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Pathogenesis
- Occlusion of the short posterior ciliary arteries (microvascular, not embolic)
Causes and risk factors for N-AION
- ocular: small disc diameter = ‘disc at risk’, optic nerve head drusen
- cardiovascular risk factors: Hypertension, diabetes mellitus, hyperlipidaemia, smoking
- obstructive sleep apnoea syndrome (OSAS)
- Medications: phosphodiesterase-5 inhibitors (e.g. Viagra/Sildenafil), interferon-alpha, amiodarone, sympathomimetics
- Nocturnal hypotension
- Surgeries = perioperative ischaemic optic neuropathy: (e.g. coronary bypass surgery, spinal surgery, radical neck dissection, etc.) -> more frequently posterior ischaemic optic neuropathy (PION)
- prothrombotic conditions, including homocysteinemia, collagenoses, vasculitides, antiphospholipid syndrome
Findings
- Acute to subacute, unilateral, painless visual loss (hours to days)
- diffuse or sectorial hyperaemic optic disc swelling, often associated with splinter-shaped peripapillary haemorrhages
- typically altitudinal, usually nasally accentuated visual field defect
Work-up
- History: symptoms of giant cell arteritis, cardiovascular risk factors, sleep apnoea syndrome, secondary diagnoses/operations, medication (see above), nicotine
- Rule out arteritic AION: Clinical findings, laboratory (blood count, CRP, ESR) (see giant cell arteritis)
- Measure blood pressure -> hypertensive crisis? Overtreatment in case of too low blood pressure?
- Cardiovascular risk factors: hypertension (24h blood pressure), blood lipids, blood glucose, creatinine (kidney function), (carotid duplex not necessary, not embolic)
- Screening for sleep apnoea syndrome
- In young patients (<50 years) consider additional work-up regarding prothrombotic conditions: Protein S, antithrombin III, lupus coagulans, anticardiolipin-antibody, ds-DNA-antibody, homocysteine, (Factor V Leiden mutation, APC resistance)
- Visual field examination
- Depending on history: MRI head/orbit to exclude infiltrative optic neuropathy
Management
- Treat cardiovascular risk factors: especially blood pressure, therapy of sleep apnoea syndrome
- In acute N-AION: consider sleeping without a pillow for the next 2 nights and raising the lower end of the bed a little -> better perfusion of the disc
- Consider lifelong Aspirin cardio 100mg/d prophylactically (controversial)
- in acute hypertensive crisis (>190mmHg/110mmHg) -> administer beta blockers as 1st choice (as beta blockers do not cause vasoconstriction), if not contraindicated (asthma)
- in case of known hypertension and overtreatment (e.g. BP of 110/60mmHg) -> consider reducing current antihypertensive medication (consult general practitioner), as hypoperfusion is bad for the optic nerve!
- Consider steroid therapy (no clear evidence)
Follow-up
- e.g. after 2 and 4 weeks, then after 3 and 6 months, possibly after 1 year (until findings are stable and work-up has been finished)
- in case of progressive visual field defects or increasing optic disc edema: repeat work-up for A-AION and consider MRI head/orbit.
Prognosis
- Visual field defects can improve over months up to >1 year (driving ability?)
- In approx. 40% of patients there is a partial recovery of visual acuity, in 50% it remains the same, in approx. 10% it worsens
- Second episode in the same eye is rare
- Risk of involvement of the other eye: 15-25%
Sources
- EyeWiki Non-Arteritic Anterior Ischemic Optic Neuropathy (NAION)
- The Wills Eye Manual: Office and Emergency Room Diagnosis and Treatment of Eye Disease; Nika Bagheri MD, Brynn Wajda MD, et al; Lippincott Williams&Wilkins; 7th Edition (2016)
- Kanski’s Clinical Ophthalmology: A Systematic Approach; Jack J. Kanski MD, Brad Bowling MD; Saunders Ltd.; 8th Edition (2015)