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Versión en español
Information for health professionals

Retinopathy of the Premature is a vasoproliferative retinopathy of multifactorial origin and produced by the existence of an immature retina and only partially vascularized at moment of premature birth.

The alteration in the development of the retinal vasculature resulting from situations of hypoxia or relative hyperoxia and the imbalance of vascular growth factors in the weeks that follow the birth, leads to the appearance of neoformation vessels that in later stages can cause a tractional detachment of the retina and the loss of its functionality.

The process of normal vascularization of the retina starts from the optic nerve in the week 16 of gestation, reaching the nasal ora serrata at approximately 36 weeks of gestation and the temporary serrata ora between 39 and 41 weeks.

The immature retina of prematurity can follow a normal development process after birth reaching retinal maturity without developing ROP. In other cases there may be a noxa that alters this process of normal retinal development generating retinopathy.

It is very important to take into account the above described to understand that children are not born with retinopathy of prematurity but that there must be some biological change after birth that causes the disease to be triggered. This is a fundamental fact to consider at the moment to plan a screening strategy. Initially that biological effect was attributed to Oxygen administration, however, today it is known that oxygen administered in controlled and rational as it is currently done would not be the causal factor in itself, being more dangerous the hypoxia and the fluctuations in the sanguineous saturation of this one.

The changes produced in the oxygen tension of the premature one, would generate a deregulation in the expression of the Vascular Endothelial Growth Factor or Vascular Endothelial Growth Factor (VEGF), a molecule present in the normal retina of the child in gestation and that would help control vascular development. This deregulation of VEGF would ultimately produce an exaggerated vaso-proliferation at the retinal level, thus giving rise to the ROP.

When the process of retinopathy has been unleashed, networks of neovessels grow on the level of the retina or at the level of the ridge and then extend towards the vitreous cavity.

Exudation of blood elements and the proliferation of fibrovascular membranes occur whose contraction will give rise to the tractional retinal detachment characteristic of retinopathy of the premature. Retinal detachment that in its most advanced stages is observed as a whitish membrane behind the lens and that gave rise to the name "retrolental fibroplasia" how this disease was originally known.

Today we can affirm that the physiopathology of ROP is complex and its multifactorial etiology where the main role is played by extreme prematurity. No study has been decisive in defining a unique causative factor of this disease. The administration of supplemental oxygen, genetic factors, the presence of candidemia, ambient light, the race, antioxidants, etc..
Today we only know that the more premature a child is, the more more tortuous is its clinical evolution and more altered is its homeostasis will have a greater risk of developing retinopathy of prematurity.
ROP México
CDMX 2017