Bilateral traumatic optic neuropathy in an unconscious patient: a diagnostic challenge.

treated with corticosteroids was found to have a statistically significant higher mortality rate compared to the placebo group [4]. This means that not only is the treatment with high dose corticosteroids not beneficial in cases of TON, it may in fact be harmful when given to patients with severe head trauma and brain injury. We present the case of a patient with bilateral TON. Bilateral TON is far less common than unilateral TON but is more meaningful functionally due to the likelihood of severe bilateral visual loss as its final outcome. In this case the diagnosis was difficult because the patient was anes-thetized and could not verbalize his visual loss following the trauma and visual acuity could not be examined. Bilateral involvement is not typical of traumatic optic neuropathy and is more commonly seen in other optic neuropa-thies such as arteritic optic neuropathy, infectious optic neuropathy in children, and toxic optic neuropathy [5]. Patient descriPtion A 75 year old Caucasian man experienced direct head, face and chest injury upon falling forward after stumbling on a low fence. His past medical history included lym-phoma in full remission for 10 years and no other known ocular or systemic pathologies. The patient arrived at the trauma unit 30 minutes after the fall. Gross neurologic examination was normal except for dilated unresponsive pupils. The patient was anesthetized and ventilated because of restlessness and nose-bleeding. Computed tomography revealed a subarachnoid hemorrhage without a mass effect. Chest t raumatic optic neuropathy is the result of an indirect optic injury caused by a contusion necrosis of the nerve fibers related to the shearing forces generated during the trauma, especially in the intra-canalicular part of the optic nerve. TON 1 may be a consequence of a relatively mild injury, especially in the case of trauma to the forehead region. TON usually causes immediate and severe visual loss which is unilateral in most cases [1]. In retrobulbar TON the optic disk appears normal at onset and atrophies within 4–8 weeks. In unilateral cases the affected eye demonstrates a relative affer-ent pupillary defect. Transethmoidal optic canal decompression and/or high dose intravenous corticosteroids were suggested as possible treatments for TON, in addition to follow-up. The International Optic Nerve Trauma study, a non-randomized multi-center comparative analysis of treatment outcomes, did not demonstrate a beneficial effect of either of these treatments [2,3]. The Corticosteroid Randomization After Significant Head Injury (CRASH) study included over …