Author Affiliations: Department of Ophthalmology, University of Basel, Basel, Switzerland (Drs Todorova and Grieshaber); and Department of Ophthalmology and Visual Sciences, School of Medicine and Public Health, University of Wisconsin–Madison (Dr Parsa).
In congenital glaucoma, the exposure to consistently elevated intraocular pressure expands the still-elastic scleral shell and leads to tissue remodeling with iris thinning, zonular stretching, posterior recession of the peripheral uvea, rarefied ciliary body, increased corneal diameter, and increased axial length of the bulbus.1
As recently demonstrated via ultrasound biomicroscopy by Roche et al,2 the well-known breaks of the Descemet membrane in primary congenital glaucoma can also be accompanied by previously unsuspected clefting of the corneal stroma, resulting in its immediate hydration and opacification known as hydrops. If the intraocular pressure is quickly normalized with reappositioning of the corneal stromal cleft wound edges, little, if any, stromal scarring then occurs owing to healing by primary rather than secondary intention.2
Todorova MG, Parsa CF, Grieshaber MC. Ciliary Body Clefting Accompanied by Rupture of the Trabecular Meshwork in Congenital Glaucoma. Arch Ophthalmol. 2012;130(4):534. doi:10.1001/archophthalmol.2011.2498
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