Traumatic Airbag Maculopathy

With the prevalence of motor vehicle crashes, airbag deployment is a significant source of ocular trauma. We describe a case of traumatic airbag maculopathy in which imaging studies document a constellation of interesting findings, including subretinal fluid with impending macular hole and persistent paracentral scotoma with underlying electrophysiological disturbance despite anatomical recovery on optical coherence tomography (OCT).

A 49-year-old woman was involved in a motor vehicle crash at 65 mph, hitting the center divide front-on with airbag deployment. She immediately noted blurry vision. The emergency department evaluation otherwise revealed no traumatic injuries beyond chest contusions. The patient had normal neurological examination findings and never lost consciousness, and no head imaging was indicated. She visited the retina service after having persistently blurry vision for 3 days. Her ocular history consisted of high myopia and retinal detachment in each eye leading to laser demarcation in the right eye. Examination of the right eye revealed visual acuity of 20/150, posterior vitreous detachment, numerous cotton-wool spots surrounding the optic disc, and subretinal fluid (Figure 1A). Fluorescein angiography revealed a transmission defect in the inferior fovea as well as minimal diffuse leakage in the peripapillary retina. Fundus autofluorescence showed a diffuse area of increased autofluorescence around the fovea, extending superiorly toward the nerve (Figure 1B). Spectral-domain OCT findings were remarkable for a foveal detachment consistent with impending macular hole (Figure 2A).

Three weeks later, the cotton-wool spots and subretinal fluid had resolved, although some photoreceptor abnormalities remained on OCT (Figure 2B). After 5 months, repeated OCT revealed recovery of her baseline architecture (Figure 2C) with visual acuity improved to 20/25. However, even a year after injury, the patient described a central doughnut-shaped area of blurry vision. Given the absence of structural evidence on fundus examination or OCT that would completely account for her persistent visual complaints, the patient underwent multifocal electroretinography, which showed reduced signal throughout the macula with some temporal sparing (Figure 1C).

Persistent airbag-associated scotoma is rarely described in the literature. We are aware of 2 other case reports of a persistent paracentral scotoma following airbag trauma. In one, the scotoma was attributed to a break in the Bruch membrane,¹ while the other demonstrated focal thinning of the juxtafoveal neurosensory retina but had normal findings on multifocal electroretinography.² In contrast, our case exhibited clear electrophysiological dysfunction on multifocal electroretinography, an outcome consistent with findings that central electroretinal activity remained depressed 6 months following acute traumatic maculopathy despite resolved OCT abnormalities.³ While no specific architectural disruption accounted for this patient's functional impairment, it is notable that the pattern of retinal injury suggested on fundus autofluorescence 3 days after the motor vehicle crash corresponded closely with the diminished signal distribution on multifocal electroretinography a year later. While the sudden shock on impact may have caused the photoreceptor injury described, the presence of subfoveal fluid with visual nadir 3 days after impact cannot be discounted. Serous retinopathy is a rare finding associated with trauma and may arise from localized concussive damage with retinal dehiscence on impact.⁴ Initially diffuse intraretinal edema has been shown to progress to outer retinal disruption.⁵ Alternatively, in the context of posterior vitreous detachment, tractional or concussive forces may have led to a fluid collection with impending macular hole, independently contributing to our patient's vision loss. Yamashita et al⁶ propose 2 mechanisms of traumatic macular hole formation: (1) immediate vision loss from primary foveal dehiscence due to concussive forces, and (2) delayed vision loss from continued vitreomacular traction. Both mechanisms may have been present in our patient. In this case, serial imaging provided insight into the evolution of traumatic maculopathy and pathogenesis of traumatic macular hole formation. Further advanced imaging may improve our ability to prognosticate and intervene following ocular trauma.

Correspondence: Dr Leng, Byers Eye Institute at Stanford, 2452 Watson Ct, Palo Alto, CA 94303 (tedleng@stanford.edu).