|Year : 2016 | Volume
| Issue : 1 | Page : 11-13
Traumatic optic neuropathy: Why leave it to chance?… Maxillofacial Surgeon's perspective
Shreyas Gupte, Punam Navnath Nagargoje
Department of Oral Maxillofacial Surgery, Y.M.T. Dental College and Hospital, Mumbai, Maharashtra, India
|Date of Web Publication||11-Aug-2016|
Department of Oral Maxillofacial Surgery, Y.M.T. Dental College and Hospital, Kharghar, Mumbai, Maharashtra
Source of Support: None, Conflict of Interest: None
Aim: To find out the efficacy of megadose steroid therapy as a treatment modality for traumatic optic neuropathy.
Materials and Methods: Six cases sustaining maxillofacial injuries without associated head injury and reporting with diminished vision were evaluated. The patient's history was noted and necessary neurologic and ophthalmologic consultations, radiologic investigations, and subjective and objective assessments of the optic nerve function were carried out. All the cases were managed nonsurgically with megadose steroid therapy. In all cases, vision improvement was noted.
Statistical Analysis: Since sample size was small, this was an observational study and could not be subjected to statistical analysis.
Results: Overall results were reasonably good with early megadose steroid therapy in traumatic optic neuropathy.
Conclusions: Early identification and management may result in better outcome of the condition. Within the limitations of the study design, this study points benefit of this treatment as salvage therapy for traumatic optic neuropathy.
Keywords: Maxillofacial trauma; megadose steroid therapy; traumatic optic neuropathy
|How to cite this article:|
Gupte S, Nagargoje PN. Traumatic optic neuropathy: Why leave it to chance?… Maxillofacial Surgeon's perspective. Indian J Multidiscip Dent 2016;6:11-3
|How to cite this URL:|
Gupte S, Nagargoje PN. Traumatic optic neuropathy: Why leave it to chance?… Maxillofacial Surgeon's perspective. Indian J Multidiscip Dent [serial online] 2016 [cited 2021 Aug 2];6:11-3. Available from: https://www.ijmdent.com/text.asp?2016/6/1/11/188218
| Introduction|| |
With the influx of high-speed automobiles, poor road conditions, and civic sense, the incidence of complex maxillofacial trauma is on a steep rise in India. Traumatic optic neuropathy is one such complex injury. Vision loss indeed is traumatic to the patients, and it is imperative on the part of an operating maxillofacial surgeon to assess investigate, diagnose, and manage promptly. The most common form of traumatic optic neuropathy is the indirect damage to the optic nerve and has been reported following 0.5-5% of all closed head trauma. , The degree of the visual acuity does not always correlate with the severity of trauma or fractures of the orbit. They neither directly predict the severity of loss of visual acuity nor determine the prognosis. 
The advocated but debated treatment modalities in the literature for the management of traumatic optic neuropathy vary from wait and watch policy to megadose steroid therapy to surgical decompression. Understanding that traumatic optic neuropathy is compartment syndrome, instead of simple observation or aggressive surgical intervention; we decided to follow the modified National Acute Spinal Cord Injury Study II (NASCIS II) rationale and protocol in the treatment of our six cases and their observations were noted.
| Materials and Methods|| |
Six cases who reported to the casualty following road traffic accident were taken up for this study. In all these six cases, head injury was ruled after evaluation of computed tomography (CT) and consultation with a neurosurgeon. All the six cases were trauma cases with associated fractures in maxillofacial region, and on examination, all of them presented with afferent papillary defect. Then, 0.2-1.5 mm slice CT was taken to rule out fracture of optic canal. CT examination revealed no signs of bony fragments, impinging on the nerve.  Thus, in consultation with ophthalmologist and neurosurgeon, a diagnosis of traumatic optic neuropathy was made [Table 1].
After subjective conformation using a CT, magnetic resonance imaging, and visual evoked potential (VEP), the necessary documentation was made. A loading dose of 30 mg/kg methylprednisolone (Solu-Medrol) was administered on admission 15 mg/kg/2 h later, followed by 15 mg/kg/6 hourly over next 48 h and then tapered thereafter. Since CT revealed no signs of bony fragments impinging on the nerve, no surgical intervention was carried out. Maxillofacial procedures were deferred until some signs of vision improvement were noted or the VEP showed signs of vision improvement.
