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Sudden visual loss
GPR, Sutton Scotney, Hampshire
E-mail: ejharding{at}doctors.org.uk
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Abstract |
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 TOP Abstract The GP curriculum--Statement...Questions to ask the...Examining the patient with...Causes of sudden visual...SummaryReferences |
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A patient presenting with sudden visual loss can be a terrifying experience for both patient and doctor. Patients want to know if they could be permanently blinded and doctors are faced with a rarely encountered highly distressing symptom which they can often do little to improve in the surgery.
GPs in training must have knowledge of:
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It may well be more important than usual to adopt a systematic approach to history taking and examination. A good working knowledge of the potential causes of sudden visual loss and a focused consultation can enable the GP to easily formulate a differential diagnosis and hence aid prompt referral to ophthalmology.
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Causes of sudden visual loss |
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TOPAbstractThe GP curriculum--Statement...Questions to ask the...Examining the patient with...Causes of sudden visual...SummaryReferences |
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The causes of sudden visual loss can be classified in many ways. Here they will be considered anatomically from superficial structures of the eye back to intracerebral causes (Table 1).
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Acute closed angle glaucoma
Acute closed angle glaucoma occurs in 1 in 1000 people over the age of 40. Impairment of normal aqueous drainage, by apposition of the iris to the trabecular meshwork, leads to a rise in intraocular pressure and subsequent painful visual impairment.
Predisposing factors include:
- Shallow anterior chamber—often associated with hypermetropia
- Thick lens—so encroaches on anterior chamber
- Pupillary dilatation—pushes the iris anteriorly to lie against the trabecular network obstructing aqueous outflow
| Clinical features of acute closed angle glaucoma History Acute loss of vision in affected eye with periocular pain Haloes around lights (secondary to corneal oedema) Nausea and vomiting—beware, this may be the acute clinical picture Examination Patient is often generally unwell Stony hard eye (due to raised pressure) with marked pericorneal injection Fixed mid-dilated pupil (often slightly oval) High intraocular pressure (normal range 10–21 mmHg)
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All patients with suspected acute angle closure glaucoma need immediate referral to ophthalmology.
Treatment involves:
- Intravenous acetazolamide to reduce aqueous secretion and hence intraocular pressure
- Topical agents to cause pupillary constriction, for example pilocarpine
- Systemic analgesia and antiemetics
- Surgical or laser iridectomy once the acute attack has resolved
Prompt treatment favours an excellent prognosis in an uncomplicated case of acute angle closure glaucoma. Consideration must be made for prophylactic treatment of the ‘unaffected’ eye since the anatomical disposition is likely to be bilateral.
Vitreous haemorrhage
Vitreous haemorrhage is one of the most common causes of sudden visual loss, particularly among the diabetic population prone to retinal neovasularization.
Fragile retinal vessels (diabetic retinopathy), stress causing rupture of normal retinal vessels (posterior vitreous detachment with or without retinal detachment trauma) or extension of blood from an adjoining source (retinal macroaneurysms, tumours) result in bleeding into the vitreous, which, when large enough, causes visual loss.
Patients presenting with sudden visual loss should be referred immediately to ophthalmology.
| Clinical features of vitreous haemorrhage History Risk factors including diabetes mellitus, trauma and previous surgery Drug history especially warfarin/aspirin Floaters (‘shower of spots’, ‘cobwebs’)—vitreous opacities casting shadows on the retina which move when the eye comes to rest Visual loss—often worse in the mornings due to pooling of blood and usually unilateral Examination Ocular examination may reveal reduced visual acuity, visual field impairment or scotoma The retina may not be seen in cases of severe haemorrhage
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Management involves exclusion of RD with subsequent treatment of the underlying aetiology, for example with photocoagulation of new vessels. Absorption of the vitreous haemorrhage should be observed and if the vitreous haemorrhage persists at 3 months, a vitrectomy may be carried out to remove the remaining blood.
Central retinal artery occlusion
Acute onset painless profound loss of vision can occur with occlusion of the central retinal artery. The central retinal artery is the first intraorbital branch of the ophthalmic artery which is, in turn, the first branch of the internal carotid artery. Its blockage, usually secondary to emboli originating in the heart, carotid arteries or intracerebrally, results in retinal infarction.
This calamitous insult on the retina can result in its swelling and opacification in as little as 15 minutes and the chance of recovery of vision is poor.
Retinal artery occlusion may be an early manifestation of widespread vascular disease and therefore a full cardiovascular examination is essential.
