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Transcript
Table of Contents
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1.0 Introduction
2.0 Sudden loss of vision
o 2.1 Sudden transient unilateral visual loss
o 2.2 Sudden persistent unilateral visual loss
o 2.3 Sudden bilateral vision loss
3.0 Progressive visual disturbances
4.0 Scintillations and flashers
5.0 Night blindness
6.0 Day blindness
7.0 'Floaters' - dots, points and lines
8.0 Headaches of extraocular origin with ocular symptoms
9.0 Cataract
10.0 Age related macular degeneration (AMD)
o 10.1 Atrophic (Dry) AMD
o 10.2 Exudative (wet) AMD
o 10.3 Treatment of AMD
References
1.0 Introduction
This lecture attempts to provide a concise, problem-based approach to disorders that affect
vision. Common causes of visual field loss, flashers, floaters and decreased visual acuity will
be covered. Primary care management of these problems will be discussed where
appropriate.
[ top ]
2.0 Sudden loss of vision
Patients with a sudden loss of vision usually seek medical aid urgently and the GP is often the
first to see the patient in what may be a crucial 'treatment window'. The following section
describes some common presentations of sudden visual loss and their implications.
Practice Tip!
As a general rule, any visual loss that is not clearly neurological needs urgent referral to
an opthalmologist.
Presentation
Possible Causes
Sudden Transient Unilateral
Visual Loss
Amaurosis fugax
Giant cell arteritis
Glaucoma
Ocular Hypoperfusion
Retinal migraine
Uhtoff's phenomenon
Obscuration due to raised ICP
Sudden Persistent Unilateral
Vision Loss
Vitreous haemorrhage
Retinal detachment
Central retinal vein & artery occlusion
Acute Glaucoma
Optic neuritis
Ischaemic optic neuropathy:

Anterior
o Giant cell arteritis

o Non arteritic·
Posterior
Optic nerve compression
Carcinoma or lymphoma
Traumatic cataract - especially children
Central serous retinopathy
Sudden Bilateral Vision Loss
Toxic optic neuropathy
Occipital cortex infarction
[ top ]
2.1 Sudden transient unilateral visual loss
Sudden transient unilateral visual loss is usually apparent at time of onset. However some
patients may only realise when they cover their good eye (in this case the visual loss is
usually gradual).
Golden Rule!
All cases presenting with visual symptoms require assessment of visual acuity, visual
fields, pupil response to light, anterior chamber depth and fundoscopy including red
reflex.
Amaurosis fugax:
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painless, uniocular visual loss
lasts < 1 hour
described as 'shutter' coming down over 1 eye
caused by an embolus passing through the retinal arteries
fundus examination - reveals refractive yellow cholesterol crystal in retinal arteries or
non-refractive calcific emboli close to optic disc.
Glaucoma:
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
intermittent angle-closure glaucoma may cause unilateral vision loss
brought on by pupillary dilation, e.g. during low light.
Ocular hypoperfusion:
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

present in patients with advanced extracranial vascular disease
caused by activities that extract blood from the retinal circulation e.g. walking,
standing after bending
diagnostic features include:- venous stasis retinopathy (hypotensive retinopathy), with
dilated retinal vein, branch occlusions, haemorrhages in the mid periphery and a
central retinal artery pulsation stopped by minimal pressure on the globe.
Obscurations:
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

unilateral or bilateral visual loss lasting a few seconds
occurs in patients with severe, raised intracranial pressure
papilloedema (bilateral disc swelling) evident on fundoscopy.
Uhtoff's phenomenon:

unilateral or bilateral loss of vision
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
occurs concurrently with rise in body temperature, eg after exercise
caused by demyelinating optic neuritis.
Retinal migraine:
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rare occurrence mainly in young adults
vision loss sudden, uniocular and painless
duration ~ 5 minutes
thought to be caused by spasm of retinal arteries
Other causes:

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giant cell arteritis (see later section)
systemic lupus.
[ top ]
2.2 Sudden persistent unilateral visual loss
Traumatic cataract:

