Assessment and Diagnosis of Visual Loss Flashcards

1
Q

Give 4 examples of causes/signs of visual loss which may suggest a broader life of function threatening problem?

A

Endogenous endeopthalmitis

Panuveitis (including viral retinitis and retinal vasculitis)

Papilloedema

Optic neuritis

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2
Q
A
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3
Q

What is the most common cause for poor vision in humans?

A

Refractive error

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4
Q

Hx: I can’t see very well and my eyes don’t seem to open properly

O/E: bilateral upper lid ptosis

DDx?

A

Neurogenic: CN III palsy, Horner’s syndrome

Myogenic: myaesthenia gravis, myotonic dystrophy

Aponeurotic: involutional

Mechanical causes: orbital tumours, oedema, scarring

Pseudoptosis: contralateral lid retraction

Mitochondrial disease: chronic progressive external opthalmoplegia

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5
Q

Hx: my R eye is red, it waters a lot and the vision is sometimes blurry

O/E: R VA 6/9, slit lamp exam shows punctuate epithelial erosions (PEEs), in this case due to ocular surface exposure

Dx?

A

Transient blurring of vision +/- epiphora (watering) = think tear-film disruption

Causes include trachoma (leading to entropion and pannus trichiasis)

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6
Q

Entropion

A

Eyelid (usually the lower lid) folds inward

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7
Q

How can entropion blur vision?

A

Tear-film disruption

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8
Q

Complications of entropion

A

Corneal scarring

Pannus trichiasis (misdirected growth of eyelashes towards the cornea)

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9
Q

What infective agent causes trachoma?

A

Chlamydia trachomatis

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10
Q

Epidemiology of trachoma

A

Prolific in arid poverty-stricken regions with poor hygiene

84 million people have active disease, 7.6 with trichiasis

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11
Q

Complications of trachoma

A

Scarring of conjunctiva

Entropion

Blindness

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12
Q

Hx: my vision has been gradually getting blurry over months; I’m in my 50s, maybe I have cataracts?

O/E: RVA 6/12, LVA 6/12, pupils equal and reactive to light (PEARL), nil RAPD, IOP normal range

Most likely Dx?

A

Fuch’s endothelial dystrophy

NB There are other corneal dystrophies, however this is the most common

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13
Q

Approach to visual loss: what structures should be considered when thinking about causes of visual loss?

A

Eyelids + tear film

Cornea

Anterior chamber/iris/pupil

Lens

Fundus

The optic nerve (and beyond, i.e. visual field defects)

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14
Q

What is the ice pack test for myaesthenia gravis?

A

Application of ice to eyes for 2-5 mins relieves bilateral ptosis of MG by at least 2mm

It is thought that by cooling the tissues, and more specifically the skeletal muscle fibres, the activity of acetylcholinesterases are inhibited

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15
Q

Pathophysiology of post-op corneal oedema

Signs?

A

Corneal endothelium is vulnerable to insult in cataract surgery

Can see visible folds in Decemet’s membrane

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16
Q

Pathophysiology of Fuch’s endothelial dystrophy

A

Decompensation of corneal endothelial pump leads to corneal oedema (usually bilateral)

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17
Q

Findings on fundoscopy in Fuch’s endothelial dystrophy

A
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18
Q

Mx of Fuch’s endothelial dystrophy

A

Topical 5% sodium chloride (dehydrates cornea)

Definitive Mx: corneal graft surgery (corneal graft of the endothelium only is usually sufficient)

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19
Q

What kind of material in the anterior chamber may decrease visual acuity?

A

RBCs

WBCs

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20
Q

Hx: my vision has been getting blurry again, I’ve had several new pairs of glasses this year but it keeps getting worse

O/E: VA with glasses R 6/12 (pinhole 6/6) and L 6/15 (pinhole 6/6), PEARL, normal IOP, Munson’s sign (V-shaped indentation observed in the lower eyelid when the patient’s gaze is directed downwards; caused by cone-shaped cornea pressing down into the eyelid)

Dx?

A

Keratoconus (progressive thinning, weakness and protrusion of the cornea)

Prevalence ~1 in 2000

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21
Q

What are the layers of the normal cornea?

