Topic outline

  • Grand Rounds

    Corneal decompensation in the setting of glaucoma surgery is a complex entity that is poorly understood. Endothelial cell loss occurs from both the glaucoma itself and from the placement of intraocular glaucoma devices. This decline in endothelial cells occurs via direct and indirect mechanisms: direct mechanisms involve the mechanical impact of the glaucoma devices on the cornea; indirect mechanisms involve factors such as aqueous turbulence, changes in intraocular pressure, and inflammatory mediators that alter the chemical makeup of the aqueous humor. Key to managing this condition is addressing each of these factors and targeting the underlying pathophysiology. Moreover, when corneal edema cannot be relieved with conservative measures, proceeding with corneal surgery is usually the treatment of choice. Here, we present a patient with corneal decompensation in the setting of previous glaucoma tube placement. We discuss the surgical options for managing corneal decompensation, as well as novel therapies targeting the inflammatory pathways of this disease. We discuss the novel concept of retrocorneal membranes and their role in corneal graft failure in patients with glaucoma tubes. The mechanism by which these membranes form requires the patient to have undergone both glaucoma tube placement and DSAEK surgery; remnant host endothelial cells then undergo an endothelial-to-mesenchymal transformation, resulting in peripheral anterior synechiae and these retrocorneal membranes. Several pathological markers have been identified in these membranes, and several research projects have looked into targeting these markers for therapeutic purposes. However, more specific and stronger therapeutics are currently needed to target these pathological markers in order to properly treat this complex condition.

    Presentation Date: 05/05/2022
    Issue Date: 06/17/2022