The transplanted endothelial cells restore the cornea’s fluid-regulating function. When this regulation improves, excess fluid can be controlled within the corneal tissue, supporting recovery of transparency and visual function. The outcome depends on the donor layer adhering to the posterior cornea so its endothelial cells can function in the appropriate anatomical position.
DMEK targets the diseased Descemet membrane and endothelial cells while leaving the cornea’s other structural layers in place. This limited tissue replacement reduces disruption to the remaining corneal architecture. Preserving those layers is therefore central to the technique’s tissue-sparing approach and helps explain its use when endothelial dysfunction is the primary problem.
After the donor graft is unrolled inside the anterior chamber, an air bubble positions it against the posterior cornea. This contact allows the donor endothelial layer to adhere where it can replace the damaged tissue’s function. The bubble therefore supports graft placement and stabilization rather than serving as the treatment itself.
The procedure begins with preparation of a donor graft, followed by insertion through a small incision. The surgeon then unrolls the tissue inside the anterior chamber and introduces an air bubble to position it against the posterior cornea. These steps place the replacement layer at the site where endothelial function is needed.
DMEK is used primarily for corneal endothelial disorders, including Fuchs endothelial dystrophy and bullous keratopathy. These conditions are relevant because the technique replaces the diseased Descemet membrane and endothelial cells rather than replacing the entire cornea. Its application is therefore focused on disorders in which endothelial dysfunction contributes to impaired corneal clarity.
By restoring endothelial fluid regulation while limiting replacement to a thin posterior tissue layer, DMEK can improve corneal clarity and visual function. The technique is also associated with limited disruption of the cornea’s other structural layers. These outcomes explain its clinical relevance in treating endothelial disease rather than broader corneal damage.