Retinal glial cells, probably transdifferentiated Müller cells, are involved in the formation of full-thickness macular hole-associated ERMs by a gliotic and fibrotic process. Such ERMs contain newly formed Type I, III, and V collagen depositions. The cell density of ERM affects its biomechanical properties and determines the difficulty of ERM peeling.

In our patient PDT with verteporfin effectively resolved the exudative retinal detachment associated with a diffuse choroidal haemangioma. Resolution of subretinal fluid occurred over several months without retreatment. We noted no side effects of the combination PDT and general anaesthesia, nor did we encounter ocular side effects of the treatment.

<b><i>Background:</i></b> High arterial oxygen saturation (SaO₂) is associated with the development of retinopathy of prematurity (ROP), but difficult to avoid. <b><i>Objective:</i></b> To assess the association between severe ROP and a burden of cerebral and arterial hyperoxia. <b><i>Methods:</i></b> We retrospectively analyzed 225 preterm infants born ≤30 weeks’ gestation. The cerebral oxygen saturation (r_cSO₂) and SaO₂ were measured within the first 96 h after birth. We determined the burden of both cerebral and arterial hyperoxia, which was defined as the percentage of time spent at saturation thresholds exceeding 85 and 90%, respectively. Their association with severe ROP (prethreshold disease type 1) was tested using logistic regression analyses. <b><i>Results:</i></b> Median gestational age (GA) was 28.0 weeks (interquartile range 26.7–29.0) and mean birth weight 1,032 g (±281 SD). Eight infants developed severe ROP. Infants with severe ROP spent more time at cerebral hyperoxic levels than infants without severe ROP (medians 30 vs. 16%). Adjusted for GA, for every 10% increase in burden of cerebral hyperoxia, the OR for developing ROP was 1.50 (95% CI 1.09 – 2.06, <i>p</i> = 0.013). A burden of arterial hyperoxia was not associated with ROP. Infants with severe ROP experienced even less arterial hyperoxia, although not statistically significant. <b><i>Conclusions:</i></b> Cerebral hyperoxia may be a better early predictor of severe ROP than arterial hyperoxia. Moreover, under strict oxygen management, cerebral hyperoxia in these infants may result from cerebral immaturity rather than a high SaO₂. Whether reducing cerebral hyperoxia is feasible and might prevent ROP needs to be further examined.