Which layer is primarily affected in keratoconus?

A
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22
Q

Mx of keratoconus

A

Hard contact lens

Cross-linking

Corneal transplant

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23
Q

Hx: 2/24 of painful unilateral red eye with worsening vision

O/E: IOP 60mmHg

Dx?

A

Acute angle closure glaucoma (this is a sight-threatening emergency!)

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24
Q

What signs are seen on inspection of the eye in acute angle closure glaucoma?

A
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25
Q

Mx of acute angle closure glaucoma

A

IOP reduction:

Acetazolamide STAT (IV and oral)

Topical B blocker (e.g. timolol)

Topical steroids

Once IOP reduced: peripheral iridotomy (LPI eliminates pupillary block by allowing the aqueous to pass directly from the posterior chamber into the anterior chamber, bypassing the pupil)

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26
Q

Hx: my vision has been getting progressively more blurry, I experience glare and colours don’t seem as bright anymore

O/E: VA 6/18 (no improvement with pinhole), PEARL, no RAPD, IOP normal, slit lamp exam revealed nuclear sclerosis (centre of lens appears white)

Dx? Types and causes?

A

Dx: cataract

Types: cortical, nuclear, subcapsular

Causes: age-related, drugs (e.g. steroids, amiodarone), trauma (including intra-ocular surgery), systemic diseases (e.g. DM, myotonic dystrophy, Wilson’s disease, atopic dermatitis), ocular diseases (uveitis, myopia)

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27
Q

What kind of VA is seen in mature cataracts?

A
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28
Q

What has happened to this lens?

A

Lens dislocation (usually due to zonular pathology)

Associated with CTDs, including Marfan’s syndrome

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29
Q

Hx: I lost vision in my L eye today, it was like a curtain came down over my vision

O/E: L VA <6/60, PEARL, no RAPD

Dx? Important causes?

A

Vitreous haemorrhage

Important causes include retinal detachment, proliferative diabetic retinopathy and trauma

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30
Q

Mx of vitreous haemorrhage

A

Often resolves slowly over weeks/months

Can require vitrectomy to clear blood

Risk of re-bleed

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31
Q

Hx: flashes of light and floaters in the visual field of my L eye

O/E: PEARL, slit lamp and dilated fundus exam performed

Dx?

A

Retinal tear and associated peripheral retinal detachment (note the peripheral location of the break - these can be hard to find!)

NB RAPD will be present when retinal detachment is extensive

32
Q

Mx of retinal detachment

A

Suspicion of retinal detachment requires urgent r/v by opthalmologist (within 24 hrs)

Mx is surgical repair

33
Q

What does this slit lamp examination show?

A

Weiss Ring (sign of posterior vitreous detachment, PVD)

34
Q

Hx: sudden, painless unilateral loss of vision

O/E: R VA <6/60, R RAPD, fundal examination performed

What are the findings of the fundal exam?

Dx?

A

Fundal exam shows pale retina, arteriolar attenuation and a “cherry red spot”

Central retinal artery occlusion (this is a sight threatening emergency; irreversible ischaemic damage to the retina occurs after ~90 mins)

35
Q

Common causes of central retinal artery occlusion

A

Atherosclerosis

Embolic sources

Haematological disorders (e.g. hypercoagulable states)

Inflammatory causes (e.g. GCA in ~3% of cases)

36
Q

Emergency Mx of central retinal artery occlusion

A

Urgent priority to rule out GCA (ESR, CRP)

Lie patient flat (to help maintain circulation)

Ocular massage (direct pressure for 5-15 secs/min for 15 mins)

Decrease IOP (e.g. with acetazolamide 500mg IV stat)

37
Q

Prognosis of central retinal artery occlusion

A

POOR

35% achieve VA of 6/60 or better

20% achieve VA of 6/12 or better

38
Q

Hx: sudden painless unilateral loss of vision

O/E: R VA <6/60, R RAPD, fundal examination performed

Findings on fundoscopy/inspection of eye?

Dx?

