Hyperoxemic retinal neuronal necrosis in the premature neonate.
A cytologically distinctive type of acute hyperoxemic injury of retinal neurons occurs in premature neonates. Ganglion cells in the central well-vascularized neonate retina are susceptible to excessive oxygen and this is expressed morphologically by karyorrhexis of their nuclei. We observed retinal neuronal necrosis in neonates who had hyperoxemia of greater than 150 torr for two hours or longer in the first week of life. Neuronal necrosis was strikingly associated with immaturity as determined by gestational age and birth weight: of 30 involved neonates, all were below 2,000 g; of 47 autopsied premature infants with birth weights under 1,500 g who survived for at least two days, 26 (55%) had acute retinal necrosis. When gestational age was used as a measure of prematurity, the highest incidence occurred in the 24- to 27-week group where 13 of 21 (62%) were involved. Hyperoxemic karyorrhectic changes, most prominent in the ganglion cells of the macula, are distinct from the classic peripheral mesenchymal vascular abnormalities of retinopathy of prematurity.
D001724:Birth Weight; D001921:Brain / Q000473:pathology; D002467:Cell Nucleus / Q000473:pathology; D005260:Female; D005865:Gestational Age; D006801:Humans; D007231:Infant, Newborn; D007245:Inferior Colliculi / Q000473:pathology; D008266:Macula Lutea / Q000473:pathology; D008297:Male; D009336:Necrosis; D009474:Neurons / Q000473:pathology; D012160:Retina / Q000473:pathology*; D012165:Retinal Ganglion Cells / Q000473:pathology*; D012178:Retinopathy of Prematurity / Q000473:pathology*; D013477:Superior Colliculi / Q000473:pathology