The optic nerve transmits visual information from the eye to the brain and traumatic optic neuropathy (TON) refers to any injury to the optic nerve secondary to trauma. After the optic nerve has been injured, it becomes more swollen and this can lead to further damage. Traumatic optic neuropathy often results in severe visual loss and the vast majority of affected people are young males in their thirties. Since the early 1980s, steroids have been used in an attempt to reduce the abnormal swelling that follows an injury to the optic nerve and improve visual recovery. However, the role of steroids in TON is controversial and clinicians remain divided over the best management strategy. The recommendations in this review are based on a critical analysis of the available evidence in the medical literature. We found only one, relatively small, randomised controlled trial of steroids in TON, which included 31 participants within seven days of their initial injury. These participants received either high dose intravenous steroids (n = 16) or placebo (n = 15). At three months follow-up, no significant difference in best corrected visual acuity was found between these two groups. There is a relatively high rate of spontaneous visual recovery in TON and no convincing data that steroids provide any additional benefit over observation alone. Each case needs to be assessed on an individual basis and the patient needs to be made fully aware of the possibility of a serious adverse reaction, although rare, to steroids. Furthermore, recent studies have highlighted possible detrimental effects of steroids when used in brain and spinal cord injuries and these new lines of evidence need to be considered seriously.
There is a relatively high rate of spontaneous visual recovery in TON and there is no convincing data that steroids provide any additional visual benefit over observation alone. Recent evidence also suggests a possible detrimental effect of steroids in TON and further studies are urgently needed to clarify this important issue. Each case therefore needs to be assessed on an individual basis and proper informed consent is paramount.
Traumatic optic neuropathy (TON) is an important cause of severe visual loss following blunt or penetrating head trauma. Following the initial injury, optic nerve swelling within the optic nerve canal can result in secondary retinal ganglion cell loss. Optic nerve decompression with steroids or surgical interventions or both has therefore been advocated as a means of improving visual prognosis in TON.
The aim of this review was to examine the effectiveness and safety of using steroids in TON.
We searched CENTRAL (which contains the Cochrane Eyes and Vision Group Trials Register) (The Cochrane Library 2013, Issue 4), Ovid MEDLINE, Ovid MEDLINE In-Process and Other Non-Indexed Citations, Ovid MEDLINE Daily, Ovid OLDMEDLINE, (January 1950 to May 2013), EMBASE (January 1980 to May 2013), Latin American and Caribbean Literature on Health Sciences (LILACS) (January 1982 to May 2013), Web of Science Conference Proceedings Citation Index- Science (CPCI-S) (January 1990 to May 2013), the metaRegister of Controlled Trials (mRCT) (www.controlled-trials.com), ClinicalTrials.gov (http://clinicaltrials.gov) and the WHO International Clinical Trials Registry Platform (ICTRP) (www.who.int/ictrp/search/en). We did not use any date or language restrictions in the electronic searches for trials. We last searched the electronic databases on 21 May 2013. We also searched the reference lists of included studies, other reviews and book chapters on TON to find references to additional trials. The Science Citation Index was used to look for papers that cited the studies included in this review. We did not manually search any journals or conference proceedings. We contacted trial investigators and experts in the field to identify additional published and unpublished studies.
We planned to include only randomised controlled trials (RCTs) of TON in which any steroid regime, either on its own or in combination with surgical optic nerve decompression, was compared to surgery alone or no treatment.
Two review authors independently assessed the titles and abstracts identified from the electronic searches.
We included one study that met our selection criteria; a double-masked, placebo-controlled, randomised trial of high dose intravenous steroids in patients with indirect TON diagnosed within seven days of the initial injury. A total of 31 eligible participants were randomised to receive either high dose intravenous steroids (n = 16) or placebo (n = 15), and they were all followed-up for three months. Mean final best corrected visual acuity (BCVA) was 1.78±1.23 Logarithm of the Minimum Angle of Resolution (LogMAR) in the placebo group, and 1.11±1.14 LogMAR in the steroid group. The mean difference in BCVA between the placebo and steroid groups was 0.67 LogMAR (95% confidence interval -1.54 to 0.20), and this difference was not statistically significant (P = 0.13). At three months follow-up, an improvement in BCVA of 0.40 LogMAR occurred in eight eyes (8/15, 53.3%) in the placebo group, and in 11 eyes (11/16, 68.8%) in the treatment group. This difference was not statistically significant (P = 0.38).