DM Rupture Alone Does Not Produce Hydrops in Keratoconic Eyes
American Journal of Ophthalmology, September 2019
Parker et al. set out to evaluate the long-held assumption that eyes with keratoconus develop corneal hydrops when the Descemet membrane (DM) breaks. In a two-center retrospective study, the investigators found that no patient had hydrops after DM endothelial keratoplasty (DMEK; in which the DM is selectively replaced). In contrast, hydrops occurred in every patient in whom the posterior corneal stroma and DM were inadvertently punctured during Bowman layer (BL) transplantation. These results discredit DM breakdown alone as the cause of corneal edema in keratoconus.
The authors hypothesized that if DM rupture is the sole reason for corneal hydrops in keratoconus, then edema should result from loss of membrane integrity, regardless of whether the DM break occurred alone or in conjunction with perforation of other corneal layers. To test this, they evaluated outcomes for 15 patients: 10 patients (16 eyes) with comorbid Fuchs endothelial corneal dystrophy and keratoconus who underwent DMEK and five patients (five eyes) with keratoconus who had inadvertent piercing of the posterior corneal stroma and DM during surgery to transplant the BL.
To determine which patients experienced hydrops, the authors reviewed data from slit-lamp biomicroscopy and anterior segment optical coherence tomography conducted intraoperatively and in the early post-op period. They found no evidence of fluid accumulation in any eye treated with DMEK, even though the procedure involves resection of the DM and, in four of the 16 eyes, led to partial or near-total detachment of the donor DM graft postoperatively. In contrast, hydrops developed immediately in all five eyes that had inadvertent perforation of the posterior stroma and DM.
For more than a century, circumstantial evidence has suggested that hydrops in keratoconic eyes is caused by disruption of DM integrity. Advances in lamellar keratoplasty have enabled precise manipulation and excision of the DM, which has led to re-evaluation of the conventional model.
The authors concluded that a defect in the DM is not sufficient to produce hydrops in keratoconus; an accompanying disruption in the posterior corneal stroma would be necessary for the edema to occur. Therefore, they suggested that researchers consider addressing the posterior corneal stroma in future efforts to prevent or treat keratoconic hydrops.
The original article can be found here.