Outcomes of Descemet Membrane Endothelial Keratoplasty

Visual Acuity

Improvement of visual acuity along with reduction of glare and haze as well as amelioration of color vision is the hallmark of DMEK surgery.

In a series of 500 patients, results for visual acuity were excellent: at 6 months. 75% of eyes reached ≥{20/25}, 41% achieved ≥{20/20}, and 13% ≥{20/18} (≥1.2) ( n = 418) when excluding eyes with ocular comorbidities. An analysis of 138 eyes without comorbidities showed equally convincing results: mean best corrected visual acuity (BCVA) at 1 year was {20/24}; 41% achieved {20/20}, 80% achieved {20/25}, and 98% achieved {20/30}. Analyzing 1700 DMEK procedures, Kruse et al. obtained similar results: at 3 months visual rehabilitation is completed; 95% of eyes see better than {20/40}, and 70% see better than {20/25}. In addition, both contrast sensitivity and color vision improve after DMEK.

Hyperopic Shift

Understanding the change in refractive power of the cornea after DMEK is critical in predicting visual recovery and managing patient expectations. This is particularly important in the setting of a combined cataract and DMEK procedure. Although DMEK does not significantly increase corneal thickness, Laaser et al. reported a hyperopic shift of +0.5 (±0.6 D) after DMEK. This hyperopic shift was also confirmed by van Dijk et al. (+0.33 ± 1.08 D) and Price et al. +0.49 (±0.63 D) in related studies. ^, Interestingly, Parker et al. found that phakic eyes undergoing DMEK had a slightly higher hyperopic shift of +0.74D. The hyperopic shift should be accounted for when trying to predict the refractive outcome for the patient.

Restoration of the Normal Anatomy

The separation of DM from the stroma uses a natural cleavage between the corneal stroma and the interfacial matrix of DM. ^, Upon successful transplantation of the DMEK graft, the natural anatomy is reconstituted, making a grafted cornea indistinguishable from a normal cornea ( Fig. 137.1 ). Postmortem analysis of DMEK confirmed the picture of a “virgin” or unoperated cornea. Evaluation of stripped donor DM reveals large inter-individual variations of the inner surface of the graft. These differences explain variable adhesion rates of DM grafts.

Morphology and Optical Properties of the Anterior Corneal Surface

As a general rule, the optical quality of the anterior corneal surface becomes almost normal in most patients after DMEK. Exceptions may occur if there was significant subepithelial scarring due and fibrosis. Nonetheless, it has been shown that patients with minimal anterior stromal scarring do not differ from controls with regard to higher order aberrations (HOAs) in the 4.0-mm zone. However, similar to DSAEK, subepithelial fibrosis, loss of keratocytes, and collagen disorganization may persist in some patients after DMEK. It is evident that anterior surface irregularities and haze are an important limiting factor in visual rehabilitation after DMEK due to increased HOAs.

Oyakawa et al. reported surface regularity of height (SR_H) as another potentially useful means of quantifying corneal irregularity before and after DMEK. It is correlated to total HOAs, as well as a direct measurement of total corneal irregularity using AS-OCT. This differs from the indirect means by which HOAs are measured using Schiempflug imaging. Anterior and posterior SR_H have been shown to improve after DMEK, with a statistically significant directional correlation with BCVA. This may help surgeons index the predictive quality of refractive outcome prior to and after DMEK.

When investigating causes for unsatisfactory visual recovery after DMEK, corneal irregularities and/or central corneal scarring were found in 8% of patients. Nine percent showed subnormal spectacle-corrected distance visual acuity (CDVA) and/or monocular diplopia due to corneal scarring, surface irregularities, or undetectable optical imperfections. These patients were managed with contact lens fitting. Surface problems are more likely to occur after severe edema, and prolonged preoperative corneal edema (>12 months) is a risk factor for irregular astigmatism after DMEK.

Epithelial and subepithelial pathology after DMEK may be prevented by epithelial debridement with mitomycin C application during DMEK surgery.