Firm ocular pressure may displace the embolus into a branch vessel if the patient presents within 1 hour. All patients should be referred as an ophthalmic emergency for diagnosis confirmation. Non-acute management involves risk factor modification and carotid doppler ultrasonography with subsequent consideration of surgery when atheromatous plaques are present.
| Clinical features of retinal artery occlusion History Patients over the age of 60 years Pre-existing embolic/atherosclerotic risk factors—diabetes, hypertension, smoking, Ischaemic heart disease, stroke or transient ischaemic attack and atrial fibrillation May reveal a history of amaurosis fugax Acute, persistent and painless loss of vision Examination Visual loss may be profound necessitating a finger count testing Relative afferent papillary defect (RAPD) (detected by the swinging torch test—stimulation of the normal eye results in bilateral papillary constriction, subsequent stimulation of affected eye results in observable bilateral papillary dilatation) White opacified retina with cherry red spot Retinal embolus potentially visible
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Amaurosis fugax
Transient retinal ischaemia, usually associated with ipsilateral carotid artery stenosis or cardiac/aortic emboli, causes temporary unilateral loss of vision. Patients often complain of a curtain of darkness descending over the eye with visual resolution after a period of time. If the cause is carotid artery stenosis, there may be a contralateral hemiparesis.
A complete cardiovascular examination is essential as the ophthalmological examination is often normal.
Amaurosis fugax may be a warning sign of future catastrophic retinal insult, for example central retinal artery occlusion (CRAO), so diagnosis of the cause may save sight.
Central retinal vein occlusion
Retinal vein occlusion is a common cause of visual loss in the UK with an incidence of 2 in 1000 in those over the age of 40. Thrombus formation involving the central or branch retinal vein causes obstruction of the retinal venous system.
Central retinal vein occlusion (CRVO) can be divided into:
- non-ischaemic—milder form of the disease with better chance of visual recovery
- ischaemic—more severe form often resulting in a painful blind eye
Branch retinal vein occlusion (BRVO) manifests as unilateral visual loss and fundal appearances confined to the corresponding area. It is twice as common as central vein occlusion with better chance of visual recovery.
Management of patients with suspected retinal vein occlusion involves:
- Identification of modifiable risk factors for example check blood pressure, blood glucose and lipids, full blood count, ESR or viscosity, VDRL and their subsequent medical management
- Recognition and management of sight-threatening complications—refer to ophthalmology for immediate review
| Clinical features of central retinal vein occlusion History Patient over the age of 50 years Risk factors—hypertension, diabetes, hyperviscosity, smoking, hyperlipidaemia and glaucoma Sudden onset painless loss of vision/blurred vision often on waking—in BRVO the visual acuity may be normal if the macula is not involved. Examination Fundoscopy—ischaemic CRVO reveals a ‘stormy sunset’—engorged veins, retinal haemorrhages and cotton wool spots. Non-ischaemic CRVO may lead to a few retinal haemorrhages and cotton wool spots only. RAPD (ischaemic CRVO)
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Fluorescein angiography can be performed to assess whether laser treatment is needed.
Panretinal laser photocoagulation prevents neovascularization. Long-term outcome is variable but chronic macular oedema leads to persistent reduction in central vision in most. Subsequent retinal vein occlusions in those with ischaemic CRVO are not uncommon.
Retinal detachment
RD, affecting 1 in 5000 people each year, involves the separation of the inner sensory retina from the outer retinal pigment epithelial layer leading to infiltration of fluid into the resulting subretinal space. Aetiologically, it can be divided into rhegmatogenous (most common) and non-rhegmatogenous (tractional or exudative).
Rhegmatogenous A retinal break (rhegma means ‘break’ in Greek) due to an acute tear or chronic retinal atrophy allows liquefied vitreous to enter the subretinal space detaching the sensory retina.
Non-rhegmatogenous
- Tractional—retinal and vitreal scarring and contraction results in separation of the retinal layers
- Exudative—subretinal fluid leaks into the subretinal space secondary to damage to the retinal pigment epithelial layer (e.g. caused by hypertension/choroidal neoplasm) dividing the retinal layers
Risk factors for RD
- Myopia
- Family history of RD
- Previous eye surgery
- Retinal disease
- Trauma
- Diabetes mellitus (fibrous bands form in the vitreous leading to tractional RD)
| Clinical features History Aged 40–70 years, male : female ratio is 1 : 1 Photopsia (flashing lights), often worse on eye movements, seen in about 50% of patients Floaters (Table 2) Visual field defect (curtain descending over vision) Examination Reduction in visual acuity with macular involvement (if normal may mean early surgical intervention may prevent macular detachment) RAPD (indicates large RD) Grey retina on fundoscopy—a tear or hole may be seen
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Patients with suspected RD should all be assessed by an ophthalmologist within 24 hours. Patients with acute onset flashers/floaters with no other symptoms may be referred urgently to ophthalmology outpatients.
Treatment options include:
- Medical treatment of inflammatory conditions causing exudative RD
- Cryotherapy or laser treatment to seal the retinal break
- Surgical treatment
Permanent visual loss is inevitable once macular detachment occurs. Fortunately, most patients present before this point and prompt treatment can allow good visual recovery. A retina that remains fixed for 6 months is unlikely to become detached again.
