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Show POINT COUNTER POINT Editor's note: In this section, two experts have debated a controversial issue based on case material and questions directed to them via E- mail. Neither contestant was aware of the other's responses until all of the questions were answered. Then they were shown all responses and asked to write a rebuttal. The editor's summary appears at the end. Leonard A. Levin MD, PhD University of Wisconsin Madison, Wisconsin Robert S. Baker MD University of Kentucky Lexington, Kentucky Management of Traumatic Optic Neuropathy A40- year- old man has sustained a traumatic brain injury in a motor vehicle accident earlier in the day. He is sedated on a ventilator, unresponsive to verbal commands. Computed tomography shows no skull fractures, brain edema, or hemorrhage. He has mild ecchymosis over the left brow and eyelids and a left afferent pupil defect. Otherwise the eye examination is normal. His wife reports that before the accident, he had had no eye problems. You diagnose traumatic optic neuropathy, OS. What diagnostic tests and treatment do you recommend? Leonard A. Levin MD, PhD: I explain to the spouse and document in the chart that the patient probably has an optic nerve injury, but that I cannot tell how severe it is. I also explain that people have tried treatments for optic nerve injuries related to trauma, but that we really don't know whether any of them are more effective than observation alone ( 1). I explain that some specialists use high- dose corticosteroids to treat unconscious patients who have optic nerve injuries, but that others just observe the patient, and that there is no consensus. Even though short- term corticosteroids are probably safe ( 2), there is no evidence that they will help. Given that the patient is unconscious and that we do not know the severity of his injury, the risks of canal decompression do not outweigh the possible benefits. Therefore, I explain that we can either treat with corticosteroids or not. If I am asked what I would want done if it were I who was injured, I answer that I might try corticosteroids, knowing they are not a proven therapy. If I were to institute steroids, I would prescribe a methylprednisolone 30 mg/ kg intravenous bolus, then 5.4 mg/ kg/ h intravenously for 48 hours ( 3). I recommend an H2 antagonist to protect the gastric mucosa. Robert S. Baker MD: I would review the computed tomography ( CT) scan carefully to assure myself that there was no missed roof fracture, especially given the bruise over the brow. If no fractures are present and there are no systemic or neurosurgical contraindications, I would start spinal cord injury protocol corticosteroid doses: a Solumedrol 30 mg/ kg load intravenously, followed by Solumedrol 5.8 mg/ kg/ h for 47 hours. Would your recommendations differ if the patient were neurologically intact apart from the traumatic optic neuropathy? Leonard A. Levin MD, PhD: If the patient were awake and cooperative, the visual loss severe, and I were at an institution with a surgeon familiar with transethmoidal canal decompression, then I would mention the possibility of doing the procedure, but still emphasize the lack of good evidence for choosing a therapy. Robert S. Baker MD: I would not change my treatment plan based on coincident neurologic impairment, unless there was risk of central nervous system infection with corticosteroids. There is evidence that comatose patients and conscious patients have similar outcomes with similar treatment plans ( 4). Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. 72 JNeuro- Ophthalmol, Vol. 23, No. 1, 2003 POINT COUNTER POINT JNeuro- Ophthalmol, Vol. 23, No. 1, 2003 What if the patient had imaging evidence of an optic canal fracture? Leonard A. Levin, MD, PhD: I am not convinced that there is good enough evidence that the presence of a displaced fragment is enough to shift the risk/ benefit equation in favor of canal decompression. Robert S. Baker MD: Optic canal fracture has been found by some authors to have a worse prognosis than no fracture, so the tempta- Leonard A. Levin MD, PhD: It has to be intrasheath hemorrhage to justify fenestration. Robert S. Baker MD: Nerve sheath hemorrhage occurs rarely and the images must be looked at together by an experienced neuro- Leonard A. Levin MD, PhD: Yes, there was a significant difference in a post- hoc analysis between patients treated with methylprednisolone and placebo greater than 8 hours after the injury, in the subgroup of patients with incomplete injuries, where motor tion to immediately decompress the canal is heightened. However, no convincing evidence to support this plan has been forthcoming ( 5). In the absence of a definitive study, I recommend individualization of patient planning. In general, I do not recommend early canal decompression for fractures unless there is a displaced fragment impinging on the optic nerve ( 6). radiologist and clinician to avoid calling peri- sheath blood an intrasheath hemorrhage. If intrasheath blood is convincingly demonstrated, I recommend optic nerve sheath fenestration. function was compared below the level of the injury. However, it is interesting that patients givenplacebo did twice as well when administered the placebo more than 8 hours after injury, compared with when placebo was given within 8 hours of injury. This suggests some fairly major differ- What if the patient had imaging evidence of hemorrhage within the optic nerve sheath in the orbit? What if the patient had had documented loss of vision in the affected eye within the previous 24 hours? What if the patient had no useful vision in the other eye? What if the patient were under 20 years of age? Leonard A. Levin MD, PhD: Robert S. Baker MD: No change in recommendations. This would not change my treatment plan. Given that the Bracken study of steroid treatment of acute spinal cord injury ( 7) showed that patients begun on treatment more than 8 hours after the injury actually fared worse than those not treated, would you alter your recommendations if more than 8 hours had elapsed from time of injury to the time of your consultation? Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. 