A 42-year-old man was seen in the emergency room with sudden vision loss in his left eye. He reportedly hit a metal pole while driving a motorized scooter. He did not recall the details of the event. He lost consciousness and upon awakening was unable to see out of his left eye. Other injuries from the event included dislocation of his right thumb and abrasions to his left forehead and face.
Medical and ocular histories were unremarkable. The patient used tobacco, alcohol and marijuana.
Distance visual acuity without correction was 20/15 in the right eye and hand motion in the left eye. IOP was 16 mm Hg in the right eye and 12 mm Hg in the left eye. Pupils measured 3.5 mm with light constriction to 2.5 mm in the right eye and 4 mm with no reaction to light in the left eye. There was a relative afferent pupillary defect in the left eye. Extraocular movements were normal. Slit lamp exam of the anterior segment and dilated fundus exam were unremarkable (Figure 1).
Figure 1. Fundus and optic nerve exams of the left eye were essentially normal.
Source: Carmody JN, Hedges TR
What is your diagnosis?
The differential diagnosis of an optic neuropathy following trauma includes traumatic optic neuropathy, optic nerve sheath hematoma and orbital hematoma. The neuropathy could also be unrelated to the trauma, such as compression by a tumor or aneurysm, optic nerve or orbital inflammation, or ischemic optic neuropathy.
The patient underwent CT imaging, which was unremarkable (Figure 2). The patient was diagnosed with a traumatic optic neuropathy of the left eye.
Figure 2. CT imaging of the orbits showed no evidence of direct optic nerve injury.
Source: Carmody JN, Hedges TR
The incidence of traumatic optic neuropathy (TON) after closed head injury is 0.5% to 5%. The majority of cases occur in men in their 20s. It is most commonly seen after motor vehicle accidents, followed by bicycle accidents, falls and assaults.
Patients present with vision loss after trauma, and this may occur after a seemingly trivial head injury. There will be an afferent pupillary defect. The optic nerve head appearance will usually be normal immediately after the injury, but optic atrophy will occur after 2 to 4 weeks. Patients often have a normal retina and anterior segment exam.
TON is most commonly caused by indirect injury to the optic nerve due to transmission of blunt forces from the frontal bone concentrated to the optic canal. The diagnosis of TON is based on history, clinical exam and imaging studies. Patients may also have TON caused by direct injury to the optic nerve resulting in avulsion or transection. Rarely does it result in anterior ischemic optic neuropathy. In up to half of patients with indirect TON, visual acuity may spontaneously recover. However, many patients are left with vision worse than hand motion. Poor prognostic factors include poor initial visual acuity, direct mechanism of injury, optic canal fractures, age older than 40 years, loss of consciousness at time of injury, and no improvement in visual acuity after 48 hours.
There is no randomized double-masked study available to clarify the effect of treatment options in indirect TON. Medical treatment with IV steroids has shown varying degrees of success and is based in part on the success of megadose steroids in recovery after spinal cord injuries. If administered within 8 hours after injury, steroids may provide an antioxidant effect and help to reduce vasospasm and swelling. Several studies, however, have not shown a clear benefit of steroid treatment vs. observation. There may also be a dose-dependent decline in axon counts with increasing doses of steroids, and megadose steroids may increase the risk of death in patients with concurrent head injury. Surgical treatment by optic canal decompression with or without optic nerve sheath decompression may be considered for patients with poor response to steroid therapy within 24 to 48 hours. The relief of compression of the optic nerve can allow it to regain function.
Treatment and follow-up
After discussion with the patient about the risks and benefits of treatment, it was decided to start high-dose steroids, which were initiated within 8 hours of the time of initial injury. As there was no improvement in vision after 24 hours of steroid treatment, the patient underwent optic canal decompression and optic nerve sheath decompression using a transethmoidal endoscopic approach. At 1-week follow-up, his visual acuity was counting fingers. Nerve fiber layer optical coherence tomography showed early optic atrophy (Figure 3).
Figure 3. Nerve fiber layer OCT shows early optic atrophy at 1 week after the injury.
Source: Carmody JN, Hedges TR
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For more information:
- Jill N. Carmody, MD, and Thomas R. Hedges III, MD, can be reached at New England Eye Center, Tufts University School of Medicine, 750 Washington St., Box 450, Boston, MA 02111; 617-636-4219; fax: 617-636-4866; website: www.neec.com.
- Edited by Catherine A. Cox, MD, and Jordana F. Goren MD, MS. Drs. Cox and Goren can be reached at New England Eye Center, Tufts University School of Medicine, 750 Washington St., Box 450, Boston, MA 02111; 617-636-4219; fax: 617-636-4866; website: www.neec.com.