Author Affiliations: Byers Eye Institute at Stanford, Stanford University School of Medicine, Palo Alto, California.
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).
Figure 1. At presentation, several areas of retinal opacification around the disc on a fundus photograph (A) corresponded to foci of decreased autofluorescence on fundus autofluorescence (B). Notably, fundus autofluorescence also shows a diffuse area of increased autofluorescence around the fovea extending superiorly toward the nerve. This distribution of photoreceptor injury appears as a near total loss of electroretinographic signal in the same pattern a year later (C).
Figure 2. Optical coherence tomography suggested an impending macular hole at presentation (A). The retinal architecture recovered by 3 weeks (B), and at 5 months it continued to show preservation of the external limiting membrane, inner segment–outer segment junction, and foveal cone structure (C).
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 (firstname.lastname@example.org).
Conflict of Interest Disclosures: None reported.
Thank you for submitting a comment on this article. It will be reviewed by JAMA Ophthalmology editors. You will be notified when your comment has been published. Comments should not exceed 500 words of text and 10 references.
Do not submit personal medical questions or information that could identify a specific patient, questions about a particular case, or general inquiries to an author. Only content that has not been published, posted, or submitted elsewhere should be submitted. By submitting this Comment, you and any coauthors transfer copyright to the journal if your Comment is posted.
* = Required Field
Disclosure of Any Conflicts of Interest*
Indicate all relevant conflicts of interest of each author below, including all relevant financial interests, activities, and relationships within the past 3 years including, but not limited to, employment, affiliation, grants or funding, consultancies, honoraria or payment, speakers’ bureaus, stock ownership or options, expert testimony, royalties, donation of medical equipment, or patents planned, pending, or issued. If all authors have none, check "No potential conflicts or relevant financial interests" in the box below. Please also indicate any funding received in support of this work. The information will be posted with your response.
Some tools below are only available to our subscribers or users with an online account.
Download citation file:
Web of Science® Times Cited: 1
Customize your page view by dragging & repositioning the boxes below.
Enter your username and email address. We'll send you a link to reset your password.
Enter your username and email address. We'll send instructions on how to reset your password to the email address we have on record.
Athens and Shibboleth are access management services that provide single sign-on to protected resources. They replace the multiple user names and passwords necessary to access subscription-based content with a single user name and password that can be entered once per session. It operates independently of a user's location or IP address. If your institution uses Athens or Shibboleth authentication, please contact your site administrator to receive your user name and password.