Progression of retinopathy of prematurity

Progression of retinopathy of prematurity: (A) Oxygen tension is low in utero and vascular growth is normal. (B) Phase 1: after birth until roughly 30 weeks postmenstrual age, retinal vascularisation is inhibited because of hyperoxia and loss of the nutrients and growth factors provided at the maternal–fetal interface. Blood-vessel growth stops and as the retina matures and metabolic demand increases, hypoxia results. (C) Phase 2: the hypoxic retina stimulates expression of the oxygen-regulated factors such as erythropoietin (EPO) and vascular endothelial growth factor (VEGF), which stimulate retinal neovascularisation. Insulin-like growth factor 1 (IGF-1) concentrations increase slowly from low concentrations after preterm birth to concentrations high enough to allow activation of VEGF pathways. (D) Resolution of retinopathy might be achieved through prevention of phase 1 by increasing IGF-1 to in-utero concentrations and by limiting oxygen to prevent suppression of VEGF; alternatively, VEGF can be suppressed in phase 2 after neovascularisation with laser therapy or an antibody. | EPO=erythropoietin. ω-3 PUFA=ω-3 polyunsaturated fatty acids. | Smith LE. Through the eyes of a child: understanding retinopathy through ROP the Friedenwald lecture. Invest Ophthalmol Vis Sci. 2008;49:5177–82.

Progression of retinopathy of prematurity

The Lancet, (2013) . doi:10.1016/S0140-6736(13)60178-6

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