Authors Saxena, Singh, and Menon (Saxena et al.) undertake the difficult task of analyzing the traumatic optic neuropathy (TON) literature. They correctly note that treatment has been controversial with a confusing array of small case series. Recent clinical series tend to indentify patients closer in time to injury compared to older series. Identifying TON patients close to the time of injury increases the opportunity to observe spontaneous visual recovery. The improved outcome is often incorrectly attributed to the use of high dose steroids or surgery rather than ascertainment bias. Saxena et al. leave the reader with the conclusion that high dose steroid treatment should be used to treat TON presenting with significant visual loss, cases diagnosed within 8 h of injury, and in cases where there has been visual deterioration after the injury (i.e. a lucid period). I disagree with the authors: High-dose steroids should not be given for TON under any circumstances.
The International Optic Nerve Trauma Study (IONTS) published in 1999, concluded that there was no clear evidence that corticosteroids or optic canal decompression were better than no treatment for TON. The IONTS authors opined that clinicians had to make individualized choices based on this limited data. In the context of the IONTS, the guidelines presented by Saxena et al. would have been reasonable. Since the publication of the IONTS, several lines of evidence, some cited by Saxena et al., have radically changed what is appropriate for high-dose corticosteroids.
The first of these studies is the Corticosteroid Randomization After Significant Head Injury (CRASH) trial published in 2004. This was a randomized, placebo-controlled study of high-dose methylprednisolone for head trauma. Patients were assigned within 8 h of trauma to treatment with placebo or high-dose methylprednisolone (30 mg/kg loading followed by an infusion of 5.4 mg/kg/h) for 48 h. The study was designed to include 20,000 patients, but recruitment was halted at 10,008 patients for patient safety reasons. Data revealed a higher risk of death from all causes 2 weeks after trauma in the corticosteroid-treated patients (21% vs. 18% mortality, P = 0.0001). This is one excess death for every 31 patients treated. TON commonly occurs in the setting of concomitant head trauma, so this study has immediate relevance. No study of TON had used death as a study end point. We now understand that treatment of TON with high-dose steroids will cause treatment-associated mortality.
What evidence exists that demonstrates the efficacy of high-dose corticosteroids for TON that might balance the potential risks? In the intervening years since the IONTS, no new studies have established such a benefit. The authors cite one animal study that suggests high-dose corticosteroids are toxic to traumatically injured optic nerve. Two other animal studies also support this conclusion. There are no well-designed clinical studies that support the use of high-dose corticosteroids for TON. The CRASH study proves this treatment causes loss of life in the setting of head trauma. Taken together, these lines of evidence suggest that TON patients treated with high dose corticosteroids are improving despite this treatment. As pointed out by Saxena et al., limited data suggests that corticosteroids treatment equivalent to methylprednisolone 1 mg/kg every 6 h may not be harmful to traumatically injured optic nerve. This means that patients with TON who might benefit from standard doses of corticosteroids for other conditions can continue to receive them. It does not imply in anyway that these corticosteroids are useful for treating TON. Unless new experimental data defines a role for high dose steroids, their use in the treatment of TON should be abandoned.
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Conflict of Interest: None declared.