Optical Properties of the Posterior Corneal Surface

The optical quality of the posterior cornea by means of HOAs improves after DMEK. Normal values for Z ₄ ² , Z ₆ ⁰ , Z ₆ ² , and Z ₆ ⁴ in the central 4.0-mm zone were previously shown. However, combined values for HOA in the 4.0-mm zone were significantly higher after DMEK. In the 6.0-mm zone only tetrafoil (Z ₄ ⁴ ) increased after DMEK. Increase in Z ₄ ⁴ may have been caused by the corneal tunnel in the 12 o’clock position in that study. Thus DMEK restores the optical properties of the posterior surface to near normal. In a similar study, van Dijk et al. described higher values of posterior HOAs (root-mean-square [RMS] third to sixth Zernike order), as well as backscattered light after DMEK.

Morphology and Function of the Corneal Endothelium

One of the most critical questions determining the future use of DMEK regards longevity and function of the grafted endothelium. It has been thought that endothelial cells after DMEK migrate from the donor tissue onto the host, possibly allowing rearrangement of the grafted endothelium. Furthermore, the grafted endothelium must maintain its original transcription program after transplantation (phenotypic differentiation), which is not the case after failed DMEK when myofibroblastic transdifferentiation occurs.

Large trials have confirmed a slow but continuous loss of endothelial cells after penetrating keratoplasty (PK), even if surgery was performed under optimal conditions and without risk factors (see Chapter 114 ; Fig. 137.2 ). In DSAEK, there is a relatively high initial endothelial cell loss followed by a more gradual depletion, which is even slower than in PK (see Chapter 134 ; see Fig. 137.2 ).

In DMEK, there is a significant loss of endothelial cells associated with graft preparation and shipment, as well as insertion and manipulation. This drop in endothelial cell count was most severe in the initial phase of the development DMEK. In his first report, Melles described a reduction from 2610 (±147) cells/mm ² to 2030 (±373) cells/mm ² at 6 months. Similar data stem from the early series of Price describing an endothelial cell loss at 1 year of 36 ± 20%, with most of the loss occurring during the first 3 months (31 ± 18%). Another study concerning initial experience showed a cell loss of 39% at 3 months and of 40% at 6 months.

The major factors determining cell loss in DMEK is surgical trauma, rebubbling, and rejection episodes. For novice surgeons cell loss at 6 months was 46% or 47%. ^, In contrast, careful preselection of patients, advanced technique, and surgeon experience can limit endothelial cell loss to 19%.

Thus increased technical skills and know-how continue to reduce cell loss in major centers. The latest report from Melles’ group describes a decrease in endothelial cell density of 35% at 6 months, 38% at 12 months, 43% at 24 months, 47% at 36 months, 52% at 48 months, and 55% at 60 months. This represents a significant decrease in the first 6 months, followed by a yearly decrease of only 7%. However, patient numbers for the 4- and 5-year follow-ups were very low (25 and 9, respectively), limiting the power of the study (see Fig. 137.2 ). In a short-term study by Price et al. investigating 492 patients, the mean endothelial cell loss remained stable at 26% between 3 and 6 months. In a long-term study, the same group reported an endothelial cell loss of 27% at 3 and 6 months as well as 1 year, 28% at 2 years, 31% at 3 years, 36% at 4 years, and 39% at 5 years. Out of 637 DMEKs in this study, 28 completed a 5-year follow-up, which limits the power of this study (see Fig. 137.2 ).

Price et al. evaluated 5 year data in 2017 consecutive cases of DSAEK and DMEK (1312 DSEK and 705 DMEK) and found that the mean ECC in DMEK was comparable to DSAEK with a cell loss of 47% ± 19% for DMEK and 48% ± 19% for DSAEK. Not surprisingly, graft rejection episodes increased endothelial cell loss; however, this was not predictive of graft failure within 5 years in either group.

Graft Preparation