73 JNeuro- Ophthalmol, Vol. 23, No. 1, 2003 POINT COUNTER POINT ence( s) between the groups given treatment before and after 8 hours. Of course, there could be no random assignment to the groups based on delay until treatment! We should therefore be very cautious in extrapolating from this post- hoc analysis. Some of this is discussed in subsequent correspondence about the quoted article ( 8). Overall, I believe that it is difficult to extrapolate timing figures from the National Acute Spinal Cord Injury studies ( NASCIS), because they studied a very different part of the central nervous system from the optic nerve. What ought to Leonard A. Levin MD, PhD: Some ophthalmologists treat their patients who have traumatic optic neuropathy with megadose corticosteroids, some do canal decompression, and others simply observe them. We have not been routinely doing surgical decompression of the optic canal via an extracranial approach. I don't believe there is a consensus of what is the best therapy Robert S. Baker MD: It is comforting and depressing that Dr Levin and I have such uniformity in our approach to this problem. Any enthusiasm we may muster in formulating a plan for these patients is based on the spinal cord decompression trial ( 3,7) or on case reports or case series. Hopefully, at some point, a controlled trial will be carried out to enlighten us, or an effective neuroprotective agent will be discovered to make the whole surgical debate moot. Detailed discussions with a patient's family in these circumstances are usually of limited benefit. The family is already overwhelmed by the tragedy of the accident and the fact that the patient is in a coma or facing other threats to survival. I differ from Dr. Levin in telling the family what I would recommend without a great deal of talk about controversy and uncertainty. This is not to say I neglect informed consent, but I simply try not to further burden the family with my insecurity. guide us are studies of traumatic optic neuropathy. Unfortunately we don't have results from a randomized controlled trial to help us. Robert S. Baker MD: I would not treat if more than 8 hours had elapsed, unless there were a fracture fragment impinging on the optic nerve, in which case I would remove it up to 48 hours post- injury. for traumatic optic neuropathy, primarily because we don't have good evidence to guide us. Robert S. Baker MD: I think my approach is similar to that of other ophthalmologists and neuro- ophthalmologists. I know oculo-plastic surgeons who believe that all traumatic optic neuropathy should be decompressed as soon as possible. I agree with Dr. Levin's point that canal decompression is recommended only if " an experienced surgeon is available.' This procedure takes place in a very small area surrounded by unforgiving structures. Outcome is influenced by the surgeon's skill and experience. Leonard A. Levin MD, PhD: I share with Dr. Baker the frustration from not having a proven therapy for this disorder. I agree that families should not be burdened by excessive information or uncertainty, but still believe that explaining there is no proven therapy is part of caring for these patients. Most importantly, I agree that results from a randomized controlled trial, perhaps of a neuroprotectant, will ultimately help us provide the best care for our patients with traumatic optic neuropathy. Do you think your approach to the management of traumatic optic neuropathy is typical of most North American ophthalmologists, neuro- ophthalmologists, or other surgical specialists who care for such patients? If not, how does it differ? Rebuttals Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. 74 © 2003 Lippincott Williams & Wilkins POINT COUNTER POINT JNeuro- Ophthalmol, Vol. 23, No. 1, 2003 Editor's Summary Not a very heated debate, is it? Forgive the contestants, for they both realize that there is very little evidence to guide their management. They acknowledge that the only basis for thinking that high- dose corticosteroid treatment helps a traumatized optic nerve is that it helps a traumatized spinal cord ( 3). But they also realize that a nonrandomized study of traumatic optic neuropathy ( 1) found that neither high dose corticosteroid treatment nor surgical optic canal decompression worked better than mere observation. Without citing any solid support or sounding very convinced, both contestants seem to favor optic canal de- 1. Levin LA, Beck RW, Joseph MP, et al. The treatment of traumatic optic neuropathy: The International Optic Nerve Trauma Study. Ophthalmology 1999; 106: 1268- 77. 2. Wing PC, Nance P, Connell DG, et al. Risk of avascular necrosis following short- term megadose mefhylprednisolone treatment. Spinal Cord 1998; 36: 633- 6. 3. Bracken MB, Shepard MJ, Holford TR et al. Administration of mefhylprednisolone for 24 or 48 hours or tirilazad mesylate for 48 hours in the treatment of acute spinal cord injury. Results of the Third National Acute Spinal Cord Injury Randomized Controlled Trial. National Acute Spinal Cord Injury Study. JAMA 1997; 277: 1597- 604. 4. Lubben B, Stoll W, Grenzenbach U. Optic nerve decompression in compression under certain circumstances- Dr. Levin if there is " a surgeon familiar with transethmoidal canal decompression" and Dr. Baker if there is imaging evidence of " a displaced fragment impinging on the optic nerve." They agree on intraorbital optic nerve sheath fenestration in the rare instance that intrasheath blood is convincingly demonstrated. Otherwise, they both long for guidance from that randomized study in the sky. Until then, treatment seems to be founded on anecdote, faith, and surgical bravado. the comatose and conscious patient after trauma. Laryngoscope 2001; 111: 320- 8. 5. Wang BH, Robertson BC, Girotto JA, et al. Traumatic optic neuropathy: a review of 61 patients. Plast Reconstr Surg 2001; 107: 1655- 64. 6. Frenkel RE, Spoor TC. Diagnosis and management of traumatic optic neuropathies. Adv Ophthalmic Plast Reconstr Surg 1987; 6: 71- 90. 7. Bracken MB, Holford TR. Effects of timing of mefhylprednisolone or naloxone on recovery of segmental and long- tract neurologic function in NASCIS 2. JNeurosurg 1993; 79: 500- 7. 8. Rosner MJ. Treatment of spinal cord injury ( comment). J Neuro-surg 1994; 80: 954- 5. REFERENCES Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. 75 |
