Retinopathy of prematurity (ROP)
Introduction
First described in 1940 and termed retrolental fibroplasia. The
incidence of ROP is inversely proportional to gestational age.
ROP probably develops in genetically susceptible infants.
Etiology
- Immature retina without full vascularization
- Hyperoxia and changes in oxygen exposure disrupt
the natural course of vascularization
- Changes in expression of VEGF (vascular endothelial
growth factor) which is strongly induced by hypoxia
- First phase (hyperoxic) — VEGF is markedly
decreased, there is retinal vasoconstriction and
endothelial cells undergo apoptosis
- Second phase (relative hypoxic) — VEGF
increases and induces abnormal growth of retinal vessels
(neovascularization) Those new vessels are fragile and
can bleed. With healing fibrous scars develop. Severe
involvement is characterized by extraretinal fibrovascular
proliferation that means spread of the abnormal vessels
into the vitreous. The retina is pulled anteriorly and may
detach. Total retinal detachement and full blindness is
the worst complication
Classification
Staging of ROP
- 1 — demarcation line lying in plane of retina,
at junction of vascularized and avascular retina
- 2 — ridge, the demarcation line extends
out of the plane of the retina
- 3 — ridge with extraretinal fibrovascular
proliferation, neovascularization may extend into vitreous
- 4 — subtotal retinal detachment
- 5 — total retinal detachment
Clinical signs
- Complications: myopia, visual impairment,
blindness, strabism and glaucoma
- Therapy: repeated examinations for ROP
in threatened infants until the retina is fully vascularized,
cryotherapy or vitrectomy in advanced ROP