A

Central retinal vein occlusion

39
Q

Clinical associations with central retinal vein occlusion

A

Atherosclerosis: HTN, DM, hyperlipidaemia, smoking

Inflammatory diseases: sarcoidosis, Behcet’s, SLE, polyarteritis nodosa

Blood dyscrasias: protein C and S deficiency, antithrombin deficiency, antiphospholipid syndrome, multiple myeloma

Opthalmic: glaucoma, orbital mass

40
Q

Mx of central retinal vein occlusion

A

Lifestyle changes

IOP control

Intra-vitreal steroids and anti-VEGF agents

41
Q

Hx: I am unable to focus on anything with my R eye, when I try to look at something it disappears

O/E: R VA 6/48 (eccentrically fixating), pupils NAD, visual fields by confrontation normal, fundus photography and OCT performed

What are the findings on fundus photography and OCT?

Mx?

Risk?

A

Macular hole

Mx: vitrectomy, removal of macular traction (through peeling of internal limiting membrane +/- epiretinal membrane), insection of gas

~10% risk of macular hole developing in other eye

42
Q

Contrast between dry and wet age-related macular degeneration in terms of typical Hx, pathophysiology and Mx

A
43
Q

Which is more common: dry or wet macular degeneration?

A

Dry (~90%)

44
Q

Contrast the expected fundus examination findings in dry vs wet macular degeneration

A
45
Q

What is the biggest RF for development of diabetic retinopathy?

List 6 other RFs

A

Duration of DM is greatest RF

Poor glycaemic control

Poorly controlled HTN

Hypercholesterolaemia

Nephropathy

Pregnancy

Obesity

46
Q

What is the most common cause of visual impairment in diabetic retinopathy?

A

Diabetic macular oedema (also the greatest cause for visual disability in working age people in developed nations)

47
Q

What signs may be seen in diabetic retinopathy on fundoscopy?

A

Circinate ring

Lipid (hard) exudates

Intra-retinal haemorrhages or vascular abnormalities

Neovascularisation of the disc (NVD) or everywhere (NVE)

Microaneurysms

Venous beading

Vitreous haemorrhage

48
Q

Hx: I’m concerned about my vision, I have nearly been in a few car accidents and my night vision is so poor that I have had to stop driving in the dark altogether - blindness tends to run in my family

O/E: R VA 6/6, L VA 6/6, PEARL, no RAPD, IOP normal, visual field testing and fundoscopy performed

Describe the findings on visual field testing and fundoscopy

Dx?

A

Retinitis pigmentosa

49
Q

What is retinitis pigmentosa?

A

Most common retinal dystrophy, may be sporadic or inherited and typically affects rods first (“rod-cone dystrophy”)

Usually presents in young adulthood

50
Q

Hx: rapid decrease in visual acuity, presentation age <20

O/E: lipid deposits beneath the macular in RPE

Dx?

A

Stargardt’s disease

51
Q

Hx: decreased central vision

O/E: vitelliform appearance of macular (i.e. egg yolk appearance)

Dx?

A

Juvenile vitelliform dystrophy (Best’s disease)

52
Q
A
53
Q

Hx: several days of decreased L visual acuity

O/E: L VA 6/12, fundoscopy performed

Dx?

A

Posterior uveitis (in this case CMV retinitis)

54
Q

What is posterior uveitis?

A

Includes retinal vasculitis, retinitis, choroiditis

55
Q

7 causes of posterior uveitis

A

Systemic inflammatory disorders (e.g. Bechet’s, sarcoidosis)

Viruses (e.g. CMV, HSV, HZV, HIV)

Fungal (e.g. candida, aspergillus, cryptococcus)

Protozoa (e.g. toxoplasmosis gondii)

Bacterial (many varieties, e.g. TB, syphilis)

Lymphoma

Many causes associated with anterior uveitis

56
Q

Mx of posterior uveitis

A

Thorough Ix of cause: antimicrobials for infective cause, topical steroids for anterior uveitis, systemic therapies

Assess risk of bilateral vision loss

Variable prognosis

57
Q

Hx: eye trauma

Findings on fundoscopy?

A
58
Q

Overweight female in her 20s presents to ED

Hx: I get terrible headaches and now my vision has got blurry

O/E: bilateral swollen optic discs (papilloedema)

What is this a sign of? What are some possible causes and what Ix should be performed?

What do you think is the most likely Dx in this patient?

