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CASE REPORT
Year : 2018  |  Volume : 11  |  Issue : 4  |  Page : 366-370  

Traumatic optic neuropathy: Surgical intervention improves vision and color perception


Department of Ophthalmology, Andaman and Nicobar Islands Institution of Medical Sciences, Port Blair, Andaman and Nicobar Islands, India

Date of Web Publication2-Aug-2018

Correspondence Address:
Sujit Das
Department of Ophthalmology, Andaman and Nicobar Islands Institution of Medical Sciences, Port Blair - 744 104, Andaman and Nicobar Islands
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/mjdrdypu.MJDRDYPU_227_17

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  Abstract 


The most common cause of traumatic optic neuropathy (TON) is indirect injury to the optic nerve, which is thought to be the result of transmitted shock from an orbital impact to the intracanalicular portion of optic nerve. Direct TON can result from penetrating injury or from bony fragments in the optic canal or orbit piercing the optic nerve. Orbital hemorrhage and optic nerve sheath hematoma can also cause TON by direct compression. There may be optic nerve avulsion and transection also. Trauma to the optic nerve rarely improves vision with best of the management. The diagnosis of TON is made clinically based on history and ophthalmic signs along with neurological investigations. The management of indirect optic nerve injury is controversial. Experimental studies of optic nerve injury have employed Corticosteroid Randomization After Significant Head injury study, National Acute Spinal Cord Injury Study (NASCIS 2 and 3) and optic canal depression surgery. Most of the therapeutic regimens have been extrapolated from the NASCIS II, which showed a statistically significant improvement in neurologic outcome (motor and sensory) in a subgroup analysis of acute spinal cord injury patients receiving a methylprednisolone 30 mg/kg bolus within 8 h of injury, followed by 5.4 mg/kg/h for 23 h, but sometimes have high death rates and other complications. Based on the studies, good results can be obtained if interventions are made within 8 h of incident and observation thereafter.

Keywords: Trauma and eye, traumatic avulsion, traumatic optic neuropathy, traumatic transection


How to cite this article:
Das S. Traumatic optic neuropathy: Surgical intervention improves vision and color perception. Med J DY Patil Vidyapeeth 2018;11:366-70

How to cite this URL:
Das S. Traumatic optic neuropathy: Surgical intervention improves vision and color perception. Med J DY Patil Vidyapeeth [serial online] 2018 [cited 2019 Oct 22];11:366-70. Available from: http://www.mjdrdypv.org/text.asp?2018/11/4/366/238174




  Introduction Top


Traumatic optic neuropathy (TON) is a condition in which acute injury to the optic nerve from direct or indirect trauma results in vision loss.[1] The most common cause of TON is indirect injury to the optic nerve, which is thought to be the result of transmitted shock from an orbital impact to the intracanalicular portion of optic nerve.[2] Direct TON can result from penetrating injury or from bony fragments in the optic canal or orbit piercing the optic nerve. Orbital hemorrhage and optic nerve sheath hematoma can also cause TON by direct compression. Direct TON is presumed to be the result of tissue disruption secondary to foreign body or bony fragments impacting on the optic nerve.[3] Several varieties of direct optic nerve injury may be recognized ophthalmoscopically or with the following imaging techniques: optic nerve avulsion, transection, optic nerve sheath hemorrhage, orbital hemorrhage, and orbital emphysema.[4] Indirect TON has been hypothesized to result from shearing injury to the intracanalicular portion of optic nerve, which can cause axonal injury or disturb the blood supply of the optic nerve. It has also been suggested that the optic nerve may swell in the optic canal after trauma, resulting in increased luminal pressure and secondary ischemic injury. Within the canal, the optic nerve dura fuses with the periosteum of the bone. Since the vasculature of the optic nerve in the canal is pial, compression and contusion of the nerve produce a compartment syndrome, whereby swelling exacerbates the ischemia.[5]

