Traumatic optic nerve damage after craniofacial injury was first described by Hippocrates.1 Although the natural history of traumatic optic neuropathy is unknown, recent studies suggest that high dose steroids and, even surgical decompression of the optic canal or the nerve sheath (in cases of nerve sheath hematoma) may restore vision in selected patients.2-8 The commonest cause of optic nerve trauma is road-traffic accidents, when the patient has poly-trauma with head injury and the visual loss is noticed only after the general condition of the patient improves. Isolated trauma of the optic nerve is usually associated with blunt skull trauma involving fractures of both skull and optical canal, but may also occur from blunt ocular trauma.9 Iatrogenic trauma to the optic nerve is not unknown.
The part of the optic nerve most vulnerable to blunt trauma of the head is the intracanalicular segment, which by virtue of its bony course is vulnerable to the fractures and compressive-elastic forces of its surrounding bone, which also being unyielding, allows for no space for inflammatory expansion or hemorrhage.10 Optic neuropathy following accidental trauma usually results from two distinct mechanisms: A primary injury as a result of a direct contusive force on the optic canal and nerve, which if untreated results in a secondary ischemia with further damage to the nerve.
Clinical assessment should include testing of visual acuity, extraocular muscle motility and papillary reactivity, visual field assessment and direct/indirect ophthalmoscopy. Visual evoked potentials (VEPs) to flash stimulation and the electroretinogram (ERG) might be supportive in unresponsive patients in the immediate aftermath of the traumatic event.11,12 The role of neuroimaging remains controversial, and practice varies between institutions. Recently, ultrasonography has been advocated to screen and detect abnormalities in optic nerve diameter.
Currently, there is no validated approach to the management of traumatic optic neuropathy. Thus, with numerous conflicting reports on the management of traumatic optic neuropathy, there is little world consensus on the optimal management of this condition. Keeping in mind the above, we have devised a management protocol for the same, simultaneously discussing the role of conservative/medical management as well as the surgical protocols followed by us.
Discussion and conclusion
In summary, optic nerve decompression alone or combined with decompression of the nerve sheath may be indicated in selected patients who fail to respond to high-dose intravenous steroids. The definitive role of surgery in the management of traumatic optic neuropathy remains unclear. There is a need for a large, prospective, randomized controlled trial to assess the different therapeutic approaches in traumatic optic neuropathy, but such a trial may be challenging given the low frequency of the condition and the difficulties inherent in randomizing patients.