Posterior Ischaemic Optic Neuropathy

Infarction of the retrobulbar optic nerve (intraorbital, intracanalicular, or intracranial portions), supplied by pial vessels and branches of the ophthalmic artery, causing visual loss with a normal optic disc in the acute phase. It is much rarer than anterior ischaemic optic neuropathy and is a diagnosis of exclusion.

• Types:
  • Perioperative (most common): after spinal fusion in the prone position (incidence 0.03 to 0.1 percent), cardiac bypass, head and neck surgery, and other long operations (more than 6 hours), with risk factors of anaemia, hypotension, large blood loss (above 1 litre) and fluid shifts, facial oedema and raised venous pressure, and compression of the globe.
  • Arteritic: giant cell arteritis, an emergency, with severe visual loss and a normal disc.
  • Non-arteritic spontaneous: associated with vascular risk factors, severe hypotension, vasculitis, and hypercoagulability.
  • Others: radiation optic neuropathy, vasculitis (lupus, polyarteritis), and sphenoid sinus mucocele.

• Sudden painless loss of vision, often noticed on waking after surgery; may be bilateral in perioperative cases.
• Acuity from mild reduction to no light perception; relative afferent pupillary defect (unilateral or asymmetric); dyschromatopsia; altitudinal, central, or cecocentral defects.
• Fundus normal at presentation, then optic disc pallor develops at 4 to 8 weeks.
• Giant cell arteritis: headache, scalp tenderness, jaw claudication, raised ESR and CRP.
• Perioperative: exclude cortical blindness and retinal ischaemia (central retinal artery occlusion after prone positioning).

• Exclusion of other causes: compressive and infiltrative lesions, optic neuritis, central retinal artery occlusion, raised intracranial pressure, and toxic and nutritional neuropathy.
• MRI brain and orbits with contrast and diffusion-weighted imaging: restricted diffusion in the optic nerve supports infarction, while excluding compression or demyelination.
• ESR, CRP, platelets, and temporal artery biopsy or ultrasound in patients over 50; blood count and haemoglobin; blood pressure review; ANA, ANCA, antiphospholipid antibodies; carotid and cardiac assessment.
• Visual fields, optical coherence tomography (retinal nerve fibre thinning later), and visual evoked potentials.
• Review of anaesthetic record (mean arterial pressure, haemoglobin, blood loss, positioning, operation time).

• Giant cell arteritis: treat immediately with intravenous methylprednisolone 1 g daily for 3 days, then prednisolone 1 mg/kg daily with slow taper, aspirin 75 mg, and steroid-sparing agents (tocilizumab 162 mg weekly).
• Perioperative: maintain mean arterial pressure and haemoglobin (transfuse if haemoglobin falls below 8 to 10 g/dL in a high-risk patient), restore blood volume, treat hypotension, elevate the head and reduce facial and orbital pressure, avoid pressure on the eyes, and optimise oxygenation. No therapy has been proven to restore vision; steroids and erythropoietin have not been shown to help.
• Stop contributing drugs and control vascular risk factors (blood pressure, diabetes, lipids, smoking), with antiplatelet therapy for vascular disease.
• Prevention for high-risk surgery: avoid prolonged prone surgery, stage lengthy operations, limit blood loss, keep head level with or above the heart, pad the face, avoid hypotension and severe anaemia, and inform patients about the risk.
• Consent and documentation, low-vision support, and psychological counselling.
• Prognosis: poor; final vision stays severely reduced in most, with partial recovery in about one-third in some series.