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Shwetha Mangalesh, Du Tran-Viet, Vincent Tai, Brittany M Wong, Christian Viehland, Joanne Finkle, Laura Edwards, Michael C Cotten, Joseph A Izatt, Sharon F. Freedman, Cynthia A Toth; Subclinical retinal manifestations in infants with hypoxic ischemic encephalopathy. Invest. Ophthalmol. Vis. Sci. 2017;58(8):4752.
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We demonstrate use of bedside eye imaging to detect severity of retinal abnormalities in infants with hypoxic ischemic encephalopathy (HIE). In prior neurodevelopmental research retinal findings on OCT were linked to brain injury and poor outcomes in preterm infants. We hypothesize that retinal injury will reflect patterns and severity of brain injury due to HIE.
We used a hand-held, bedside, non-contact spectral-domain optical coherence tomography (SDOCT) imaging system (Envisu 2300, Bioptigen, North Carolina) under a protocol approved by Duke Institutional Review Board and after obtaining consent from a parent/guardian. All infants were imaged without pharmacologic dilation. Eligible preterm and term infants with HIE were imaged within 24 hours of hypothermia initiation (cooling), 72 hours after birth (re-warming), 5 days (time of magnetic-resonance imaging (MRI)) and weekly thereafter until discharged depending on the systemic stability of the infant. We compared retinal findings to clinical MRI findings in all infants.
We enrolled 6 infants born 35-42 weeks gestational age. We recorded macular edema in two infants, sub-retinal fluid (SRF) in one infant, absence of ellipsoid zone at the fovea in 2 infants, thinning of the retinal nerve fiber layer with rake-like defects in 5 infants and hyper-reflective speckles in the ganglion cell layer in all 6 infants. The average retinal nerve fiber layer thickness at the papillomacular bundle was 53µm. 5/6 infants had abnormal MRI findings. Of these, two infants with macular edema showed diffuse signal and edema involving the supra-tentorial region of the brain consistent with severe hypoxic injury. We had more than one imaging time points in 5/6 infants. Those with SRF and macular edema showed progress towards resolution in subsequent imaging. The RNFL thickness increased over time in 2/5 infants.
Non-dilated handheld OCT imaging may be used to assess patterns of neural injury such as neuroinflammation (macular edema), neuronal development (photoreceptor development) and visual pathway axonal loss (RNFL thinning). Future studies are proposed to help in identifying specific markers predictive of brain abnormalities useful to monitor intervention for infants at high risk for brain damage due to birth asphyxia.
This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.
RNFL defects (white arrows) and cystoid spaces (yellow arrow) and over all nerve fiber layer thinning in a term infant with HIE.
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