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2013 ; 382
(9902
): 1445-57
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Retinopathy of prematurity
#MMPMID23782686
Hellström A
; Smith LE
; Dammann O
Lancet
2013[Oct]; 382
(9902
): 1445-57
PMID23782686
show ga
The immature retinas of preterm neonates are susceptible to insults that disrupt
neurovascular growth, leading to retinopathy of prematurity. Suppression of
growth factors due to hyperoxia and loss of the maternal-fetal interaction result
in an arrest of retinal vascularisation (phase 1). Subsequently, the increasingly
metabolically active, yet poorly vascularised, retina becomes hypoxic,
stimulating growth factor-induced vasoproliferation (phase 2), which can cause
retinal detachment. In very premature infants, controlled oxygen administration
reduces but does not eliminate retinopathy of prematurity. Identification and
control of factors that contribute to development of retinopathy of prematurity
is essential to prevent progression to severe sight-threatening disease and to
limit comorbidities with which the disease shares modifiable risk factors.
Strategies to prevent retinopathy of prematurity will depend on optimisation of
oxygen saturation, nutrition, and normalisation of concentrations of essential
factors such as insulin-like growth factor 1 and ?-3 polyunsaturated fatty acids,
as well as curbing of the effects of infection and inflammation to promote normal
growth and limit suppression of neurovascular development.
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