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Endothelial Keratoplasty & Graft Complications
DMEK
Descemet membrane endothelial keratoplasty (DMEK) transplants only Descemet membrane and its attached endothelial cell monolayer, with no donor stroma at all. Its predecessor, DSEK/DSAEK, carries a thin layer of donor posterior stroma along with the endothelium as a handling carrier; DMEK does away with that carrier entirely. The thinner, more physiologic graft recovers faster and rejects less often than DSEK, which is why DMEK has become the preferred technique for isolated endothelial disease. Fuchs endothelial corneal dystrophy is the most common indication and remains the leading reason for corneal transplantation overall (see Penetrating & Anterior Lamellar Keratoplasty for the broader picture).
The tradeoff is technical difficulty. Once inside the eye, a DMEK graft is a fragile, acellular scroll of tissue that has to be unfolded, oriented correctly, and held against the host stroma with an air or gas bubble until it adheres. Full-thickness PK has no equivalent step: the donor button there is simply sutured into place.
Both DMEK and DSAEK grafts depend on that air or gas bubble to stay apposed to the host stroma while they adhere. When adhesion fails, a gap opens between donor and host, often with graft edema returning over the area that lost contact. This is the single most common complication of modern endothelial keratoplasty, with reported rates ranging from a few percent to as much as a third of cases depending on the series. Most dislocations show up early, within the first one to two weeks after surgery. They're treated by reinjecting air or sulfur hexafluoride gas into the anterior chamber, a step called rebubbling, after which the large majority of grafts reattach and recover normally.
Corneal Graft Rejection
Acute graft rejection is an immune-mediated attack on donor tissue. Its symptom pattern is worth memorizing: redness, sensitivity to light (photophobia), decreased vision, and pain, sometimes recalled by the mnemonic "RSVP." Any of these after a corneal transplant warrants urgent evaluation. Rejection caught early responds well to intensive topical corticosteroids; a delayed diagnosis risks permanent damage to the graft.
Endothelial Rejection and the Khodadoust Line
Rejection can target any donor layer, but endothelial rejection threatens graft survival the most, since the endothelium's pump function is what keeps the cornea clear in the first place. Its hallmark is the Khodadoust line: a line of keratic precipitates advancing across the donor endothelium, marking a moving front of lymphocytes destroying endothelial cells as it goes, usually with accompanying graft edema. Endothelial dropout left behind the line is irreversible, so prompt recognition matters. Initial treatment is intensive topical corticosteroid therapy, sometimes with systemic therapy added, aimed at halting the line's advance before decompensation sets in.
A Khodadoust line marks a rejection episode, treated urgently with steroids. It is not the same thing as chronic graft failure and does not call for repeat transplantation as a first response. Reaching for repeat keratoplasty instead of intensive topical steroids at the first sign of a new Khodadoust line is a common exam trap.
Long-Term Graft Failure
Separate from acute rejection, corneal grafts also fail through a slower, cumulative process: gradual endothelial cell loss over years, the most common cause of late graft failure after penetrating keratoplasty. Transplanted endothelium does not regenerate by cell division, so cell density only ever falls from its post-transplant baseline, and episodes of rejection along the way accelerate the decline. Once density drops below the threshold needed to keep the cornea dehydrated and clear, corneal edema and graft decompensation follow: the same endpoint an untreated Khodadoust line reaches by a faster, acute route.
Glaucoma After Keratoplasty
Elevated intraocular pressure is a common complication after penetrating keratoplasty, most often from surgical trauma to the anterior chamber angle, peripheral anterior synechiae, or other angle distortion that impairs trabecular outflow. Chronic postoperative topical steroids, needed to control the same rejection risk covered above, add a second mechanism: a subset of patients mount a steroid response with elevated IOP from the medication itself. Elevated IOP after keratoplasty threatens the graft as well as the optic nerve, so monitoring it is not a brief postoperative formality. It stays part of long-term follow-up for as long as the graft is in place.
- DMEK = Descemet membrane + endothelium only, no stromal carrier: faster recovery, lower rejection than DSEK, but a technically demanding unscroll/orientation step.
- "RSVP" = redness, sensitivity to light, vision decrease, pain: the classic graft rejection warning symptoms.
- Khodadoust line = a moving line of keratic precipitates = active endothelial rejection → urgent intensive topical steroids.
- Long-term graft failure is usually endothelial cell attrition, often accelerated by prior rejection episodes: distinct from an acute rejection event.
- Post-keratoplasty glaucoma has two drivers: angle damage/synechiae from surgery, and steroid response from the very drops used to prevent rejection.
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