Non-Arteritic Anterior Ischemic Optic Neuropathy (N-AION)

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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)