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Year 2 Clinical > Visual Loss and Blindness > Flashcards

Visual Loss and Blindness Flashcards

1
Q

2 types of visual loss?

A

Sudden visual loss (inc. sudden transient visual loss)

Gradual visual loss

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2
Q

Main causes of sudden visual loss?

A
  • Vascular aetiology
  • Retinal detachment
  • Age-related macular degeneration (ARMD - wet-type
  • Closed-angle glaucoma
  • Optic neuritis
  • Stroke
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3
Q

Arterial supply to the eye?

A

Major blood supply to eye:
• Various branches of ophthalmic artery (branch of the ICA)

Branches include:
• Central retinal artery
• Posterior ciliary arteries

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4
Q

Blood supply to the layers of the retina?

A

Inner 2/3rds supplied by the central retinal artery

Outer 1/3rd supplied by the posterior ciliary artery

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5
Q

Vascular causes of sudden visual loss?

A

OCCLUSION of:
• Retinal circulation (CRAO or BRAO)
• Optic nerve head (AKA optic disc) circulation

HAEMORRHAGE from:
• Abnormal blood vessels, e.g: diabetes, wet ARMD
• Retinal tear

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6
Q

Symptoms of central retinal artery occlusion (CRAO)?

A

SUDDEN, profound visual loss that is PAINLESS

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7
Q

Examination findings with CRAO?

A

RAPD (relative afferent pupil defect)

Pale, oedematous retina with thread-like retinal vessels

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8
Q

Causes of CRAO?

A

It is a type of stroke and causes include:
• Carotid artery disease (atherosclerotic) is the main cause
• Emboli from the heart (unusual)

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9
Q

Ophthalmic management of CRAO?

A

If it presents within 24 hours, try ocular massage (which attempts to dislodge the embolus to an area further down the vascular tree)

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10
Q

Vascular management of CRAO?

A

Vascular management:
• Establish source of the embolus (Ix with a carotid doppler)
• Assess and manage risk factors

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11
Q

Examination signs with BRAO?

A

Only a small area of the retina is pale, e.g: if the retina is pale inferiorly, they are likely to have a superior visual field defect

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12
Q

Symptoms of amaurosis fugax (AKA transient CRAO)

A

Transient, painless visual loss (like a curtain coming down)

It lasts only 5 minutes and then their is full recovery

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13
Q

Examination signs with amaurosis fugax?

A

Usually, nothing abnormal is seen

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14
Q

Mx of amaurosis fugax?

A

Immediate referral to a TIA clinic

Aspirin

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15
Q

Other causes of transient visual loss?

A

Migraine (although the visual loss typically follows a headache)

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16
Q

Systemic causes of central retinal vein occlusion (CRVO)?

A

Virchow’s triad:
• Atherosclerosis (change in vessel walls)
• Hypertension (change in blood flow)
• Hyperviscosity (change in blood constituents)

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17
Q

Ocular causes of CRVO?

A

Raised intra-ocular pressure (with venous stasis)

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18
Q

Symptoms of CRVO?

A

Sudden visual loss

Moderate to severe visual loss

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19
Q

Examination signs of CRVO?

A

Retinal haemorrhages

Dilated tortuous veins

Disc swelling and macular swelling

Cotton-wool spots (small infarcts of the nerve fibre layer)

THERE IS NO PALLOR

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20
Q

Complication of CRVO?

A

Ischaemic eye grows new blood vessels, which are fragile and prone to bleeding

Can cause, e.g: a vitreous haemorrhage

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21
Q

Treatment of CRVO?

A

Treat the systemic or ocular cause, e.g: hypertension, diabetes, glaucoma

Anti-VEGF (vascular endothelial growth factor) can stop budding of new vessels

Monitoring for complications (new vessels require laser treatment to avoid issues like a vitreous haemorrhage)

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22
Q

Summarise the cause and locations for occlusion of the retinal circulation?

A

Arterial (embolic):
• Central retinal artery
• Branch retinal artery

Venous (stasis):
• Central retinal vein
• Branch retinal vein

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23
Q

Colour of the retina in arterial vs vein occlusion?

A

Pale in arterial occlusion

Dark in venous occlusion

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24
Q

Describe occlusion of the optic nerve head circulation

A

AKA ischaemic optic neuropathy

The posterior ciliary arteries (PCA) become occluded, resulting in infarction of the optic nerve head

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25
Q

Types of ischaemic optic neuropathy (ION)?

A

Arteritis (50%) - inflammation (Giant Cell Arteritis)

Non-arteritis (50%) - atherosclerosis

26
Q

Symptoms of ION?

A

Both types cause SUDDEN, PROFOUND visual loss with a SWOLLEN DISC

27
Q

Pathogenesis of GCA?

A

Inflammation of medium-large sized arteries (multinucleate giant cells)

Lumina of the posterior ciliary arteries become occluded and there is ischaemia of the optic head, leading to visual loss

28
Q

Examination signs of ION?

A

Pale, swollen optic disc

29
Q

Visual symptoms of GCA?

A

Amaurosis fugax

SUDDEN, profound visual loss and irreversible blindness

Diagnosis and immediate treatment can prevent bilateral visual loss (as there is a risk of sudden complete blindness in the second eye)

30
Q

Other symptoms of GCA (temporal arteritis)?