Patients with TON may have decreased central visual acuity, decreased color vision, an afferent pupillary defect, and/or visual field deficits. A history consistent with TON would be vision loss after blunt or penetrating trauma that could not be explained by slit-lamp or dilated fundus findings.[6] TON can be bilateral, so an afferent pupillary defect may not be seen in patients with bilateral injury and vision loss. The optic nerve head will appear normal initially, but optic atrophy can be seen 3–6 weeks after the initial traumatic event.[7]

It is important to obtain neuroimaging, usually a computed tomography (CT) to visualize the optic nerve as well as the optic canal, especially the fractures, whereas magnetic resonance imaging (MRI) is for soft-tissue injury, especially optic nerve hematoma. Automated visual field testing such as a Humphrey visual field can be used to characterize visual field defects/scotomas in patients with TON over time. Finally, a visual-evoked potential (VEP) can be used to characterize the electrical activity of the optic nerve.[2]


  Case Report Top


A 24-year-old male patient presented to the emergency department with the complaints of vomiting, left eye swelling with ecchymosis, and nasal bleeding after a road traffic accident (car injury) with head injury after 24 h. There was no history of loss of consciousness and seizure episodes. On systemic examination, the patient was conscious and oriented, blood pressure was 120/80 mmHg, pulse was 90/min, and respiratory rate was 14/min. Systemic cardiovascular, respiratory, central nervous system (Glasgow Coma Scale score – 15/15), and per abdomen examination were all normal. He was admitted and called for ophthalmological opinion. On examination, distance visual acuity (DVA) in the right eye was 6/6 and in the left eye it was hand movement close to the face with perception of ray positive in all directions. Intraocular pressure in the right eye was normal digitally and the left eye was swollen. On eye examination, cornea was normal and conjunctiva was congested and chemosed with subconjunctival hemorrhage [Figure 1]. Anterior chamber was normal with relative afferent pupillary defect in the left eye. Fundus examination revealed normal findings. Extraocular movements were full and free. There was no red and green color perception. Clinically, a diagnosis of TON was made and he was put on intravenous methylprednisolone 30 mg/kg bolus dose followed by 5.4 mg/kg/h for 48 h under continuous electrocardiogram monitoring as per the National Acute Spinal Cord Injury Study (NASCIS). Along with injection neurobion, chymoral forte was prescribed. He was advised noncontrast CT (NCCT) brain with orbit. After 24 h of treatment, his vision was as before, but there was improvement of red color perception only. NCCT brain revealed normal brain parenchymal structure with no subdural hematoma/epidural hematoma. There was a fracture in the anterior and posterior maxillary antra with floor and medial wall of the left orbit with herniation of fat. Fracture was also noted in the greater wall of greater sphenoid extending along the superolateral aspect of the left optic canal, with a bony chip in the inferior part of the optic canal [Figure 2] and [Figure 3] and a fracture of zygoma. Complete hemogram, sugar, urea, and creatinine were all normal. He was referred to mainland for further management where he underwent MRI brain with orbit and paranasal sinus. In MRI, there was thickening of the intraorbital part of optic nerve with bleeding in the paranasal sinus. There were multiple fractures in the paranasal sinuses [Figure 4] and [Figure 5] with bony chips in the optic canal. VEP from the left eye was not elicited compared to normal response [Figure 6] and [Figure 7], whereas in the right eye, there was normal response. Visual field testing could not be done in the left eye, whereas in the right eye, there was normal visual field testing [Figure 8]. He then underwent optic nerve and optic canal decompression with optic nerve sheath fenestration surgery along with ethmoidectomy and sphenoidectomy. Postoperative period was uneventful. On follow-up, there was mild improvement in the vision (DVA-LE-1/60) with recovery of both red and green color perception.
Figure 1: Chemosed eye with relative afferent pupillary defect (RAPD) with subconjunctival hemorrhage

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Figure 2: Fracture optic canal with bony chip inferiorly

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Figure 3: Fracture intra-cranial part of optic canal

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Figure 4: Multiple sinus wall fracture

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Figure 5: NCCT paranasal sinus shows bleeding in the sinus cavity

