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  • 2020–2021 BCSC Basic and Clinical Science Course™

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    8 External Disease and Cornea

    Chapter 15: Clinical Approach to Corneal Transplantation

    Endothelial Keratoplasty

    Postoperative Care and Complications

    Dislocation or decentration of the donor graft

    In DSEK and DMEK, the donor tissue should be well centered over the pupil, without fluid in the interface. To promote tissue adherence over the ensuing days, 40%–60% of the air bubble injected intraoperatively should remain after DSEK on postoperative day 1 (Fig 15-17), and 80% of the gas (SF6) or air bubble should remain after DMEK on day 1 (Fig 15-18). The air bubble resorbs within 2–3 days, and SF6 resorbs within 4–6 days after DMEK. The rate of dislocation of donor tissue decreases for both DSEK and DMEK as surgeon experience increases. See Table 15-8 for dislocation rates for DSAEK and DMEK.

    Figure 15-16 A, Hemorrhage in the interface after DSEK. B, Slit-lamp photograph showing blood in the interface.

    (Courtesy of Robert W. Weisenthal, MD.)

    Figure 15-17 Residual air bubble following DSEK (postoperative day 1).

    (Courtesy of Robert W. Weisenthal, MD.)

    DSEK

    Dislocation or decentration of the donor graft (Fig 15-19) typically occurs within the first 24 hours after DSEK. A soft eye due to a preexisting tube shunt or uncontrolled release of the air increases the likelihood of a decentered or dislocated graft. Retained viscoelastic or the presence of vitreous in the interface may prevent proper adherence of the graft. If the graft remains attached on postoperative day 1, subsequent dislocation is unlikely, although inadvertent trauma or eye rubbing during the first week may displace the donor tissue. Wearing glasses or a shield to protect the eye is recommended, along with exercising caution during instillation of eyedrops.

    It is still not clear how long the air bubble should be retained after DSEK, as some surgeons remove the air completely on the day of surgery without an increased incidence of tissue dislocation. This raises the possibility that long-term retention of an air bubble is not necessary for graft adherence in DSEK.

    Figure 15-18 Residual air bubble after Descemet membrane endothelial keratoplasty (DMEK) (postoperative day 1). The S stamp is shown for orientation.

    (Courtesy of Robert W. Weisenthal, MD.)

    Figure 15-19 Slit-lamp photograph of a detached donor corneal button following DSEK.

    (Courtesy of Robert W. Weisenthal, MD.)

    DMEK

    The donor tissue is more delicate, and as a result, peripheral or central detachments are much more common in DMEK than in DSEK (Fig 15-20). Anterior segment OCT allows visualization of the area of detachment (Fig 15-21). Peripheral detachments not involving the visual axis can be observed over several weeks to ensure there is no progression. They usually seal without adverse impact.

    If the graft detachment extends into the visual axis or is greater than one-third of the graft area, the surgeon may consider additional injection of air (rebubbling) to tamponade the graft against the host. Initially, rebubbling was not advised because of reports of extensive, visually significant detachments resolving spontaneously. Yet longer-term follow-up of these cases has been instructive. Baydoun et al reported that, in patients with clinically significant graft detachments managed without rebubbling, there was a significant reduction in endothelial cell counts at 5-year follow-up, which led to a higher rate of late graft failure. In some cases, permanent stromal haze developed secondary to chronic corneal edema, worsening the visual outcome after repeated DMEK. Thus, early rebubbling seems to be the best course in these cases. If rebubbling is necessary, it can be performed in the office or surgery center.

    Figure 15-20 Slit-lamp photograph of a peripheral detachment following DMEK.

    (Courtesy of Robert W. Weisenthal, MD.)

    Figure 15-21 Anterior segment optical coherence tomography images of a peripheral detachment following DMEK.

    (Courtesy of Robert W. Weisenthal, MD.)

    In the event that the graft is attached but the cornea still has visually significant edema after 1–2 months, repeated surgery is indicated prior to the development of chronic corneal edema, which can lead to bullous keratopathy, epithelial breakdown, and possible secondary infection. Repeated EK, either DMEK or DSEK, before the development of permanent corneal changes has a good visual prognosis, similar to that of the original procedure.

