Histopathologic Features of Descemet Membrane Endothelial Keratoplasty Graft Remnants, Folds, and Detachments

Müller, Thomas; Verdijk, Robert M.; Lavy, Itay; Bruinsma, Marieke; Parker, Jack; Binder, Perry S.; Melles, Gerrit R.J.

doi:10.1016/j.ophtha.2016.08.014

Cited by 39 publications

(23 citation statements)

References 16 publications

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“…Descemetorhexis without endothelial transplantation has been investigated as a potential treatment for Fuchs’ dystrophy corneas that decompensate, and encouraging results have been reported with this approach because viable endothelial cells remain in the periphery of these diseased corneas and appear to migrate and, possibly, proliferate. 45-47 However, posterior stromal fibrosis has been noted in some human corneas after Descemetorhexis without endothelial transplant, 48,49 similar to what we have noted in rabbits that have Descemetorhexis without endothelial transplantation. 5 Rabbit corneas have more tendency to develop fibrosis than human corneas.…”

Section: Descemetorhexis Without Endothelial Transplantationsupporting

confidence: 79%

Coordinated Modulation of Corneal Scarring by the Epithelial Basement Membrane and Descemet's Basement Membrane

Wilson¹

2019

J Refract Surg

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Purpose: To provide an overview of the importance of the coordinated role of the epithelial basement membrane (EBM) and Descemet's basement membrane (DBM) in modulating scarring (fibrosis) in the cornea after injuries, infections, surgeries and diseases of the cornea. Methods: Literature review. Results: Despite their molecular and ultrastructural differences, the EBM and DBM act in coordinated fashion to modulate the entry of transforming growth factor beta (TGFβ), and other growth factors, from the epithelium/tear film and aqueous humor, respectively, into the corneal stroma where persistent levels of these modulators trigger the development and persistence of myofibroblasts that produced disordered, opaque extracellular matrix not usually present in the corneal stroma. The development of these myofibroblasts and the extracellular matrix they produce is often detrimental to visual function of the cornea after PRK, LASIK buttonhole flaps, persistent epithelial defects, microbial keratitis, DSEAK, DMEK, while being beneficial in other situations such as the scarred edge of LASIK flaps and donor-recipient interface in penetrating keratoplasty (PKP). Efforts to modulate the repair or replacement of the EBM and DBM, and thereby the development or disappearance of myofibroblasts should be a major emphasis of treatments provided by refractive and corneal surgeries, infections trauma or diseases of the cornea. Conclusions: The EBM and DBM are critical modulators of the localization of pro-fibrotic growth factors, such as TGFβ, that modulate the development and persistence of myofibroblasts that produce corneal scars (stromal fibrosis). Therapeutic efforts to regenerate or repair EBM and/or DBM, and interfere with the development of myofibroblasts or facilitate their disappearance, are often the key to clinical outcomes. The critical role of the EBM and DBM in modulating corneal myofibroblast development and scarring The central role of the epithelial basement membrane (EBM) 1-4 and Descemet's basement membrane (DBM) 4,5 in modulating scarring (stromal fibrosis) that may develop after surgeries, injuries, infections and diseases of the cornea has been illustrated by numerous

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Section: Descemetorhexis Without Endothelial Transplantationsupporting

confidence: 79%

Coordinated Modulation of Corneal Scarring by the Epithelial Basement Membrane and Descemet's Basement Membrane

Wilson¹

2019

J Refract Surg

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“…Third, others have noted that surgical difficulties, including poor graft decentration [ 61 , 62 ], anterior band layer fragments [ 63 ], and incomplete removal of host Descemet membrane [ 64 ], associate with increased graft detachment. Moreover, a study using prospective transplant registry data on 752 DMEK-treated eyes showed with multivariate analysis that surgical difficulty was a risk factor for both rebubbling (Odds Ratio = 2.28, 95% confidence intervals = 1.20–4.33, p = 0.012) and early graft failure (Odds Ratio = 2.93, 95% confidence intervals = 1.42–6.04, p = 0.012) [ 65 ].…”

Section: Discussionmentioning

confidence: 99%

Identification of the preoperative and perioperative factors that predict postoperative endothelial cell density after Descemet membrane endothelial keratoplasty: A retrospective cohort study

