entity is usually subtle rather than gross, as in our patient. 2,3 Furthermore, whiplash maculopathy has been associated with OCT appearances of a hyperreflective lesion at the vitreoretinal interface, rather than the macular edema we observed. 3,4 A case report by Parsons et al. 5 described an association between a severe whiplash injury and serous retinal pigment epithelial detachments and retinoschisis most likely attributable to a shearing mechanism, although in this case the patient's injuries were so extensive they led to death.Previous cases of traumatic retinal angiopathy have also been described, although these were invariably unilateral and less significant visual deterioration was manifest. 4 Macular edema has been reported in cases after minor head trauma (with normal Glasgow Coma Score) and after blunt ocular trauma, as in commotio retinae; however, our patient had no evidence of head or systemic trauma, and commotio retinae is characterized by retinal pallor, which our patient did not display. 6,7 Cases bearing resemblance to our patient have been described; however, the pattern of macular thickening was different in these cases and 1 case did suffer minor ocular trauma and concussion. 8 Airbag deployment in road traffic accidents has also been associated with retinal findings such as cotton wool spots, subretinal fluid, and impending macular hole, along with persistent central visual disturbance, which again were not seen in our case presentation. 9 In summary, the clinical presentation and ocular findings noted in our case appear distinct from other such ophthalmic manifestations of trauma, making this a unique and instructive report. A discussion of the potential pathophysiology of the bilateral macular edema in this case is difficult given the absence of fundus fluorescein angiography. However, given the rapidity of resolution of the edema and lack of recurrence over 1 year of follow-up, it was believed to be unethical to undertake fundus fluorescein angiography. In other cases of retinal trauma, the manifestations are postulated to be a combination of localized microcirculatory insufficiency caused by localized endothelial damage, coagulation, and complement activation caused by raised intraluminal pressure secondary to factors such as seat belt compression, systemic coagulopathy, and traumatic posterior vitreous detachment at the macula. 3 We are unable to make such assertions in this case. However, ophthalmologists should still be aware of such scenarios of rapid, bilateral visual loss after indirect trauma, as well as the subsequent good prognosis for visual improvement. Correspondence to: Mark Sigona, MBChB (Hons): mark.sigona@doctors.org.uk REFERENCES 1. Trikha S, Tiroumal S, Hall N. Purtscher's retinopathy following a road traffic accident. Emerg Med J. 2011;28:453. 2. Mavrakanas N, Dreifuss S, Safran AB. OCT III imaging of whiplash maculopathy. Eye. 2008;22:860-1. 3. Haslett RS, Duvall-Young J, McGalliard JN. Traumatic retinal angiopathy and seat belts: pathogenesis of whiplash inj...