Retinal detachments associated with retinopathy of prematurity (ROP) are predominantly tractional [1], occasionally exudative [2], and rarely rhegmatogenous. The configuration of the tractional retinal detachment in ROP is guided by the fibrous tissue growing over the shunt at the junction of the vascular- avascular retina [3] and the hyaloid stalk. Various tractional forces in the vitreous and previous treatment, if any, modulate these changes. The tractional forces can include ridge to ridge (trans-ridge), ridge to the retina, lens, hyaloid or ciliary body, etc. ROP detachment assumes a tent-shaped configuration when the tractional vectors from the contracting fibrovascular tissue over the ridge and around the optic disc predominate [1]. Isolated exudative detachment in ROP is often peripheral and can extend posteriorly but is relatively uncommon and can, at times, follow laser treatment. The detachment, occasionally, can have a bullous configuration when it is secondary to exudation. Rhegmatogenous retinal detachment, uncommon in active ROP, can happen in subjects with regressed cicatricial ROP at a later stage secondary to firmly attached contracting posterior hyaloid or fibrous tissue. In this article, we report a series of 5 babies (10 eyes) with atypically configured bleb- shaped posterior combined tractional and exudative retinal detachment in severe ROP, not yet reported in the literature (Medline search).

The atypically configured bleb-shaped predominantly exudative and combined with focal tractional posterior only detachments in babies with ROP described here are not reported before (Medline search with keywords, ‘bleb or blister-like detachment’, ‘ROP’, ‘atypical detachment’, ‘configuration of Stage 4B ROP’, ‘combined ROP detachment’). These are different from classical tractional or exudative retinal detachments in ROP by their physical configuration (Fig. 1 and Supplementary Figs. 1–4) and response to treatment. (Online supplement Table 1). Because all affected babies had a stormy post-natal course and received 100% unblended oxygen, we suspect oxygen-induced retinopathy could be the predominant pathogenesis. However, the extensive posterior exudation along the developing arcades has an unknown mechanism and needs further studies. The disorganized retinal vasculature and relatively posterior location than expected for the age (GA 28–30 weeks; PMA 36–39 weeks) or birth weight seen in these babies strike a resemblance to oxygen-induced retinopathy in the experimental animal [4]. We suspect the extensive avascular periphery with high vascular endothelial growth factor (VEGF) drive could have accounted for severe fibrovascular proliferation over the posterior pole, as reported by Yokoi et al. [3].

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