Traumatic Vision Loss With Clear Media
Many patients report decreased vision following periocular trauma. It is imperative that a complete ophthalmic examination be performed to rule out direct globe injury or OCS. Reduction in visual acuity may be due to associated injuries of the cornea, lens, vitreous, retina, or orbit. In addition, eyelid edema may impede opening of the eyes to sufficiently clear the visual axis. However, a small percentage of patients have true vision loss without any evidence of globe injury. Vision loss in these cases suggests traumatic dysfunction of the optic nerve, also known as traumatic optic neuropathy. Such vision loss results from 1 of the 2 following mechanisms:
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direct injury to the optic nerve from a penetrating wound, bone fragment, or nerve avulsion
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indirect injury caused by force from a frontal blow transmitted to the intracanalicular portion of the optic nerve
The presence of an afferent pupillary defect in patients with an intact globe strongly suggests traumatic optic neuropathy. However, detection of an afferent defect may be difficult if the patient has received narcotics that cause pupillary constriction or if the traumatic optic nerve injury is bilateral and symmetric.
The details of the injury and orbital imaging can help differentiate direct optic nerve injury from indirect. A penetrating wound likely indicates direct injury. History of blunt trauma to the frontal region or rapid deceleration of the cranium, often in patients who have experienced loss of consciousness, is suggestive of indirect injury. CT imaging of the orbits can demonstrate disruption of the optic nerve or fracture involving the orbital apex and/or optic canal in cases of direct injury but is often unremarkable in patients with indirect injury (Fig 6-9).
The proper management of neurogenic vision loss after blunt head trauma is controversial. Observation alone, high-dose corticosteroids, and surgical decompression of the optic canal have been considered as treatment options for indirect traumatic optic neuropathy. However, recent studies have shown that high-dose corticosteroid therapy may not provide any additional vision benefit over observation alone, and such treatment is contraindicated in patients with concomitant traumatic brain injury. In addition, other studies have shown that decompression of the optic nerve provides no additional benefit over observation alone while subjecting patients to the risks associated with surgery. The optimal management of indirect traumatic optic neuropathy remains unresolved. Future research focused on neuroprotection and regeneration is needed.
Ultimately, vision loss after trauma can have serious consequences relating to employment, education, driving, and/or other daily activities. Referral for a comprehensive vision rehabilitation assessment and intervention should be an integral part of the treatment plan for the patient. Significant psychosocial issues may also need to be addressed.
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American Academy of Ophthalmology PPP Vision Rehabilitation Committee, Hoskins Center for Quality Eye Care. Preferred Practice Pattern® Guidelines. Vision Rehabilitation. San Francisco: American Academy of Ophthalmology; 2017. Available at www.aao.org/ppp.
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Steinsapir KD, Goldberg RA. Traumatic optic neuropathy: an evolving understanding. Am J Ophthalmol. 2011;151(6):928–933.
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Yu-Wai-Man P, Griffiths PG. Steroids for traumatic optic neuropathy. Cochrane Database Syst Rev. 2013;6:CD006032.
Excerpted from BCSC 2020-2021 series: Section 10 - Glaucoma. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.