Assessment and Diagnosis of Visual Loss Flashcards
Give 4 examples of causes/signs of visual loss which may suggest a broader life of function threatening problem?
Endogenous endeopthalmitis
Panuveitis (including viral retinitis and retinal vasculitis)
Papilloedema
Optic neuritis
What is the most common cause for poor vision in humans?
Refractive error
Hx: I can’t see very well and my eyes don’t seem to open properly
O/E: bilateral upper lid ptosis
DDx?
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
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?
Transient blurring of vision +/- epiphora (watering) = think tear-film disruption
Causes include trachoma (leading to entropion and pannus trichiasis)
Entropion
Eyelid (usually the lower lid) folds inward
How can entropion blur vision?
Tear-film disruption
Complications of entropion
Corneal scarring
Pannus trichiasis (misdirected growth of eyelashes towards the cornea)
What infective agent causes trachoma?
Chlamydia trachomatis
Epidemiology of trachoma
Prolific in arid poverty-stricken regions with poor hygiene
84 million people have active disease, 7.6 with trichiasis
Complications of trachoma
Scarring of conjunctiva
Entropion
Blindness
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?
Fuch’s endothelial dystrophy
NB There are other corneal dystrophies, however this is the most common
Approach to visual loss: what structures should be considered when thinking about causes of visual loss?
Eyelids + tear film
Cornea
Anterior chamber/iris/pupil
Lens
Fundus
The optic nerve (and beyond, i.e. visual field defects)
What is the ice pack test for myaesthenia gravis?
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
Pathophysiology of post-op corneal oedema
Signs?
Corneal endothelium is vulnerable to insult in cataract surgery
Can see visible folds in Decemet’s membrane
Pathophysiology of Fuch’s endothelial dystrophy
Decompensation of corneal endothelial pump leads to corneal oedema (usually bilateral)
Findings on fundoscopy in Fuch’s endothelial dystrophy
Mx of Fuch’s endothelial dystrophy
Topical 5% sodium chloride (dehydrates cornea)
Definitive Mx: corneal graft surgery (corneal graft of the endothelium only is usually sufficient)
What kind of material in the anterior chamber may decrease visual acuity?
RBCs
WBCs
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?
Keratoconus (progressive thinning, weakness and protrusion of the cornea)
Prevalence ~1 in 2000
What are the layers of the normal cornea?
Which layer is primarily affected in keratoconus?
Mx of keratoconus
Hard contact lens
Cross-linking
Corneal transplant
Hx: 2/24 of painful unilateral red eye with worsening vision
O/E: IOP 60mmHg
Dx?
Acute angle closure glaucoma (this is a sight-threatening emergency!)
What signs are seen on inspection of the eye in acute angle closure glaucoma?
Mx of acute angle closure glaucoma
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)
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?
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)
What kind of VA is seen in mature cataracts?
What has happened to this lens?
Lens dislocation (usually due to zonular pathology)
Associated with CTDs, including Marfan’s syndrome
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?
Vitreous haemorrhage
Important causes include retinal detachment, proliferative diabetic retinopathy and trauma
Mx of vitreous haemorrhage
Often resolves slowly over weeks/months
Can require vitrectomy to clear blood
Risk of re-bleed
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?
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
Mx of retinal detachment
Suspicion of retinal detachment requires urgent r/v by opthalmologist (within 24 hrs)
Mx is surgical repair
What does this slit lamp examination show?
Weiss Ring (sign of posterior vitreous detachment, PVD)
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?
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)
Common causes of central retinal artery occlusion
Atherosclerosis
Embolic sources
Haematological disorders (e.g. hypercoagulable states)
Inflammatory causes (e.g. GCA in ~3% of cases)
Emergency Mx of central retinal artery occlusion
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)
Prognosis of central retinal artery occlusion
POOR
35% achieve VA of 6/60 or better
20% achieve VA of 6/12 or better
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?
Central retinal vein occlusion
Clinical associations with central retinal vein occlusion
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
Mx of central retinal vein occlusion
Lifestyle changes
IOP control
Intra-vitreal steroids and anti-VEGF agents
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?
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
Contrast between dry and wet age-related macular degeneration in terms of typical Hx, pathophysiology and Mx
Which is more common: dry or wet macular degeneration?