    Baydoun L, Ham L, Borderie V, et al. Endothelial survival after Descemet membrane endothelial keratoplasty. Effect of surgical indication and graft adherence status. JAMA Ophthalmol. 2015;133(1):1277–1285.

    Baydoun L, van Dijk K, Dapena I, et al. Repeat Descemet membrane endothelial keratoplasty after complicated primary Descemet membrane endothelial keratoplasty. Ophthalmology. 2015;122(1):8–16.

    Dirisamer M, van Dijk K, Dapena I, et al. Prevention and management of graft detachment in Descemet membrane endothelial keratoplasty. Arch Ophthalmol. 2012;130(3):280–291.

    Lehman RE, Copeland LA, Stock EM, Fulcher SF. Graft detachment rate in DSEK/DSAEK after same-day complete air removal. Cornea. 2015;34(11):1358–1361.

    Price FW Jr, Price MO. To intervene or not to intervene: that is the question. Ophthalmology. 2015;122(1):6–7.

    Pupillary block

    Anterior pupillary block or iris bombé may occur if the anterior chamber bubble migrates posteriorly, preventing aqueous flow through the pupil; Figures 15-22 and 15-23 show such a block after DSEK and DMEK, respectively. The resultant acute rise in IOP produces pain and can exacerbate preexisting optic nerve damage. Pupillary block may also lead to iridocorneal adhesion, damaging the graft and increasing the risk of rejection. Pupil dilation and supine positioning may relieve the pupil block; if this fails, some air should be removed. An inferior iridectomy performed prior to or at the time of the surgery reduces the likelihood of this scenario.

    Figure 15-22 Slit-lamp photograph showing pupillary block following DSEK.

    (Courtesy of Robert W. Weisenthal, MD.)

    Figure 15-23 A, Slit-lamp photograph of pupillary block following DMEK. B, The same patient after the release of air, leading to resolution of the block.

    (Courtesy of Robert W. Weisenthal, MD.)

    Epithelial ingrowth

    Epithelial ingrowth following DSEK can be seen as a gray-white deposit within the graft– host interface (Fig 15-24). It typically remains stable and is asymptomatic unless it occurs in the visual axis. The source of epithelium may be either the host or the donor. Host epithelium can be pushed into the eye through the main wound, side ports, or venting incisions used to drain interface fluid. It can also enter the eye through a fistulous track. Loose donor epithelium may enter the eye if adherent to the donor corneal button because of eccentric trephination beyond the microkeratome excision. In rare cases, epithelial ingrowth leads to graft failure that is missed on clinical examination but recognized on histologic examination of the tissue after removal. In a large series of cases, the majority of patients with epithelial ingrowth were simply observed and continued to see well without further intervention. In the atypical cases that resulted in graft failure, a second DSEK or PK produced a good outcome without recurrent ingrowth. This is in contrast to the progressive and devastating course of intraocular epithelial downgrowth associated with intracapsular cataract extraction or full-thickness PK. Epithelial ingrowth has not been described in DMEK.

    Dalal RR, Raber I, Dunn SP, et al. Epithelial ingrowth following endothelial keratoplasty. Cornea. 2016;35(4):465–470.

    Suh LH, Shousha MA, Ventura RU, et al. Epithelial ingrowth after Descemet stripping automated endothelial keratoplasty: description of cases and assessment with anterior segment optical coherence tomography. Cornea. 2011;30(5):528–534.

    Other interface pathology

    Infections can occur in the graft–host interface by several means: pathogens passing through venting incisions, contaminated donor tissue, or bacteria from the ocular surface dragged into the eye during insertion.

    Figure 15-24 Slit-lamp photograph of epithelial ingrowth (arrow) in the interface after DSEK.

    (Courtesy of Robert W. Weisenthal, MD.)

    In a recent review by the EBAA, 0.7% of donor rim cultures were positive for fungi, and infections developed in 17.1% of corneas with positive fungal rim culture results. The incidence of postoperative fungal infections is significantly higher for EK than PK. These infections have occurred primarily in eyes that have undergone DSEK, but there are case reports of infections after DMEK as well. It is possible that these infections are related to the tissue warming that occurs during preparation of donor tissue for EK.