A

Temporal headache

Jaw claudication

Scalp tenderness (combing hair is painful) and tender, enlarged scalp arteries

Malaise

31
Q

Ix for GCA?

A

Very high inflammatory markers

Temporal artery biopsy (skip lesions)

32
Q

Where does haemorrhage often occur?

A

Into the vitreous cavity (AKA vitreous haemorrhage)

33
Q

How does haemorrhage occur?

A

From abnormal vessels - assoc. with retinal ischaemia and new vessel formation, e.g:
• After retinal vein occlusion
• Diabetic retinopathy

From normal retinal vessel - usually assoc. with a retinal tear

34
Q

Symptoms of vitreous haemorrhage?

A

Loss of vision

Floaters

35
Q

Examination signs of vitreous haemorrhage?

A

Loss of red reflex

Fundoscopy may show the haemorrhage

36
Q

Mx of vitreous haemorrhage?

A

Identify the cause; often, it resolves physiologically

For non-resolving cases, a vitrectomy can be done

37
Q

Symptoms of retinal detachment?

A

Painless loss of vision

Sudden onset of flashes and/or floaters (due to mechanical separation of the sensory retina from the retinal pigment epithelium)

38
Q

Examination signs of retinal detachment?

A

May have RAPD

Ophthalmoscopy may show a tear

39
Q

Mx of retinal detachment?

A

Usually surgical

40
Q

Presentation of retinal detachment?

A

Depends on site, e.g: an inferior tear can cause a superior visual defect

41
Q

Types of age-related macular degeneration (ARMD)?

A

Dry (causes a GRADUAL reduction in vision)

Wet (causes a SUDDEN reduction in vision)

42
Q

Pathology of wet ARMD?

A

New blood vessels grow under the retina; leakage causes build-up of fluid/blood, which separates the layers and leads to scarring

43
Q

Symptoms of wet ARMD?

A

Rapid CENTRAL vision loss - cannot see black dot in the centre of the Amsler grid

Distortion (metamorphosis) -straight lines become wavy when looking at the Amsler grid

44
Q

Examination signs of wet ARMD?

A

Haemorrhage/exudate on ophthalmoscopy

45
Q

Treatment of wet ARMD?

A

Anti-VEGF treatment injected into the vitreous cavity; prevents new blood vessel growth by binding to VEGF

Previously used laser and photodynamic therapy

46
Q

Presentation of bilateral visual loss?

A

Usually bilateral and often asymmetrical (worse in one eye)

May present either:
• Early with reduced visual acuity
• Late with decreased visual field

47
Q

Mnemonic for the causes of gradual visual loss?

A

CARDIGAN

Cataract
Age-related macular degeneration (dry type)
Refractive erroe
Diabetic retinopathy
Inherited diseases, e.g: retinitis pigmentosa
Glaucoma
Access (to eye clinic) that is Non-urgent

48
Q

What is a cataract?

A

Cloudiness of the lens that has many different causes and there are many different types

49
Q

Causes of cataract?

A
  • Age-related
  • Congenital (due to an intra-uterine infection; must check red reflex in neonates)
  • Traumatic
  • Metabolic (diabetes, etc)
  • Drug-induced (e.g: steroids)
50
Q

Types of cataracts?

A

Nuclear cataract (rainbow appearance); impaired distance vision

Posterior subcapsular cataract; profoundly affects vision

Polychromatic cataract (Christmas tree cataract)

Congenital cataract

…others

51
Q

Treatment of cataract?

A

If the patient is symptomatic, surgical removal with intra-ocular lens implant

52
Q

Symptoms of dry ARMD?

A

Gradual decline in vision

Central vision is ‘missing’ (scotoma)

53
Q

Examination signs of dry ARMD?

A

Drusen (build up of waste products below the RPE)

Atrophic patches of retina

54
Q

Treatment of dry ARMD?

A

No cure

Supportive treatment with low vision aids, e.g: magnifiers

55
Q

Types of refractive errors?

A
  • Myopia (short-sighted)
  • Hypermetropia (long- sighted)
  • Astigmatism (usually irregular corneal curvature)
  • Presbyopia (loss of accommodation with aging)
56
Q

Pathogenesis of glaucoma?

A

Unclear aetiology but raised IOP may be implicated

It causes progressive optic neuropathy and visual loss

57
Q

Types of glaucoma?

A

Open-angle (irido-corneal angle is open and as wide as usual)

Closed-angle (narrowed or closed irido-corneal angle)

58
Q

Presentation of closed-angle glaucoma?

A 
May be acute (ophthalmic emergency) with:
• Painful, red eye 
• Visual loss
• Headache 
• Nausea and vomiting
59
Q

Treatment of glaucoma?

A

Lower IOP with:

• Drops/oral mediation

60
Q

Presentation of open-angle glaucoma?

A

Often asymptomatic and an incidental finding by the optician

61
Q

Examination signs of open-angle glaucoma?

A

Cupped disc

Visual field defect

May/may not have a high IOP

62
Q

Treatment of open-angle glaucoma?

A

Preserve vision by lowering IOP (improve drainage or reduce production)
• Eye drops
• Laser
• Surgery (trabeculectomy)

Regular monitoring

Year 2 Clinical (119 decks)

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