Chaussard¹,

Bloch²,

Elnar

et al. 2022

PLoS ONE

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Low postoperative endothelial-cell density (ECD) plays a key role in graft failure after Descemet-membrane endothelial keratoplasty (DMEK). Identifying pre/perioperative factors that predict postoperative ECD could help improve DMEK outcomes. This retrospective study was conducted with consecutive adult patients with Fuchs-endothelial corneal dystrophy who underwent DMEK in 2015–2019 and were followed for 12 months. Patients underwent concomitant cataract surgery (triple-DMEK) or had previously undergone cataract surgery (pseudophakic-DMEK). Multivariate analyses assessed whether: patient age/sex; graft-donor age; preoperative ECD, mean keratometry, or visual acuity; triple DMEK; surgery duration; surgical difficulties; and need for rebubbling predicted 6- or 12-month ECD in the whole cohort or in subgroups with high/low ECD at 6 or 12 months. The subgroups were generated with the clinically relevant threshold of 1000 cells/mm2. Surgeries were defined as difficult if any part was not standard. In total, 103 eyes (95 patients; average age, 71 years; 62% women) were included. Eighteen eyes involved difficult surgery (14 difficult graft preparation or unfolding cases and four others). Regardless of how the study group was defined, the only pre/perioperative variable that associated significantly with 6- and 12-month ECD was difficult surgery (p = 0.01, 0.02, 0.05, and 0.0009). Difficult surgery also associated with longer surgery duration (p = 0.002). Difficult-surgery subgroup analysis showed that difficult graft dissection associated with lower postoperative ECD (p = 0.03). This association may reflect endothelial cell loss due to excessive graft handling and/or an intrinsic unhealthiness of the endothelial cells in the graft that conferred unwanted physical properties onto the graft that complicated its preparation/unfolding.

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“…However, this complication has been noted in human corneas after descemetorexis without endothelial transplant 27. Similarly, there is likely to be a risk of posterior fibrosis in corneas that have complicated Descemet's membrane endothelial keratoplasty (DMEK) and Descemet's stripping automated endothelial keratoplasty (DSAEK) surgeries where a portion of the posterior surface of the recipient cornea is not covered by donor tissue containing the Descemet's membrane, as has also been noted in clinical studies 28,29. A goal of DMEK and DSAEK should be to cover all exposed posterior stromal tissue to decrease posterior stromal fibrosis as a potential complication of these surgeries.…”

Section: Discussionmentioning

confidence: 92%

Descemet's Membrane Modulation of Posterior Corneal Fibrosis

Medeiros

Saikia

Oliveira

et al. 2019

Invest. Ophthalmol. Vis. Sci.

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PurposeThe purpose of this study was to evaluate the effect of removal of Descemet's basement membrane and endothelium compared with removal of the endothelium alone on posterior corneal fibrosis.MethodsTwelve New Zealand White rabbits were included in the study. Six eyes had removal of the Descemet's membrane–endothelial complex over the central 8 mm of the cornea. Six eyes had endothelial removal with an olive-tipped cannula over the central 8 mm of the cornea. All corneas developed stromal edema. Corneas in both groups were cryofixed in optimum cutting temperature (OCT) formula at 1 month after surgery. Immunohistochemistry (IHC) was performed for α-smooth muscle actin (SMA), keratocan, CD45, nidogen-1, vimentin, and Ki-67, and a TUNEL assay was performed to detect apoptosis.ResultsSix of six corneas that had Descemet's membrane–endothelial removal developed posterior stromal fibrosis populated with SMA+ myofibroblasts, whereas zero of six corneas that had endothelial removal alone developed fibrosis or SMA+ myofibroblasts (P < 0.01). Myofibroblasts in the fibrotic zone of corneas that had Descemet's membrane–endothelial removal were undergoing both mitosis and apoptosis at 1 month after surgery. A zone between keratocan+ keratocytes and SMA+ myofibroblasts contained keratocan-SMA-vimentin+ cells that were likely CD45− corneal fibroblasts and CD45+ fibrocytes.ConclusionsDescemet's basement membrane has an important role in modulating posterior corneal fibrosis after injury that is analogous to the role of the epithelial basement membrane in modulating anterior corneal fibrosis after injury. Fibrotic areas had myofibroblasts undergoing mitosis and apoptosis, indicating that fibrosis is in dynamic flux.

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Histopathologic Features of Descemet Membrane Endothelial Keratoplasty Graft Remnants, Folds, and Detachments

Cited by 39 publications

References 16 publications

Coordinated Modulation of Corneal Scarring by the Epithelial Basement Membrane and Descemet's Basement Membrane

Coordinated Modulation of Corneal Scarring by the Epithelial Basement Membrane and Descemet's Basement Membrane

Identification of the preoperative and perioperative factors that predict postoperative endothelial cell density after Descemet membrane endothelial keratoplasty: A retrospective cohort study

Descemet's Membrane Modulation of Posterior Corneal Fibrosis

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