Retinopathy of prematurity

Lancet. 2013 Oct 26;382(9902):1445-57. doi: 10.1016/S0140-6736(13)60178-6. Epub 2013 Jun 17.

Abstract

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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Cryotherapy / methods
  • Disease Progression
  • Early Diagnosis
  • Humans
  • Hyperglycemia / complications
  • Hypoglycemic Agents / adverse effects
  • Infant, Newborn
  • Insulin-Like Growth Factor I / metabolism
  • Insulins / adverse effects
  • Laser Therapy / methods
  • Oxygen / administration & dosage
  • Oxygen / adverse effects
  • Prenatal Diagnosis
  • Retinopathy of Prematurity / etiology*
  • Retinopathy of Prematurity / pathology
  • Retinopathy of Prematurity / therapy
  • Risk Factors
  • Weight Gain

Substances

  • Hypoglycemic Agents
  • Insulins
  • Insulin-Like Growth Factor I
  • Oxygen