Sudden Painless Visual Loss
A sudden onset of visual loss is alarming to the patient. Only a few diagnoses
require immediate
ophthalmic referrals for management:
Central or branch retinal artery occlusion <6h
Giant cell arteritis
Any sudden visual loss <6h and the cause can not be established
All other causes of visual loss can be referred within 24 hours.
Most common causes seen in ED:
Central or branch retinal artery occlusion
Central or branch retinal vein occlusion
Vitreous haemorrhage
Retinal detachment
Ischaemic optic neuropathy including giant cell arteritis
Optic neuritis
History
Transient visual loss like a curtain coming down (suggestive of amourosis
fugax)
Visual loss or field loss preceded by sudden onset floaters and flashing light
(photopsia),
this is suggestive of retinal detachment
History of poorly controlled DM and laser treatment to the retina (vitreous
haemorrhage)
Headache +/- jaw claudication in the elderly (giant cell arteritis)
Pain on eye movement in young patients (optic neuritis)
Examination:
Visual acuity
Assess the visual field by confrontation some patients may have homonymous
hemianopia
and yet complain of uniocular visual loss.
Full ocular examination which should include:
opupil reaction for afferent papillary defect (this occurs in optic nerve
disorder and
extensive retinal pathology.)
oretinal examination for any obvious signs
Differential Diagnosis
Central/Branch Retinal Artery Occlusion,
TIA
Central/Branch Retinal Vein Occlusion
Endophthalmitis
Episcleritis/Scleritis
Intraocular Foreign Body
Giant Cell Arteritis
Headache/Migraine
Hyphema
Optic Neuritis
Ischemic/Compressive Optic Neuropathy
Papilloedema
Retinal Detachment
Sickle Cell Disease
Corneal Abrasion/Ulcer
Occipital lobe ischaemia, infarction
or trauma
Rapidly progressive chiasmal
compression
Methanol poisoning
Hysteria
Vitreous haemorrhage
May occur post-trauma or spontaneously (posterior vitreous detachment
retinal breaks,
proliferative diabetic retinopathy, central retinal vein occlusion and subretinal
neovascular
membrane in age-related macular degeneration with breakthrough bleeding).
Features:
Sudden onset of floaters causing impaired vision
If severe, may obscure all the retina on fundoscopy. So examine other eye for
clues
Management:
Refer within 24 hours
Bed rest. Check for DM, USS to exclude retinal detachment if view obscured.
Central or branch retinal artery occlusion
Caused by
arteriosclerotic
changes, emboli,
(from heart or
carotids) or occ
inflammation
(temporal
arteritis)
Features:
Sudden painless unilateral visual loss: complete (central artery) or partial
(branch artery)
May be transient (a form of TIA amaurosis fugax) with return of normal
vision.
Patient usually have a history of hypertension or heart disease
Relative afferent pupillary defect is present in central retinal artery occlusion
The retinal arteries are narrow or collapsed and emboli may be seen.
In CRAO, the fovea shows a cherry-red spot against the white infarcted
retina.
Management:
Immediate referral if the visual loss <3h as Rx may restore some or most of
the function.
Rx: globe massage, IV acetazolamide, TOP beta-blockers, aqueous humour
paracentesis
to IOP, or rebreathe CO2 to dilate vessels and hopefully re-establish the
arterial flow.
Further management aim to uncover any underlying diseases such as
hypertension,
cardiac or carotid thrombus.
Inv: BSL, FBC, EUC, Lipids, ESR, Thrombophilia screen, ECG, ECHO, carotid
Doppler.
Long term low dose aspirin is advised to reduce the risk of occurrence.
Central or branch retinal vein occlusion
Retinal vein occlusion is relatively
common with infarction (not
ischaemia) caused by impaired
venous blood flow. Seen mainly in
elderly, DM & HT.
It is second only to diabetes
mellitus as a vascular cause of
impaired vision.
Features:
Sudden onset painless blurred vision
Less commonly painful red eye due to neovascular glaucoma as a result of
recent CRVO.
Visual acuity dependent on the severity of the occlusion. May be normal in
branch
retinal vein occlusion, if the fovea is not involved.
Relative afferent pupillary defect if severe CRVO
Ophthalmoscopy reveals extensive intraretinal and pre-retinal haemorrhage
with
distended retinal veins.
Management:
Check for hyperviscosity, DM, hypertension and glaucoma
Inv: BSL, BP, IOP, FBC, ESR and in young patients auto-immune screening.
Refer within 24 hours & follow-up in eye clinic to monitor for neovascular
glaucoma
Retinal detachment
Features:
Commonly, a recent history of floaters and flashes of light
Curtain coming across the vision
Assoc with myopia, cataract removal, ocular trauma & vitreous diseases
Visual acuity variable depending if the macula is involved. Visual field defect
Ophthalmic examination in a dilated pupil shows greyish retina. A tear may be
seen or
wrinkled retina. Loss of red reflex.
Management:
Bed rest. Pad eye
Refer the patient the same day for surgical management + laser photocoagulation.
Ischaemic optic neuropathy
In ischaemic optic neuropathy, there is occlusion of the small
arteries around the optic disc. Arteritic ischaemic optic neuropathy
is caused by giant cell arteritis and prompt systemic steroids can
prevent involvement of the contralateral eye. Patients usually >50y.
Features:
Sudden visual loss in a patient with a history of temporal headache or jaw
claudication
suggests giant cell arteritis
In giant cell arteritis there is tenderness & pulsation over the affected
temporal artery.
Profound visual loss usually in giant cell arteritis and less severe if nonarteritic.
Commonly an afferent pupillary defect.
Fundoscopy: swollen optic disc caused by occlusion of the arteries around the
optic disc.
Management:
ESR and CRP
Refer to ophthalmology for review, steroids & temporal artery biopsy.
Optic neuritis
This condition typically affects patients in the 20 45y
age range and may be associated with demyelination (most
often MS) or not (infection, autoimmune).
Features:
Impaired vision over hours days. Usually unilateral.
Central field defect
Visual acuity may be as poor as perception of light
Central scotoma is typical
Impaired colour discrimination (esp red object)
Relative afferent pupillary defect of the affected eye
Pain on eye movement especially on adduction.
Fundoscopy is normal (retrobulbar neuritis) or swollen. Other disc may look
pale.
Management:
Refer for review, ESR, MRI (r/o demyelination) or CXR (TB, sarcoid).
Normal or near-normal vision usually returns within 6wk
No specific therapy though IV steroids may slow onset of MS.
