Traumatic Optic Neuropathy

Acute injury to the optic nerve from trauma, causing visual loss. Occurs in about 0.5 to 5 percent of closed head injuries and 2.5 percent of facial fractures; commonest in young men after motor vehicle crashes, falls, assaults and cycling accidents.

• Direct: penetrating injury, bone fragment, intraneural or sheath haematoma, nerve avulsion or transection (immediate and usually irreversible).
• Indirect (more common): transmission of force through the skull to the intracanalicular optic nerve, usually after a frontal or frontotemporal blow, with shearing, contusion and ischaemia from oedema in the tight optic canal, even with minor visible injury.
• Associated injuries: frontal bone and orbital roof fractures, sphenoid and optic canal fractures, intracranial haemorrhage, loss of consciousness.

• Immediate or delayed (hours to days) reduced vision, from mild to no light perception (about 40 to 50 percent present with light perception or worse).
• Relative afferent pupillary defect (the key sign, may be the only sign, particularly in unconscious patients), dyschromatopsia, field defects (central, altitudinal or arcuate), normal fundus initially, disc pallor developing at 3 to 8 weeks.
• Eyebrow laceration, periorbital bruising, frontal haematoma, and signs of skull base fracture.
• Retrobulbar haemorrhage, orbital compartment syndrome, and globe injury must be distinguished.

• Visual acuity, pupil examination with swinging flashlight (the afferent defect), colour vision, visual fields, dilated fundus examination; document baseline.
• CT head and orbits with thin cuts through the optic canal (fracture of the canal, orbital apex, sphenoid sinus haematoma, haematoma in nerve sheath, retrobulbar haemorrhage); MRI orbit if no metal and when CT is non-diagnostic (nerve oedema, haematoma).
• Visual evoked potentials: useful in unconscious patients (reduced amplitude and delayed latency).
• Optical coherence tomography at follow up shows retinal nerve fibre layer thinning.
• Exclude other causes of visual loss (globe rupture, retinal detachment, vitreous haemorrhage, commotio, chiasmal injury, cortical injury).

• Treat reversible compressive lesions urgently: retrobulbar haemorrhage by lateral canthotomy and cantholysis, optic canal or sheath haematoma by surgical decompression, orbital compartment syndrome by decompression.
• Stabilise and treat life threatening injuries first, and continue careful monitoring of vision every 1 to 2 hours in the first 24 hours.
• Observation alone is a valid option: spontaneous improvement occurs in about 40 to 60 percent of cases.
• Corticosteroids: high dose methylprednisolone (30 mg/kg IV bolus, then 15 mg/kg after 2 hours and every 6 hours for 24 to 48 hours) has been used for indirect injury within 8 hours, but benefit is unproven; it increases mortality when there is significant head injury with intracranial involvement and should be avoided in such patients and when injury is more than 8 hours old. Many centres use a lower dose or none, after discussing risks with the patient.
• Surgical optic canal decompression (endoscopic transethmoidal or transcranial) for progressive visual loss, bony fragments impinging on the nerve, or lack of improvement after steroids, particularly when decompression is possible within 7 days; outcomes are not clearly better than observation.
• Other adjuncts under study: erythropoietin (5000 units/kg IV daily for 3 days) and neuroprotective agents, with insufficient evidence.
• Rehabilitation: low vision aids, driving and occupational advice; protective eyewear for the fellow eye.
• Prognosis: poor with no light perception initially, loss of consciousness, absent improvement after 48 hours, or optic canal fracture; better with initial light perception or better, no loss of consciousness, and early recovery in the first 48 hours.