Dry (~90%)
Contrast the expected fundus examination findings in dry vs wet macular degeneration
What is the biggest RF for development of diabetic retinopathy?
List 6 other RFs
Duration of DM is greatest RF
Poor glycaemic control
Poorly controlled HTN
Hypercholesterolaemia
Nephropathy
Pregnancy
Obesity
What is the most common cause of visual impairment in diabetic retinopathy?
Diabetic macular oedema (also the greatest cause for visual disability in working age people in developed nations)
What signs may be seen in diabetic retinopathy on fundoscopy?
Circinate ring
Lipid (hard) exudates
Intra-retinal haemorrhages or vascular abnormalities
Neovascularisation of the disc (NVD) or everywhere (NVE)
Microaneurysms
Venous beading
Vitreous haemorrhage
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?
Retinitis pigmentosa
What is retinitis pigmentosa?
Most common retinal dystrophy, may be sporadic or inherited and typically affects rods first (“rod-cone dystrophy”)
Usually presents in young adulthood
Hx: rapid decrease in visual acuity, presentation age <20
O/E: lipid deposits beneath the macular in RPE
Dx?
Stargardt’s disease
Hx: decreased central vision
O/E: vitelliform appearance of macular (i.e. egg yolk appearance)
Dx?
Juvenile vitelliform dystrophy (Best’s disease)
Hx: several days of decreased L visual acuity
O/E: L VA 6/12, fundoscopy performed
Dx?
Posterior uveitis (in this case CMV retinitis)
What is posterior uveitis?
Includes retinal vasculitis, retinitis, choroiditis
7 causes of posterior uveitis
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
Mx of posterior uveitis
Thorough Ix of cause: antimicrobials for infective cause, topical steroids for anterior uveitis, systemic therapies
Assess risk of bilateral vision loss
Variable prognosis
Hx: eye trauma
Findings on fundoscopy?
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?
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
Mx of idiopathic intracranial HTN
Weight loss is the most effective treatment
Medical Rx: acetazolamide, other diuretics, corticosteroids
Surgical Rx: optic nerve sheath fenestration, lumbar-peritoneal (LP) shunt
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?
Optic neuritis
Incidence in general population is low (5/100,000) while prevalence in MS patients is 70%
Mx of optic neuritis
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
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
No lesions: 16% chance
2+ lesions: 51% chance
DDx for bilateral disc swelling
Generally papilloedema; nerve fibre layer swelling due to raised ICP due to delay of axoplasmic flow
Malignant HTN
Pseudopapilloedema (partially myelinated nerve fibre layer
Causes of raised ICP
Mass effect: haemorrhage, haematoma, tumours
Increased CSF production: choroid plexus tumour
Reduced CSF production: venous sinus thrombosis, aqueduct/foramen stenosis, idiopathic intracranial HTN
DDx for unilateral disc swelling
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
Causes of pseudopapilloedema
Optic disc drusen
Hypermetropia (i.e. shorter eye axial length can give the disc a swollen appearance)
Tilted discs
Papilloedema and psuedopapilloedema: which is which?
What is GCA?
Medium to large vessel vasculitis involving arteries with a greater quantity of elastic tissue in media and adventitia
Clinical features of GCA
Headache
Scalp tenderness
Jaw claudication
Associated PMR
Acute unilateral loss of vision (usually due to ischaemic optic retinopathy but can be due to CRAO)
Key Ix for GCA
ESR (classically >100)
CRP
Temporal artery biopsy
What is the risk of the second eye losing vision if one eye is affected with a presentation of GCA?
20-50%
This is a sight threatening emergency!
Mx of GCA
High dose prednisolone (40-60mg/day), usually good response to steroids
Classical signs of POAG
Increased optic cup-to-disc ratio
Progressive visual field loss (often not noticed by the patient until glaucoma is very advanced; commonly detected incidentally)
POAG
A chronic degenerative condition affecting the optic nerve
RFs for POAG
Positive FHx
High myopia
DM
Elevated IOP
Mx of POAG
Lowering IOP (even from normal levels) is associated with delayed progression of disease
What causes of visual loss require referral to an opthalmologist?
Any that can be explained by refractive error alone (i.e. cannot be corrected with pinhole)
