Ischaemic Optic Neuropathy After Surgery

Ischaemic optic neuropathy (ION) after surgery is infarction of the optic nerve head (anterior) or retrobulbar nerve (posterior), causing painless, often severe and irreversible visual loss. Posterior ION accounts for most spine surgery cases.

Epidemiology. It is the commonest cause of postoperative vision loss after non-ocular surgery (about 1 in 30,000 to 1 in 125,000 overall; about 0.03% to 0.2% after spinal fusion, and 0.06% to 0.113% after cardiac surgery). Bilateral involvement is common (about 50% of posterior ION).

Risk factors. Prone position, surgery over 6 hours, blood loss over 1 L, anaemia, hypotension, large volume crystalloid resuscitation, male sex, obesity, Wilson frame, small cup-to-disc ratio ("crowded disc"), vascular disease, diabetes, hypertension, smoking and sleep apnoea.

Pathophysiology.

The optic nerve head has a precarious blood supply from short posterior ciliary arteries, and the retrobulbar nerve is supplied by the pial network. Reduced perfusion pressure (blood pressure minus intraocular pressure or venous pressure), anaemia and optic nerve oedema in a tight canal cause infarction.

Painless visual loss noticed on waking up to 3 days after surgery, central or altitudinal field loss, reduced colour vision, relative afferent pupillary defect (if unilateral), and disc swelling with haemorrhages (anterior) or a normal disc initially (posterior). Disc pallor appears at 4 to 6 weeks.

Red flags.

• Bilateral loss.
• Eye pain or ophthalmoplegia (arterial occlusion, compressive).
• Headache with jaw claudication (arteritis).
• Neurological deficit.

Ophthalmology examination with fundoscopy, visual fields, optical coherence tomography and visual evoked potentials. MRI brain and orbits with diffusion (restricted diffusion in the nerve) to exclude cortical infarct, compression and pituitary apoplexy. Inflammatory markers to exclude arteritis.

Differential diagnosis.

• Central retinal artery occlusion.
• Cortical blindness.
• Optic neuritis.
• Giant cell arteritis.
• Compressive optic neuropathy.
• Pituitary apoplexy.

No proven treatment reverses damage. Provide supportive care and correct predisposing factors.

• Correct anaemia: transfuse red cells to haemoglobin 80 to 100 g/L when ischaemia is suspected, and maintain mean arterial pressure at 65 mmHg or more (at baseline in chronic hypertension); keep head at or over heart level when possible.
• Aspirin 75 mg orally daily may be given for vascular risk after specialist advice; maximum 300 mg daily; monitor bleeding.
• Acetazolamide, steroids, erythropoietin and neuroprotection lack proven benefit; use only in specialist settings.

Arrange visual rehabilitation, low vision aids, driving assessment, psychological support and secondary prevention (control of hypertension, diabetes and sleep apnoea).

Prevention. In high risk prone spine surgery: keep the head neutral at or over heart level, free of pressure, maintain mean arterial pressure near baseline, limit crystalloid and use colloid or blood as needed, keep haemoglobin over 80 g/L, stage long operations, and inform patients of the risk before surgery.

Monitoring. Vision checks on waking, then at 24 hours, with ophthalmology follow up at 1 week, 4 to 6 weeks and 3 months.

Referral and escalation. Urgent ophthalmology and neuro ophthalmology. Disclosure and reporting.