Injury with initially unsuspected globe penetration (eg small sharp metal foreign body)
may cause a uveitis and a loss of vision if the lens has been damaged. Be aware of
this possibility especially in children with the added issue of developing amblyopia
from the cataract.
Vitreous haemorrhage
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fundus obscured due to vitreous haemorrhage.
Retinal detachment:
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patient 1st perceives a dark shadow in peripheral vision
if macula becomes involved, visual acuity is lost
total detachment may be associated with afferent pupil defect
Suspect the possibility of early detachment with the recent onset of flashes and
floaters. Consider prompt ophthalmic referral in all cases because of the possibility of
an early retinal hole before the retina becomes detached.
Cental retinal vein occlusion
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

relatively common
fundoscopy reveals dilated, tortuous veins, flamed shaped haemorrhages and soft
exudates
visual loss occurs when macular is involved.
Central retinal artery occlusion
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painless, sudden loss of vision (visual acuity reduced to light perception only)
pupil unreactive to light (afferent pupil defect)
fundus near-normal in early stages
retinal arteries may appear smaller and macula may have cherry-red spot
later stages - retina displays pale, cloudy swelling due to infarction
if seen within minutes, emergency treatment involves massaging the globe,
intravenous acetazolamide and paracentesis of the globe (urgent, immediate referral
for the ophthalmologist to perform this procedure is required).
Acute glaucoma:
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severe pain, haloes around lights, nausea and vomiting
globes are hard to touch and very tender
acute glaucoma is a medical emergency and the patient should be sent to a hospital
with a specialist eye unit immediately.
Optic neuritis:
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visual loss occurs over several days
pain on eye movement
often described as a "lace curtain" over eye but degree of vision loss varies
visual field loss (esp. central scotoma) common
fundoscopy may reveal swollen optic disc sometimes including haemorrhages and
exudates
afferent pupil defect
partial recovery between 2-6 weeks after onset.
Ischaemic optic neuropathy:
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
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sudden painless loss of vision in the elderly
fundoscopy reveals pale, swollen optic disc, haemorrhages may be present
visual field loss
caused by infarction of the optic nerve head
important to refer early as may be caused by giant cell arteritis which needs
corticosteroid therapy ASAP
afferent pupil defect usually present.
Optic nerve compression:
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not usually of sudden onset
decreased visual acuity
poor colour vision
central scotoma
pale optic disc
a relative afferent pupillary defect is usually present.
Carcinomatous or lymphomatous:


unilateral or bilateral vision loss
may be suspected in patients with known lymphoma, carcinoma or leukaemia.
Central serous retinopathy:



typically affects younger men
impaired central vision with distortion and micropsia
macular lesion may be apparent on fundoscopy.
[ top ]
2.3 Sudden bilateral vision loss
Toxic optic neuropathy:

painless

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
bilaterally symmetrical
progressive
scotomatous field defects
colour vision loss
can be due to ethanol, methanol, tobacco, ethambutol, quinine.
Occipital cortex infarction:


presents with bilateral homonymous hemianopia with variable macular sparing
patients are cortically blind and hence may be unaware of their visual loss until fully
examined.
[ top ]
3.0 Progressive visual disturbances
Progressive permanent cloudiness of vision.
May be due to:


cataract
vitreous opacities.
Mobile opacities
May be due to:


vitreous floaters
retinal detachment.
Central scotoma
May be due to:
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
macula haemorrhage, macular hole, central serous retinopathy
macular degeneration.
Peripheral field losses
May be due to:



inflammation
glaucoma
intraocular, orbital and brain tumours.
[ top ]
4.0 Scintillations and flashers
Posterior vitreous detachment is the most common cause of scintillations and flashers.
Scintillations may also be associated with fainting and migraines. In migraine, a scotoma
associated with flickering sparks and zigzags (which may move through visual fields) may be
present. This is followed by headache minutes - hours later. Retinal detachment and
choroiditis also cause scintillations.
Caution!
Patients with acute onset of flashers or floaters should be seen promptly by an
ophthalmologist to exclude a retinal tear or detachment.
[ top ]
5.0 Night blindness
The causes of night blindness include:



decreased vitamin A intake (due to malabsorption, gastritis, liver disease etc)
advanced glaucoma
macular degeneration (diminished light to dark adaptation).
[ top ]
6.0 Day blindness
Patients complaining of day blindness may have central opacities of the cornea or lens.
Albinism and total colour blindness are other causes of day blindness.
[ top ]
7.0 'Floaters' - dots, points and lines
"Floaters" are caused by vitreous opacities, primarily due to haemorrhages, cellular opacities,
parasites and pigment. As the eye moves, these distracting floaters move synchronously, with
a slight lag caused by inertia of the vitreous gel.
Caution!
All complaints of recent or increasing floaters that come to the patient's attention are
significant and require ophthalmoscopic examination. Serious retinal traction is likely
when floaters are accompanied by 'flashers' (streaks of light).
[ top ]
8.0 Headaches of extraocular origin with ocular symptoms
Migraine:
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most significant of the vascular headaches
aura and/or scintillating scotoma a frequent prodrome
headaches usually hemicranial, above eye, brow, temple and occiput
photophobia may occur.
Ophthalmoplegic migraine:
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neurologic deficits (oculomotor nerve paralysis) follow hemicranial migraine
paralysis may last for 12-24 hours
aneurysms, basilar tumours and arteriosclerosis must be ruled out.
Sinusitis:
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may cause eye pain.
Giant cell temporal arteritis:
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radiating pain from temple
temporal arteries are tortuous, nodular, pulseless and painful when pressure is
applied
pain on mastication, brushing hair, wearing a hat
low grade fever, muscle aches and weight loss