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Figure 6: Right eye normal visual evoked potential (VEP)

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Figure 7: Left eye poor response on -VEP (Visual evoked potential)

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Figure 8: Visual field test in the right eye

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  Discussion Top


The management of indirect optic nerve injury is controversial. Experimental studies of optic nerve injury have employed Corticosteroid Randomization After Significant Head (CRASH) injury study, NASCIS 2 and 3 study, and optic canal decompression surgery to decompress the optic canal, via intracranial, transethmoidal, and endonasal routes, and even sublabial approaches have been advocated in many retrospective reports.[8],[9],[10],[11] The rationale was strengthened by studies on spinal cord injury. High or “mega” dose of corticosteroids in TON includes methylprednisolone 30 mg/kg bolus within 8 h of injury followed by 5.4 mg/kg/h for 23 h.[12] The second NASCIS 2 study was a multicentric, randomized, double-blind, placebo-controlled study of patients with acute spinal cord injury. Patients were treated with placebo, naloxone, or methylprednisolone and administered with an initial dose of 30 mg/kg followed by an infusion at 5.4 mg/kg/h for 24 h. Patients were evaluated by pinprick, light touch, and motor function initially, and then at 6 weeks and 6 months. The study showed that the treatment with methylprednisolone within 8 h of injury resulted in a significant improvement in motor and sensory functions compared to that of placebo-treated patients. Further analysis of the data suggested that methylprednisolone treatment initiated more than 8 h after spinal cord injury may be detrimental.[13] NASCIS 3 study established that treatment should be continued for 24 h if initiated within 3 h after injury, but for 48 h if initiated within 3–8 h.[12]

Subsequently, however, the CRASH study showed an increased relative risk of death in patients given this regimen after significant head injury.[14]

The International Optic Nerve Trauma Study also did not show a difference in final visual acuity between patients with TON who were observed compared with those given steroids.[10]

Surgical intervention for TON was shown not to be beneficial in the International Optic Nerve Trauma Study.[10] Some have supported the use of surgery in certain scenarios such as when a bony fragment is abutting to optic nerve or in the case of an optic nerve sheath hematoma, but there is no good data supporting surgery for indirect TON.[15] Optic nerve decompression surgery may entail further complications as a result of damage to the neighboring structures in the orbit and region of the sella.[16]

Several authors have reported that spontaneous recovery may occur in at least a third of patients.[17] A study of the current practice in 16 countries was carried out between 1994 and 1997. A total of 133 patients were included in this study (127 were unilateral cases, 6 were bilateral cases) and were access 3 days after optic nerve injury. They divided into 3 groups -corticosteroid group-85, surgery group- 33 and 15 patients were left untreated and observation. At least 1 month of follow-up was required for inclusion. Nine patients were untreated, 85 were treated with corticosteroids, and 33 with decompression surgery. Visual acuity increased by three or more lines in 32% of the surgery group, 57% of the untreated group, and 52% of the steroid group.[18] After adjustment for the initial vision, there were no significant differences between any of the treatment groups.[19]

Serious surgical complications specific to decompression surgery for TON include infection (meningitis), cerebrospinal fluid leaks, and exacerbation of TON. Complications from high or “mega” dose steroids include wound infection and gastrointestinal bleed.[20]

In the International Optic Nerve Trauma Study, visual acuity improvement of >3 lines was seen in 57% of the untreated group, 52% of the group that received steroids alone, and 32% of the group that underwent surgery. This was not a statistically significant result.

