Multiple cotton wool
spots

RAPD likely

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10
Q

Compare the signs of non-ischaemic and ischaemic CRVO.

A
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
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11
Q

Name and explain a CRVO complication.

A

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

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12
Q

Outline the Optometric Management of CRVO.

A

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

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13
Q

Outline the Opthalmological Management of CRVO.

A

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

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14
Q

Explain Branch Retinal Vein Occlusion.

A

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

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15
Q

Outline the Optometric Management of BRVO.

A

Measure visual acuity

Fundus examination
- Dilated BIO

Pupil reactions

Visual field

Refer to GP cardiovascular investigation

Ophthalmological referral

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16
Q

Outline the Opthalmological Management of BRVO

A

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

17
Q

Define Anterior Ischaemic Optic
Neuropathy and its Epidemiology
Name the two types of AION

A

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)

18
Q

Explain A-AION

A

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

19
Q

Outline the Optometric Management of A-AION

A

Investigation
VA, Pupils, Colour vision, VFs,
IOP
Dilated fundus examination?

Management
Emergency referral to casualty
Contact ophthalmologist

20
Q

Outline the Opthalmological Management of A-AION

A

Investigation:
Blood tests
Temporal artery biopsy
Scans (Doppler, MRI)

Management:
Aspirin, treatment of
cardiovascular problem
If arteritic, high doses of
systemic steroids for years

21
Q

What is Temporal Arteritis?

A

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

22
Q

Explain NA-AION

A

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