The Treatment of Indirect Traumatic Optic Neuropathy with Corticosteroids

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Dear Simon,

I agree that, in a perfect world, basing our treatment choices on evidence-based medicine (EBM) from RCT is the preferred method. However, as we see from the discussion thus far, we are not always afforded this kind of information. Should we simply refuse to treat patients in the absence of EBM from RCT? Or should we use clinical judgement combined with the available evidence coupled with our individual past experience in combination with what we think is the best for the individual patient? Sackett and colleagues state it this way, and I favour their approach:

“External clinical evidence can inform, but can never replace, individual clinical expertise, and it is this expertise that decides whether the external evidence applies to the individual patient at all and, if so, how it should be integrated into a clinical decision. Similarly, any external guideline must be integrated with individual clinical expertise in deciding whether and how it matches the patient’s clinical state, predicament, and preferences, and thus whether it should be applied.”¹

The study by Entezari et al. is cited as the only RCT available on the use of corticosteroids to treat i-TON.² This was a small study with only 16 patients in the treatment group and 15 in the placebo group. After 3 months, 11 of the treated patients improved (68.8%) whereas 8 of the placebo group improved (53.3%). Although the difference between the two groups was not statistically significant, the trend for improvement was preserved at all times tested (2 weeks, 1 month, and 3 months) with no crossover at any time of the average visual acuities in each group.² With larger numbers would these difference result reach statistical significance?

The International Optic Nerve Trauma Study by Levin et al. is difficult to interpret regarding i-TON.³ They noted that initial visual acuity was a strong predictor of final visual acuity. One of three untreated i-TON patients improved from hand movement vision to a final visual acuity of 20/40 or better with a follow-up interval of at least 1 month, whereas 7 of 34 treated patients demonstrated similar improvement. All in all, they concluded the following:

“These results and the existing literature provide sufficient evidence to conclude that neither corticosteroids nor optic canal surgery should be considered the standard of care for patients with traumatic optic neuropathy. It is therefore clinically reasonable to decide to treat or not treat on an individual patient basis.”³

Similar conclusions, affording at least the option of treatment, have been reached by others.^4,5

Your comments about the NASCIS^6,7 and CRASH⁸ trials are noted. The Steinsapir et al. article refers to corticosteroid doses in this range⁹ and in a later article Steinsapir acknowledges that lower doses of methyprednisolone were not studied.¹⁰ I personally do not use NASCIS or CRASH doses of steroids, preferring to rely on the intravenous and oral dose used in the Optic Neuritis Treatment Trial.¹¹ My personal experience with the safety of this dose regimen in treatment of optic neuritis is confirmed by the statistics reported by the ONTT.¹¹ If indeed the corticosteroids were responsible for the two “more serious” cases cited, they represent a little more than 1% of those treated.

Carta and others studied 35 patients with i-TON who were all treated within 72 hours of injury with intravenous corticosteroids at NASCIS doses.¹² Thirteen percent of patients had visual improvement that began within 48 hours of initiating treatment; the remaining 87% did not improve, and failure to improve after 48 hours of corticosteroid treatment was a poor prognostic sign for further visual improvement. Three other variables heralded a poor prognosis for visual recovery: (1) presence of blood in the posterior ethmoidal air cells; (2) age over 40 years; and (3) loss of consciousness at time of head injury.

In another study, Lee and colleagues, found a spontaneous improvement in 24% of 33 patients not treated and in 20% of 56 patients treated with steroids or surgery.¹³ Poor visual outcomes were associated with poor initial visual acuities, orbital fractures and significant head injury.

Given the foregoing, my present approach to patients with i-TON who have visual acuities of 20/200 or less in the affected eye(s) is to give them the option of treatment with the ONTT regimen of 1 g of intravenous methylprednisolone for 3 consecutive days. If no improvement is noted, I discontinue treatment. If improvement occurs, oral prednisone is started after the third intravenous dose and tapered according to improvement in visual acuity.

I would not routinely treat an unconscious patient with corticosteroids for presumed i-TON.

For patients with initial visual acuities better than 20/200 I would also include the option of oral prednisone 1 mg/kg/day, with similar stipulations on a 3-day time window for improvement. I have treated two such patients who presented 6 and 7 days after injury, both of whom responded rapidly to oral corticosteroids at the above dose (Tomsak, unpublished observations).

The use of neuroprotective agents in treatment of i-TON holds promise, as discussed by Warner and Eggenberger.⁵

SIMON J. HICKMAN

Dear Bob,

I admire your approach and certainty and I am in no doubt that you always acts with your patients’ best interests at heart. Taking the approach of Sackett et al. is certainly tempting.¹ If I analyse my clinical practice in a more self-critical light than I would be comfortable with, then I am sure that there are many times when I have manipulated the clinical evidence in my mind to get to the answer that I want. There is a danger, however, of using Sackett et al. as a “Get Out Of Jail Free” card to justify the management decided upon. My concern here though, is that high-dose corticosteroids are not risk free and, in the absence of clear evidence of benefit, I will continue not to recommend them in cases of i-TON.

ROBERT L. TOMSAK

Dear Simon,

I would like to end our correspondence with a quote from Oscar Wilde:

“The truth is rarely pure and never simple.”¹

EDITOR’S COMMENT

We are grateful to Simon Hickman and Robert Tomsak for these thoughtful remarks. This controversy brings into sharp focus some of the limitations of evidence-based medicine. Firstly that the absence of evidence (or the absence of adequate evidence) in favour of an intervention is not the same as evidence against that intervention, as was facetiously emphasized in the “parachute” controversy.¹ Secondly the value of any intervention must take into account both any beneficial outcome demonstrated in a trial and the adverse effects: a judgement that can be difficult to quantify. Thirdly medical decisions are taken in the context of the individual case in front of the clinician, in the real world we do not have the luxury of “exclusion criteria”. We also see clearly in the above correspondence the influence of personality as an important component of the context: both the personality of the practitioner (who may prefer to avoid errors of omission on the one hand or errors of commission on the other) and not to forget the personality of the patient (who may desire everything going or to avoid all treatment unless mandatory).

In English law there are two levels of evidence, one is “beyond all reasonable doubt”, the criterion used for serious crimes and serious punishments where the consequences of an incorrect judgement are catastrophic. For lesser matters evidence is based on the “balance of probabilities”, this accepts that some judgements will go the wrong way but that overall more just than unjust decisions are made. We cannot allow ourselves to be paralysed by lack of evidence and neither can we promise at all times to “do no harm”: sometimes, like judges, politicians, generals, and other professionals, we have to use our experience, intuition, and common sense to make a judgement in the belief that overall we do more good than we do harm,

   Gordon Plant

What is your opinion of the use of corticosteriods in I-TON? The editors would like to publish readers’ short contributions (supported by references) on this issue. Why not share your experience with clinical colleagues elsewhere and help to establish a dialogue within our readership? If you have a particular view on this matter, please send an e-mail to the Editors (Gordon T. Plant: [email protected] or Walter Jay: [email protected]). Early responses would be appreciated.

   Gordon Plant and Walter Jay, 18th May 2011

Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.