Given the uncertainties about the value of intervention, particularly after 8 h, specific treatment may not be indicated for many patients with indirect optic nerve injury.[21]

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Steinsapir KD, Goldberg RA. Traumatic optic neuropathy. Surv Ophthalmol 1994;38:487-518.  Back to cited text no. 1
    
2.
Crompton MR. Visual lesions in closed head injury. Brain 1970;93:785-92.  Back to cited text no. 2
    
3.
Fukado Y. Results in 400 cases of surgical decompression of the optic nerve. Mod Probl Ophthalmol 1975;14:474-81.  Back to cited text no. 3
    
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Sawhney R, Kochhar S, Gupta R, Jain R, Sood S. Traumatic optic nerve avulsion: Role of ultrasonography. Eye (Lond) 2003;17:667-70.  Back to cited text no. 4
    
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Turner JW. Indirect injuries of the optic nerve. Brain 1943;66:140-51.  Back to cited text no. 5
    
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Hooper RS. Orbital complications of head injury. Br J Surg 1951;39:126-38.  Back to cited text no. 6
    
7.
Seiff SR. High dose corticosteroids for treatment of vision loss due to indirect injury to the optic nerve. Ophthalmic Surg 1990;21:389-95.  Back to cited text no. 7
    
8.
Edwards P, Arango M, Balica L, Cottingham R, El-Sayed H, Farrell B, et al. Final results of MRC CRASH, a randomised placebo-controlled trial of intravenous corticosteroid in adults with head injury-outcomes at 6 months. Lancet 2005;365:1957-9.  Back to cited text no. 8
    
9.
Young W. NASCIS. National acute spinal cord injury study. J Neurotrauma 1990;7:113-4.  Back to cited text no. 9
    
10.
Levin LA, Beck RW, Joseph MP, Seiff S, Kraker R. The treatment of traumatic optic neuropathy: The international optic nerve trauma study. Ophthalmology 1999;106:1268-77.  Back to cited text no. 10
    
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Levin LA, Joseph MP, Rizzo JF 3rd, Lessell S. Optic canal decompression in indirect optic nerve trauma. Ophthalmology 1994;101:566-9.  Back to cited text no. 11
    
12.
Bracken MB, Shepard MJ, Holford TR, Leo-Summers L, Aldrich EF, Fazl M, et al. Administration of methylprednisolone 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.  Back to cited text no. 12
    
13.
Bracken MB, Holford TR. Effects of timing of methylprednisolone or naloxone administration on recovery of segmental and long-tract neurological function in NASCIS 2. J Neurosurg 1993;79:500-7.  Back to cited text no. 13
    
14.
Zuo L, Khan RS, Lee V, Dine K, Wu W, Shindler KS, et al. SIRT1 promotes RGC survival and delays loss of function following optic nerve crush. Invest Ophthalmol Vis Sci 2013;54:5097-102.  Back to cited text no. 14
    
15.
Nishida S, Otani N, Inaka Y, Morinaga Y, Kimura S, Tomura S, et al. Usefulness of extradural optic canal unroofing and decompression of the optic nerve for improvement of visual acuity in traumatic optic neuropathy. No Shinkei Geka 2014;42:1035-8.  Back to cited text no. 15
    
16.
Moreau A, Lao KC, Farris BK. Optic nerve sheath decompression: A surgical technique with minimal operative complications. J Neuroophthalmol 2014;34:34-8.  Back to cited text no. 16
    
17.
Wolin MJ, Lavin PJ. Spontaneous visual recovery from traumatic optic neuropathy after blunt head injury. Am J Ophthalmol 1990;109:430-5.  Back to cited text no. 17
    
18.
Wu N, Yin ZQ, Wang Y. Traumatic optic neuropathy therapy: An update of clinical and experimental studies. J Int Med Res 2008;36:883-9.  Back to cited text no. 18
    
19.
Maegele M. Reversal of isolated unilateral optic nerve edema with concomitant visual impairment following blunt trauma: A case report. J Med Case Rep 2008;2:50.  Back to cited text no. 19
    
20.
Entezari M, Rajavi Z, Sedighi N, Daftarian N, Sanagoo M. High-dose intravenous methylprednisolone in recent traumatic optic neuropathy; A randomized double-masked placebo-controlled clinical trial. Graefes Arch Clin Exp Ophthalmol 2007;245:1267-71.  Back to cited text no. 20
    
21.
Warner N, Eggenberger E. Traumatic optic neuropathy: A review of the current literature. Curr Opin Ophthalmol 2010;21:459-62.  Back to cited text no. 21
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8]



 

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