associated with a clinical picture similar to polymyalgia rheumatica
erythrocyte sedimentation rate elevated.
treatment - systemic steroids in high doses (80mg prednisone/day for 46 weeks).
Trigeminal neuralgia:

may have localized eye pain.
Brain / Intracranial:
The following may all cause pain localised "behind the eye":
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increased intracranial pressure
o headache
o vomiting
o papilleodema
o fixed pupil
o unilateral mydriasis
meningitis
brain tumours.
[ top ]
9.0 Cataract
Cataracts are opacifications of the lens. Lens opacities appear grey with oblique illumination
and black in light reflected from the fundus. Patients present with symptoms such as blurred
and unclear vision, monocular diplopia, photophobia and dazzling. Vision may be improved in
low light because dilation of the pupil may allow patients to see around the lens opacity.
Cataract has highest incidence in patients who:
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are aged 65+
have a history of ocular trauma
have a history of uveitis
have diabetes mellitus
have genetic diseases such as myotonic dystrophy and galactosaemia
have a history of radiation or glucocorticoid therapy.
Patients suspected of cataract should be referred to an ophthalmologist for surgical extraction
and replacement of the lens. Surgery is extremely successful with very low associated risk.
[ top ]
10.0 Age related macular degeneration (AMD)
Incidence
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most common cause of irreversible blindness in people over 65 years
25% of people 65+ and 40% of people 80+ have some form of AMD
90% of all AMD cases are atrophic (dry) and 10% are exudative (wet)
exudative AMD produces the most severe visual loss.
Risk factors:
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age
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genetic influences
environmental
o smoking
o lack of antioxidants in diet
o nutritional supplements such as vitamin A, C & E and minerals such as zinc,
copper and selenium may reduce risk
[ top ]
10.1 Atrophic (Dry) AMD
Dry AMD is characterised by gradual cell (rods & cones) death in the retinal pigment
epithelium and the choroid. Fundoscopy may reveal drusen (pale spots deep within the retina,
as distinct from the pale superficial retinal spots due to exudate in hypertension or diabetic
retinopathy), pigment clumping and atrophy around the macula. Dry AMD is occurring in
increasing prevalence in Australia and as yet no truly effective preventative measures are
available. Treatment of dry AMD is not satisfactory and early detection of a change to the
exudative state is of primary importance.
(Illustration: Optic drusen around the macula in atrophic age-related macula degeneration.
Photo courtesy of Dr Alex Hunyor.)
[ top ]
10.2 Exudative (wet) AMD
Wet AMD is due to aberrant choroidal angiogenesis. The newly formed vessels in wet AMD
are weak and prone to haemorrhage, causing sudden, severe visual loss. Fibrovascular
scarring is the end-stage of the disease.
(Illustration: Choroidal neovascularisation in exudative age-related macular degeneration.
Photo courtesy of Dr Alex Hunyor.)
[ top ]
10.3 Treatment of AMD
Laser treatment is the mainstay of therapy for exudative AMD. It aims to cauterise new
vessels, thus reducing oxidative stress and preventing further neovascularisation. Generally
these treatments offer reduced progression of the scotoma from the retinal damage, but little
prospect of improvement. New and experimental treatment options include photodynamic
therapy, pharmacological therapy and surgical intervention.
[ top ]
References
1. King, J. 2000, 'Sudden loss of vision: a GP's guide to the many causes',
MedicineToday, vol. 1, no. 7, pp. 76-83
2. Reich, J. 2000, 'Sudden loss of vision in an elderly woman', Australian Family
Physician, vol. 29, no. 9, pp. 870-871
3. Nuffield Institute for Health, 'Management of Cataract', Effective Health Care, vol. 2,
no. 3, pp 1-12
4. Wun, Y.T., Lam, C.C. & Shum, W. K. 1997, 'Impaired vision in the elderly: a
preventable condition', Family Practice, vol. 14, no. 4, pp. 289-292
5. Pau, H. 1978, Differential Diagnosis of Eye Diseases, Georg Thieme Publishers,
Stuttgart
6. Kanski, J.J., 1989, Clinical Ophthalmology, Butterworth & Co. Ltd, Hong Kong
7. Hunyor, A.P., 2001 Age related macular degeneration and diabetic eye disease.
Chatswood Retinal Service.