A

Sign of raised ICP

Causes include causes of mass effect (haemorrhage, haematoma, tumours), increased CSF production (choroid plexus tumour) and reduced CSF reabsorption (venous sinus thrombosis, aqueduct/foramen stenosis, idiopathic intracranial HTN)

Ix: urgent neuroimaging to exclude space-occupying lesion, then LP if cause not clear

Most likely: idiopathic (benign) intracranial HTN

59
Q

Mx of idiopathic intracranial HTN

A

Weight loss is the most effective treatment

Medical Rx: acetazolamide, other diuretics, corticosteroids

Surgical Rx: optic nerve sheath fenestration, lumbar-peritoneal (LP) shunt

60
Q

Hx: I woke this morning and have very poor vision in one eye

No PHx

O/E: R VA 6/6, L VA 6/60, left RAPD, IOP normal, reduced L colour saturation, fundoscopy performed

Describe the findings on fundoscopy

Dx? What are the possible implications of this Dx with regard to the long term prognosis?

A

Optic neuritis

Incidence in general population is low (5/100,000) while prevalence in MS patients is 70%

61
Q

Mx of optic neuritis

A

MRI brain and urgent referral to neurologist to Ix for MS

High dose prednisolone regime (IV methylprednisolone 1g/day for 3/7, then oral 1mg/kg daily for 11/7, then wean over 4/7) may speed up visual recovery but does not appear to impact on long term visual prognosis

62
Q

Compare the 5 year risk of developing MS in patients with optic neuritis but no lesions on MRI vs those with 2+ lesions on MRI

A

No lesions: 16% chance

2+ lesions: 51% chance

63
Q

DDx for bilateral disc swelling

A

Generally papilloedema; nerve fibre layer swelling due to raised ICP due to delay of axoplasmic flow

Malignant HTN

Pseudopapilloedema (partially myelinated nerve fibre layer

64
Q

Causes of raised ICP

A

Mass effect: haemorrhage, haematoma, tumours

Increased CSF production: choroid plexus tumour

Reduced CSF production: venous sinus thrombosis, aqueduct/foramen stenosis, idiopathic intracranial HTN

65
Q

DDx for unilateral disc swelling

A

Arteritic anterior ischaemic optic neuropathy (AION)

Non-arteritic anterior ischaemic optic neuropathy (NAION)

Inflammatory disorders (i.e. optic neuritis)

Orbital compressive lesion (i.e. tumours)

Infections

Causes of unilateral swelling related to raised ICP: Foster-Kennedy syndrome, raised ICP where one optic disc is already atrophic

NB These conditions can occur bilaterally

66
Q

Causes of pseudopapilloedema

A

Optic disc drusen

Hypermetropia (i.e. shorter eye axial length can give the disc a swollen appearance)

Tilted discs

67
Q

Papilloedema and psuedopapilloedema: which is which?

A
68
Q

What is GCA?

A

Medium to large vessel vasculitis involving arteries with a greater quantity of elastic tissue in media and adventitia

69
Q

Clinical features of GCA

A

Headache

Scalp tenderness

Jaw claudication

Associated PMR

Acute unilateral loss of vision (usually due to ischaemic optic retinopathy but can be due to CRAO)

70
Q

Key Ix for GCA

A

ESR (classically >100)

CRP

Temporal artery biopsy

71
Q

What is the risk of the second eye losing vision if one eye is affected with a presentation of GCA?

A

20-50%

This is a sight threatening emergency!

72
Q

Mx of GCA

A

High dose prednisolone (40-60mg/day), usually good response to steroids

73
Q

Classical signs of POAG

A

Increased optic cup-to-disc ratio

Progressive visual field loss (often not noticed by the patient until glaucoma is very advanced; commonly detected incidentally)

74
Q

POAG

A

A chronic degenerative condition affecting the optic nerve

75
Q

RFs for POAG

A

Positive FHx

High myopia

DM

Elevated IOP

76
Q

Mx of POAG

A

Lowering IOP (even from normal levels) is associated with delayed progression of disease

77
Q

What causes of visual loss require referral to an opthalmologist?

A

Any that can be explained by refractive error alone (i.e. cannot be corrected with pinhole)