Anterior Ischaemic Optic Neuropathy
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Anterior ischaemic optic neuropathy (AION) = sudden loss of blood supply to the head of the optic nerve (part of the nerve which enters the eye)
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results from occlusion of the short posterior ciliary arteries
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Split into 2 categories:
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Arteritic (giant cell arteritis) ​
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Non-arteritic​​
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Arteritic anterior ischaemic optic neuropathy (AAION)
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Occurs as a result of giant cell arteritis
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this refers to a disease where there is swelling and inflammation of medium to large arteries, including major branches of the aorta and the superficial temporal artery, ophthalmic artery, and posterior ciliary arteries
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Patients are typically aged >65 years
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Associated with polymyalgia rheumatica (PMR) - pain and stiffness of the shoulders and proximal lower limbs
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GCA may occur without causing an arteritic AION but it is extremely important to ask and assess for vision problems, as once they occur, the visual prognosis is poor
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if no ocular involvement, management by medical teams - usually rheumatologists​
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If vision loss occurs - pain rarely reported in the eye itself (but scalp tenderness/headache typical)
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may describe transient obscurations within visual field in preceding weeks, or sudden painless unilateral vision loss​
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Extremely important not to miss this diagnosis - can be fatal (cause myocardial infarction and strokes), and can lead to rapid, irreversible vision loss - may progress to second eye if untreated
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Non-arteritic anterior ischaemic optic neuropathy (NAAION)
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Associations
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may be seen with an anatomically small optic disc (optic nerve head), which is crowded meaning there is less room for the vessels supplying it, so they are predisposed to occlusion
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cardiovascular risk factors (same as for stroke)​
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hypertension​
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diabetes mellitus
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hyperlipidaemia
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smoking
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antiphospholipid syndrome
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cataract surgery
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age >50 years
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Need to rule out giant cell arteritis in a patient; if no inflammatory cause, tends to be related to same risk factors as other forms of stroke/ vein occlusions
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Symptoms
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sudden, unilateral, painless loss of vision
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often noted on waking from sleep - likely a result of reduced perfusion of the optic nerve at night due to nocturnal hypotension​
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if arteritic - other typical findings include scalp tenderness, jaw claudication (pain on eating/talking), headache, weight loss, fevers, night sweats
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Examination findings
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reduced visual acuity - moderate to severe impairment most often in non-arteritic; if arteritic, typically severe
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visual field defects
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may be altitudinal - loss of superior or inferior part of vision which stops at the horizontal midline​
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pale, swollen optic disc on slit lamp examination
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pale due to loss of blood supply​
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in arteritic AION - prominent superficial temporal artery, tender, may be pulseless, cord-like
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Investigations for AION
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Investigations for GCA
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Blood tests - high ESR, CRP, platelets, anaemia
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Temporal artery biopsy
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should occur within 3 days of starting steroids​ - should not delay initiation of steroid treatment
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Colour Doppler and duplex ultrasonography of superficial temporal artery - shows oedema (swelling ) within artery wall​
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Investigations for causes of non-arteritic AION
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blood pressure​
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fasting lipid blood test, HbA1c, clotting screen
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Management
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Arteritic:
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IV steroids (methylprednisolone) usually for 3 days​
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followed by high dose oral steroids (prednisolone) for 4 weeks
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followed by a tapering course of oral steroids
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antiplatelet therapy e.g. aspirin started & continued indefinitely
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Prognosis is poor - vision loss usually permanent
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treatment mainly aims to prevent recurrence in the other eye​
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Non-arteritic: ​
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no specific treatment available​
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some ophthalmologists treat with a short course of oral steroids
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sometimes treated with aspirin - but not shown to reduce risk of recurrence in fellow eye
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manage underlying conditions e.g. hypertension, antiphospholipid syndrome
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some improvement in vision may be seen
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References
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Salmon, J. F. (2019) Kanski’s clinical ophthalmology. 9th edn. London, England: Elsevier Health Sciences.