Klin Monbl Augenheilkd 2013; 230(9): 894-901
DOI: 10.1055/s-0033-1350764
Übersicht
Georg Thieme Verlag KG Stuttgart · New York

Kindliche Ablationes: ROP und Myopie

Childhood Retinal Detachment: ROP and Myopia
B. Müller
Augenklinik der Charité Universitätsmedizin Berlin (Standorte Virchow Klinikum und Klinikum Benjamin Franklin)
,
A. M. Joussen
Augenklinik der Charité Universitätsmedizin Berlin (Standorte Virchow Klinikum und Klinikum Benjamin Franklin)
› Author Affiliations
Further Information

Publication History

eingereicht 09 July 2013

akzeptiert 29 July 2013

Publication Date:
28 August 2013 (online)

Zusammenfassung

Dieser Übersichtsartikel diskutiert die pathophysiologischen Mechanismen und Behandlungsoptionen, die zu einer traktiven Ablatio bei der Frühgeborenenretinopathie und bei ROP-Residuen in der Jugend und im frühen Erwachsenenalter führen. Die retinale Vaskularisation ist inkomplett bei Frühgeborenen. Die Phase I der ROP besteht aus einem verzögerten Wachstum der Gefäße und einem Gefäßverlust nach der Geburt, die zu einer Hypoxie führt. Die anschließende Phase II resultiert in hypoxieinduzierten Gefäßproliferationen und – in der Konsequenz – in vitreoretinaler Traktion. Das anatomische und funktionelle Ergebnis bei der ROP ist abhängig von der vorherigen Therapie (z. B. Laserphotokoagulation in der peripher avaskulären Peripherie oder eine Anti-VEGF-Injektion). Während in der Literatur Wiederanlageraten von > 70 % bei der ROP Stadium IV a beschrieben wurden, sind die funktionellen und anatomischen Ergebnisse späterer Stadien limitiert. Residualformen der ROP können eher zu rhegmatogenen als traktiven Ablationes in der Kindheit bis zum frühen Erwachsenenalter führen. Die Myopie ist dabei mit der ROP assoziiert und kann die retinale Situation weiter beeinträchtigen und das Risiko für eine rhegmatogene Amotio erhöhen. Retinale Veränderungen in Assoziation mit einer ROP erfordern lebenslängliche Kontrollen.

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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