Superficial and Deep Capillary Plexus Nonperfusion in Nonaccidental Injury on OCTA. (January 2023)

• Record Type: Journal Article
• Authors: Echegaray, Jose J.; Iyer, Prashanth; Acon, Dhariana; Negron, Catherin; El Hamichi, Sophia; Berrocal, Audina M.
• Is Part Of: Journal of vitreoretinal diseases. Volume 7:Number 1(2023)
• Page Start: 79
• Page End: 82
• Publication Date: 2023-01
• Subjects: nonaccidental injury -- shaken baby syndrome -- macular ischemia -- OCT angiography -- superficial vascular plexus -- deep capillary plexus -- ocular trauma; Retina -- Diseases -- Periodicals; Vitreous body -- Diseases -- Periodicals; Retina -- Diseases; Vitreous body -- Diseases; Periodicals; 617.735005
• DOI: 10.1177/24741264221120643
• Languages: English
• ISSNs: 2474-1264

Abstract

Purpose: To report OCTA findings in a case of nonaccidental injury (NAI). Methods: Retrospective review of a clinical case. Results: A 5-year-old White child with a history of NAI at age 1 year presented with reduced vision in the left eye resulting from a closed funnel retinal detachment. The right eye had optic nerve pallor, peripheral vascular attenuation, and leakage. Optical coherence tomography angiography (OCTA) showed significant parafoveal attenuation of the superficial vascular plexus, intermediate capillary plexus, and deep capillary plexus. This correlated with inner and middle retinal layer thinning temporal to the fovea and preservation of the ellipsoid zone. The peripapillary vascular plexus was preserved. Laser photocoagulation was performed to the nonperfused peripheral retina, and intravitreal bevacizumab was injected. Attenuation of the superficial, intermediate, and deep capillary plexuses might represent chronic ischemic retinal changes from traumatic injury to the vitreoretinal interface and inner retina in NAI. Conclusions: OCTA identified nonperfusion of the superficial and deep vascular plexuses as late sequelae of NAI. Traumatic injuries to the vitreoretinal interface in NAI might lead to inner retinal ischemia and atrophy with vascular attenuation present on OCTA.