Optic neuritis
Optic neuritis or inflammation of the optic nerve, affecting 1–5 in 100 000 per year, causes subacute visual impairment. Demyelination is the main cause of inflammation but infectious and autoimmune disease processes may also be responsible.
Multiple sclerosis (MS) is the most common demyelination disease which affects the optic nerve, and up to 20% of cases of MS manifest initially as optic neuritis. The risk of developing MS following a single episode of optic neuritis is 30% at 5-year follow-up.
| Clinical features of optic neuritis History Increased risk in women—male : female ratio is 1 : 1.8 Mean age of onset 30 years Warning triad (70% unilateral) Subacute visual loss Ocular pain Impaired colour discrimination (dyschromatopsia) Extraocular symptoms may be present, for example weakness, numbness and frontal headache Examination Reduced visual acuity—6/18–6/60 RAPD in affected eye Fundal examination is usually normal as most patients have retrobulbar neuritis A full neurological examination is mandatory
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If demyelinating optic neuritis is suspected clinically, the patient must be referred to neurology/ophthalmology for MRI brain and orbits.
Management involves a 2-week course of intravenous followed by oral steroids. Visual recovery begins at 3 weeks and is maximal at 6 months with 85% of patients by that stage obtaining a visual acuity of at least 6/12. Recurrence of optic neuritis is not uncommon and can occur in the ipsi- or contralateral eye in 35% of patients at 10 years.
Temporal arteritis
Temporal arteritis is a chronic systemic vasculitic syndrome which can present as sudden visual loss due to inflammation of branches of the ophthalmic artery leading to ischaemic optic neuropathy. Visual manifestations can also include diplopia (due to third, fourth or sixth cranial nerve palsies), blurred vision, amaurosis fugax and CRAO.
| The American College of Rheumatology requires three of the five diagnostic criteria: Age over 50 years New onset headache Temporal artery abnormality—tenderness on palpation or reduced temporal artery pulse ESR of over 50 mm/hour Positive temporal artery biopsy
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As the underlying vasculitis can affect a wide range of arteries, the subsequent modes of presentations are diverse. A full multi-system examination is essential including blood pressure readings in both arms to exclude aortic arch involvement. Clinical features which may support a diagnosis are:
- Scalp tenderness
- Jaw claudication
- General malaise and fatigue
- Fever
- Polymyalgia rheumatica (30% of patients also have temporal arteritis)
- Hemiplegia or epilepsy if intracerebral artery involvement
- Angina or myocardial infarction
Ophthalmic examination often reveals evidence of ischaemic disease. Once the diagnosis is suspected, an immediate referral to ophthalmology is necessary. Biopsy of the temporal artery remains the gold standard for diagnosis although the presence of skip lesions reduces its accuracy to 60–80%.
Prednisolone is the mainstay of treatment, 40 mg/day in the absence of ocular symptoms increased to up to 80 mg/day with visual loss. If temporal arteritis is not treated, the unaffected eye may become involved within 2 weeks. The dosage of steroids should be tapered down depending on the severity of symptoms and may take more than 1 year. Monitoring the ESR assesses the effectiveness of the treatment.
Relapses are relatively common and usually require the steroid dose to be increased to the level at which symptoms were previously controlled. Despite treatment, 10–15% of patients will develop complete or partial permanent blindness and steroid-related complications such as osteoporosis and corticosteroid myopathy can be an added problem.
Stroke
Stroke is a common cause of a homonymous hemianopia, although patients may complain of monocular loss of vision. It is important to consider stroke in the differential diagnosis, especially in patients with high cardiovascular risk. There is no specific treatment for the visual loss in stroke but visual recovery may occur over time.
Migraine
Migraine may be associated with transient monocular loss of vision, probably occurring secondary to choroidal or retinal arterial vasospasm. It is often associated with photopsia or teichopsia (zigzag lines).
The International Headache Society defines retinal migraine as the occurrence of at least two attacks of monocular scotoma or blindness lasting less than 1 hour and associated with headache within 1 hour of the event, occurring in the absence of ocular or structural vascular disorder. Refer all patients with suspected retinal migraine to an ophthalmologist to exclude other causes of visual loss.
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Summary |
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TOPAbstractThe GP curriculum--Statement...Questions to ask the...Examining the patient with...Causes of sudden visual...SummaryReferences |
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Seeing patients presenting with sudden visual loss need not be daunting.
- Take a thorough history, perform a focused examination and have a systematic approach enabling consideration of all possible causes of visual loss
- Invest in an ophthalmoscope early in your GP training career in order to get as much practice in using the equipment.
- If you do not feel confident with eye examinations, sit in with consultants in ophthalmology outpatients. This will not only enable you to understand what the patient will experience on referral but also will give you lots of practice at fundal examination through dilated pupils in a dark room.
Key points
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References |
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TOPAbstractThe GP curriculum--Statement...Questions to ask the...Examining the patient with...Causes of sudden visual...SummaryReferences |
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