Abstract
This article reviews the cause and treatment options for retinopathy of prematurity (ROP)-related tractional detachment and detachments in ROP residuals during childhood and early adulthood. Retinal vascularisation is incomplete after premature birth. Phase I of ROP consists of a delayed retinal vascular growth and vessel loss after premature birth resulting in hypoxia, phase II results in hypoxia-induced vascular proliferation and as a consequence to vitreoretinal traction. The anatomic and functional outcome of tractional detachment in ROP is determined by the previous treatment (e.g., laser to the avascular periphery or anti-VEGF). While the literature reports re-attachment rates > 70 % in ROP IV a, functional and anatomic outcome in the later stages is limited. ROP residuals may cause rhegmatogenous rather than tractional detachments in childhood or early adulthood. Myopia is associated with ROP and may further complicate the retinal situation and the risk for rhegmatogenous detachment. The retinal changes due to ROP warrant lifelong controls.
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