Retinopathy of prematurity

Summary 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). Su...

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Bibliographic Details
Published in:The Lancet (British edition) 2013-10, Vol.382 (9902), p.1445-1457
Main Authors: Hellström, Ann, Prof, Smith, Lois EH, Prof, Dammann, Olaf, Prof
Format: Article
Language:English
Subjects:
Age
Babies
Biological and medical sciences
Birth weight
Cryotherapy - methods
Disease Progression
Early Diagnosis
General aspects
Government grants
Growth factors
Humans
Hyperglycemia - complications
Hyperoxia
Hypoglycemic Agents - adverse effects
Hypoxia
Infant, Newborn
Insulin-Like Growth Factor I - metabolism
Insulins - adverse effects
Intensive care
Internal Medicine
Laser Therapy - methods
Medical sciences
Mortality
Neonates
Oftalmologi
Ophthalmology
Oxygen - administration & dosage
Oxygen - adverse effects
Polyunsaturated fatty acids
Premature birth
Prenatal Diagnosis
Retina
Retinopathies
Retinopathy of Prematurity - etiology
Retinopathy of Prematurity - pathology
Retinopathy of Prematurity - therapy
Risk Factors
Studies
Vascular endothelial growth factor
Weight Gain
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Summary:Summary 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 ω-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.
ISSN:0140-6736
1474-547X
DOI:10.1016/S0140-6736(13)60178-6