In one case where complete preoperative vision was obtained in addition to megadose protocol, a lateral canthotomy was performed to evacuate the retrobulbar hemorrhage on emergency basis. The final outcomes in which hand close to face movements were perceived were considered to be positive improvement from no light perception by ophthalmologist. The VEPs from absolute flat graphs showed considerable improvements.
| Discussion|| |
The most common site of indirect optic nerve injury is the optic canal.  Review of literature shows 4-11.3% of midfacial, supraorbital, frontal, and sphenoid bone fractures contribute to traumatic optic neuropathy. The intracanalicular portion of the optic nerve is tightly adherent to the canal by the dural sheath which is situated in the optic canal within the greater wing of sphenoid. This bone being elastic absorbs the decelerating forces causes bending of the bone resulting in shearing, stretching, contusions, and lacerations, which further lead to edema, hemorrhage in the canal, strangulating and compromising the blood supply to the nerve. On unfortunate and rare occasions, an impinging bony spicule might cause the same effect.
Pathologic examination of the optic nerve from autopsied individuals after closed head trauma revealed that 83% had dural sheath hemorrhage and 44% experienced ischemic necrosis. It is important from for maxillofacial surgeons to recognize and diagnose traumatic optic neuropathy because, on many occasions, the first chance might be the last chance. It is of paramount importance to diagnose and take a decision whether to treat or delay the treatment of associated maxillofacial fractures. Imagining with 1.5-2 mm axial and coronal cuts of CT and VEP is very important in locating the pathology and documenting it subjectively. One of our patient demonstrated hyphema (bleeding in the anterior chamber of the eye) that there was a delay in diagnosis. In such cases, light reflexes cannot be made out and VEP comes into the picture to evaluate the optic nerve function. VEP is not only an important diagnostic aid but also a good prognostic indicator.
Megadose steroid therapy has been the gold standard in treatment of acute spinal cord injuries, and similar protocol has been extrapolated to traumatic optic neuropathy as it is a part of compartment syndrome the difference is that the soon after dose is reduced. The NASCIS was a multicenter, randomized, double-blind, placebo-controlled study of patients with acute spinal cord injury to test the megadose steroid therapy in which 30 mg/kg of steroid was administered IV followed by a continuous infusion of 5.4 mg/kg/h within 8 h resulted in statistically significant improvement to another study. 
Rationale based on the ability of the steroids to reduce trauma induced edema, microvascular spasm, neural cell necrosis. A loading dose of methylprednisolone 30 mg/kg, IV administration followed by 15 mg/kg 2 hourly later and followed by 15 mg/kg/6 hourly over next 48 h and then tapered thereafter if no improvement was observed within 48-72 h the steroid doses were aborted.  Methylprednisolone therapy was advocated as the initial treatment of choice because of its neuroprotective mechanism. 
The exact mechanism of corticosteroids in reducing optic nerve injury is still unclear. Steroids may have the neuroprotective effects of decreasing the intraneural or extraneural edema and relieving compression of the nerve fibers. By reducing vasospasm, steroids may also limit contusion necrosis of the nerve and block neuronal death in the setting of trauma is through inhibition of free radicals.  Review of literature also mentions various surgical modalities although reports are not conclusive, compared to the intracranial routes, and transethmoidal and transnasal routes of nerve decompression seem to be less invasive and more effective. 
| Conclusions|| |
Our observations showed occurrence of traumatic optic neuropathy in association mainly with zygomatic complex and sphenoidal bone fractures. Treatment of all maxillofacial fractures should be delayed until some vision improvements occur. Early identification and management may result in better outcome of the condition. Some patients will recover completely and spontaneously while others many still have residual vision defects. Steroid therapy in our cases gave us reasonably good results. Within the limitations of the study design, this study points benefit of this treatment as salvage therapy for traumatic optic neuropathy.
We would like to acknowledge the parent institute KLE's Institute of Dental College and Hospital and Professor Dr. Kotrashetti SM and Professor Dr. Pascal Pinto for having given an opportunity.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
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