De novo glaucoma and ocular hypertension occur significantly less frequently following Descemet membrane endothelial keratoplasty (DMEK) than after Descemet stripping automated endothelial keratoplasty (DSAEK), according to a systematic review and meta-analysis published in the American Journal of Ophthalmology. Researchers analyzed 33 studies encompassing 5,235 eyes up to June 2025, finding pooled de novo glaucoma incidence rates of 3.3% for DMEK compared with 10.7% for DSAEK.
Post-Keratoplasty Glaucoma Rates: DMEK vs. DSAEK Data
Post-keratoplasty glaucoma threatens optic nerve function and graft survival, yet surgeons often lack procedure-specific estimates to guide technique selection. The meta-analysis found that pooled incidence was lower after DMEK across multiple metrics. Medication initiation or escalation occurred in 5.8% of DMEK eyes versus 19.9% of DSAEK eyes. Ocular hypertension developed in 9.1% of DMEK cohorts compared with 33.7% in DSAEK groups.
Observation times differed between the groups, with DSAEK cohorts averaging 68.1 months of follow-up time compared to 35.3 months for DMEK cohorts. However, calculated incidence rate ratios still favored DMEK, registering at 0.45 for glaucoma diagnosis and 0.31 for ocular hypertension. When investigators restricted glaucoma definitions strictly to structural optic-nerve change or visual field loss, the incidence gap narrowed to 5% for DMEK versus 8.1% for DSAEK, though that strict subset was limited to five study arms.
Anatomic Differences and Steroid Exposure Mechanisms
The lower event rates observed in DMEK stem from distinct anatomical and pharmacological factors. DMEK involves the transplantation of only Descemet’s membrane and endothelium with a graft thickness of approximately 10μm to 15μm. In contrast, DSAEK grafts measure 50μm to 200μm in thickness. Francis Price, Jr., MD, provided clinical imagery for the research.
Did you know? Thicker DSAEK lenticules sit more anteriorly in the eye and have historically been favored for complex eyes, which may amplify postoperative intraocular pressure stress and outflow limitation.
Researchers noted that post-keratoplasty glaucoma reflects both steroid responsiveness and structural outflow compromise. Corticosteroids induce lasting trabecular meshwork changes that do not always fully reverse when doses drop, requiring continued therapy or secondary glaucoma surgery. Mechanical factors such as peripheral anterior synechiae, anteriorly positioned grafts or intraocular lenses, shallow anterior chambers, and pre-existing angle narrowing convert early postoperative pressure spikes into sustained outflow issues.
Greater steroid exposure independently correlated with ocular hypertension in meta-regression models. The thinner DMEK tissue profile reduces interface inflammation and rejection rates, enabling clinicians to transition patients to less potent topical corticosteroids more quickly.
Clinical Decision-Making and Future Monitoring
These findings support individualized surgical planning that balances glaucoma risk against visual outcomes, rejection rates, anatomic complexity, and surgeon expertise. Authors of the study recommend that clinicians maintain vigilant intraocular pressure monitoring following both endothelial keratoplasty procedures and adopt steroid-sparing strategies when clinically appropriate, particularly in borderline eyes.
Frequently Asked Questions
What is the main difference in glaucoma incidence between DMEK and DSAEK?
De novo glaucoma diagnosis occurs in 3.3% of DMEK eyes compared to 10.7% of DSAEK eyes, according to pooled data from 33 studies.
Why does DMEK have a lower rate of ocular hypertension?
DMEK utilizes an ultra-thin graft (10μm to 15μm) that reduces interface inflammation and allows for faster visual recovery and earlier reduction of potent topical corticosteroids compared to thicker DSAEK grafts.
How does graft thickness affect intraocular pressure?
Thicker grafts, such as those used in DSAEK (50μm to 200μm), sit more anteriorly in the eye, which can contribute to mechanical and anatomic outflow limitations when combined with postoperative inflammation and steroid response.
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