A 59-year-old Black male presented to the clinics for follow-up. His chief complaint was blurry vision and a central dark spot in his right eye that started immediately after his car accident 5 years ago where he was hit on the right side of his body.

On exam, his best-corrected visual acuity was 20/200 OD and 20/20 OS and there was an afferent pupillary defect in the right eye.

Compared to last year’s documentation, vision and symptoms were stable although this year, an orange lesion was noted temporally to his previously noted macular scar (see arrow on fundus photo). We decided to run an OCT through that area (see OCT picture).

Our patient was diagnosed with a choroidal rupture and subsequent macular scarring. The orange lesion is highly suggestive of an active Choroidal Neovascularization (CNV) due to the presence of fluid. The patient was sent to the retinal specialist for management.

Based on this patient’s fundus appearance only, one could suspect this lesion to be an old toxoplasmosis scar due to its similitude and location within the posterior pole, but the sudden onset of vision loss experienced by our patient following his car accident makes it less likely to be of an infectious etiology.

Discussion

A choroidal rupture happens when a disruption of the choriocapillaris, Bruch’s membrane, and the retinal pigment epithelium (RPE) occurs secondary to traumatic ocular compression in which stretching and folding of these structures lead to its rupture. Ruptures are typically located within the posterior pole and are most often concentric to the optic disc(1). Sports injuries and car accidents involving the deployment of airbags are common causes of choroidal rupture although systemic conditions such as Pseudoxanthoma elasticum, Ehlers-Danlos, Paget disease, Sickle cell anemia, or virtually any condition involving Angioid streaks may predispose a patient for choroidal ruptures with impacts of minimal intensity as these represents breaks in Bruch’s membrane as well.

In the acute phase, the breaks are commonly associated with subretinal and sub-RPE hemorrhages. Later on in the chronic phase, choroidal neovascularizations (CNV) may develop and are often found at the edges of the rupture2. Choroidal neovascularization may occur months to years post-trauma and can result in fibrotic scarring(2).

The prognosis is highly dependent on the location of the rupture and whether it involves the foveal area or not and if subretinal or sub-RPE hemorrhages are present. Patients with choroidal rupture should be followed carefully as they carry the risk of developing secondary choroidal neovascularization at any time post-trauma which may decrease further visual acuity(2).

The treatment of choroidal rupture often involves observation and close follow-up to monitor for spontaneous improvement of vision as there is no medical nor surgical therapy indicated in the treatment of acute choroidal rupture. Patients are often provided with an Amsler grid as a self-monitoring device in order to detect any changes in vision as these patients carry the risk of developing choroidal neovascularization in the future. In cases where CNV develops, intraocular injections of anti-vascular endothelial growth factor (Anti-VEGF) can be used.

References 

1. K.Bailey Freund, David Sarraf, William F. Mieler, Lawrence A. Yannuzzi. Choroidal Rupture. The Retinal Atlas. Second Edition. Elsevier: 2017: p1011
2. Mitchell S. Fineman, Allen C. Ho. Choroidal Rupture. Color Atlas & Synopsis of Clinical Ophthalmology. Second Edition. Wolters Kluwer: 2012: p316