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Shin and Kim: Clinical Manifestations and Prognosis of Patient with Traumatic Optic Neuropathy
Original Article

J Korean Ophthalmol Soc 2016;57(11):1770-1776.

Published online: 25 September 2016

DOI: https://doi.org/10.3341/JKOS.2016.57.11.1770

Clinical Manifestations and Prognosis of Patient with Traumatic Optic Neuropathy

Gwang Rae Shin, MD, Dae Hyun Kim, MD, PhD

Department of Ophthalmology, Chosun University School of Medicine, Gwangju, Korea

Address reprint requests to Dae Hyun Kim, MD, PhD Department of Ophthalmology, Chosun University Hospital, #365 Pilmun-daero, Dong-gu, Gwangju 61453, Korea Tel: 82-62-220-3190, Fax: 82-62-225-9839 E-mail: eyelovehyun@hanmail.net

Received 28 July 2016       Revised 6 October 2016       Accepted 2 November 2016

Copyright © 2016 Korean Ophthalmological Society

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Purpose

To investigate the clinical manifestations, management, ophthalmologic complications, and prognosis of traumatic optic neuropathy.

Methods

A retrospective survey of 55 patients who visited Chosun Hospital from April 2009 to February 2016 was performed. The sex, age, causes, fracture characteristics, neurologic injury, and combined craniofacial bone fractures of patients who were diagnosed with traumatic optic neuropathy were statistically analyzed. Also, we investigated the rate of visual impairment in the patients with intracranial hemorrhaging and craniofacial fracture on radiologic examination and development of sensory strabismus.

Results

Traffic accidents were the most common cause of traumatic optic neuropathy. Among the patients, more than 60% showed severe visual impairment of less than 0.1 that lasted until the final observation. Altitudinal visual defects were the most common visual field defect and presented as marginal atrophy and central scotoma. While intracranial hemorrhaging was showed in 52.4% of the patients, craniofacial fracture was observed in 90.5% of the patients. The initial visual acuity was decreased when the patient presented with orbital fracture located in the retrobulbar area. Intravenous high-dose steroid injection did not affect visual prognosis. Sensory strabismus occurred more commonly under conditions of poor initial vision (p = 0.007) or young age (p < 0.001).

Conclusions

Traumatic optic neuropathy in Korea has a high rate of initial visual impairment with poor prognosis of vision. In addition, high-dose intravenous steroid injection did not result in visual improvement.

Keywords: High-dose corticosteroid, Traumatic optic neuropathy, Visual prognosis

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Figure 1.
Initial visual acuity difference between the groups of patients classified by involvement of posterior wall fracture in craniofacial fracture. fx. = fracture; Post. = posterior. * Mann whitney U-test.
jkos-57-1770f1.tif
Figure 2.
Initial and final visual acuity in group of patients classified by steroid treatment. * Wilcoxson signed rank test.
jkos-57-1770f2.tif
Table 1.
Visual acuity and color vision of traumatic optic neuropathy patients
  First visit Final visit
Visual acuity    
 >0.5 4 (7.0%) 5 (8.7%)
 0.1–0.5 18 (31.5%) 17 (29.8%)
 <0.1 35 (61.4%) 35 (61.4%)
Ishihara test 2.4 ± 1.5 1.9 ± 1.1

Values are presented as mean ± SD unless otherwise indicated.

Table 2.
Visual field defect distribution in traumatic optic neuropathy patients
Visual field defect No. of patients (%)
Altitudinal defect 13 (24.0)
Peripheral atrophy 12 (22.2)
Total scotoma 12 (22.2)
Central scotoma 10 (18.5)
Generalized defect 5 (9.2)
Cecal scotoma 2 (3.7)
Arcuated scotoma 1 (1.8)

Values are presented as n (%). No. = number.

Table 3.
Accompanying injury of traumatic optic neuropath patients
Accompanying injury of TON patients No. of patients (%
Accompanying nerve palsy (N = 10)  
 Oculomotor nerve 3 (30)
 Abducens nerve 2 (20)
 Facial nerve 2 (20)
 Oculomotor nerve + Abducens 1 (10)
 Trochlear nerve 1 (10)
 Internuclear ophthalmoplegia 1 (10)
Intracranial hemorrhage (N = 22)  
 EDH 8 (36.3)
 ICH 7 (31.8)
 SDH 6 (27.2)
 SAH 1 (4.5)
Craniofacial fracture (N = 38)  
 Orbital 31 (81.5)
 Sphenoid or Posterior Ethmoid 12 (31.5)
 Optic canal (lesser wing of sphenoid) 4 (10.5)
 Malar 23 (60.5)
 Maxillar 19 (50.0)
 Frontal 10 (26.3)
 Temporal 6 (15.7)
 Nasal bone 4 (10.5)

TON = traumatic optic neuropathy; EDH = epidural hemorrhage ICH = intracerebral hemorrhage; SDH = subdural hemorrhage SAH = subarachnoid hemorrhage; No. = number.

Table 4.
Univariate analysis with visual prognostic factor for traumatic optic neuropathy
Independent variable No. of cases No. of recovery of visual acuity (N, %) RR* CI (95%)
Initial visual acuity below finger count 29 27 (93.1) 3.77 1.65–6.78
Sphenoid or Posterior ethmoid Fx. 12 10 (83.3) 2.12 1.26–3.74
Optic canal Fx. 4 3 (75.0) 1.98 1.43–2.79
Loss of consciousness 35 32 (91.4) 4.18 1.52–2.47
Nerve palsy associated 10 5 (50) 0.87 0.84–3.51

Visual acuity recovery: >0 from initial exam. RR = relative risk; CI = confidence interval; Fx = fracture; No. = number.

* Pearson's chi-square test.

Table 5.
Influencing factors, angle of deviation, and type of sensory strabismus after traumatic optic neuropathy
  Sensory strabismus (+)(N = 8) Sensory strabismus (−)(N = 12) p-value*
Age (years) 14.1 ± 4.4 43.0 ± 15.8 p < 0.001
BCVA (log MAR) 2.8 ± 0.4 1.6 ± 1.1 p = 0.007
Angle of deviation 26.3 ± 14.4 (exotropia)    

Values are presented as mean ± SD unless otherwise indicated. BCVA = best corrected visual acuity.

* Mann whitney U-test.

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