    Interface opacification may occur because of retention of fibers, incomplete removal of the Descemet membrane, and persistence of interface fluid. Textural interface opacity describes a recently reported finding that results from retained viscoelastic or from the shearing of stromal fibrils during an irregular microkeratome donor preparation. The opacity has 2 forms: elongated (a lacy honeycomb pattern of deposits with intervening clear zones) (Fig 15-25) and punctate (small, discrete deposits). Textural interface opacity may be associated with reduced vision, but it typically improves or disappears completely over many months. There have been no reports of interface problems after DMEK.

    Aldave A. The utility of donor corneal rim culture: a report of the EBAA Medical Advisory Board Subcommittee on fungal infection following corneal transplantation. Subspecialty Day Program: Cornea. Las Vegas: American Academy of Ophthalmology; 2015.

    Vira S, Shih CY, Ragusa N, et al. Textural interface opacity after Descemet stripping automated endothelial keratoplasty: a report of 30 cases and possible etiology. Cornea. 2013; 32(5):e54–59.

    Progression of cataracts

    DSEK performed in a phakic eye may induce cataract progression, particularly in patients with narrow anterior chambers (<3.0 mm); therefore, DSEK with cataract extraction has been recommended in patients older than 50 years or in the presence of mild to moderate cataract. In a large series of patients with Fuchs dystrophy, DSEK combined with cataract extraction did not increase the risk of graft dislocation, endothelial cell loss, or other complications. There has not been a similar study in patients after DMEK, but many surgeons routinely combine DMEK with cataract surgery.

    Figure 15-25 Slit-lamp photograph of textural interface opacity after DSEK.

    (Courtesy of Jeffrey Goshe, MD.)

    Terry MA, Shamie N, Chen ES, et al. Endothelial keratoplasty for Fuchs’ dystrophy with cataract: complications and clinical results with the new triple procedure. Ophthalmology. 2009;116(4):631–639.

    Tsui JY, Goins KM, Sutphin JE, Wagoner MD. Phakic Descemet stripping automated endothelial keratoplasty: prevalence and prognostic impact of postoperative cataracts. Cornea. 2011;30(3):291–295.

    Primary graft failure

    In published reports, the primary graft failure rates for DSEK and DMEK range from 2.2% to 8.0%, with a mean of 5.0% for DSEK (see Table 15-8); higher rates are associated with less experienced surgeons. The lower rates probably reflect better surgical technique, which results in less tissue manipulation and a lower rate of graft dislocations and thus less endothelial trauma.

    Graft rejection

    The incidence of corneal graft rejection following DSEK seems to be lower than that after PK; in several long-term studies, the incidence was between 0% and 10% in the first year, increasing slightly at 2 years. In a paper by Wu et al, the incidence of graft rejection in DSEK was reported to be 22% at 5 years, although this result may be skewed, as these investigators routinely discontinued steroids, in some cases at 4 months postoperatively and typically at 1 year. In contrast, in a study by Ratanasit and Gorovoy, where all patients were maintained on topical steroids indefinitely, the rejection rate was 2% after 5 years in 51 eyes. Several studies on graft rejection after DSEK suggest that long-term prophylaxis with a steroid once daily, regardless of the strength of the steroid, is important in reducing the incidence of graft rejection.

    For DSEK patients, topical steroids such as prednisolone acetate (1%) 4 times a day are prescribed initially and then tapered over time to once per day at 1 year. A patient who is pseudophakic and not at risk of IOP elevation can continue to use a topical steroid once daily indefinitely, but periodic IOP measurement is recommended. If the patient is a steroid responder, loteprednol etabonate or fluorometholone may be substituted.

    The clinical presentation of graft rejection in DSEK patients differs from that in PK patients. The classic endothelial rejection line of PK is not seen; instead, multiple keratic precipitates scattered across the cornea are typically noted (Fig 15-26).

    Figure 15-26 Slit-lamp photograph showing endothelial graft rejection after DSEK, characterized by scattered keratic precipitates without an endothelial rejection line.

    (Courtesy of Robert W. Weisenthal, MD.)

    The rate of graft rejection after DMEK seems to be even lower than that after DSEK (eg, less than 1%). Further, the medication regimen after DMEK offers more flexibility in terms of dosage, strength, and tapering of the topical steroids. In a randomized prospective study, prednisolone acetate 1% was used for only 1 month following DMEK, after which loteprednol etabonate 0.5% gel was used without increased incidence of graft rejection. The authors of that study report that the incidence of graft rejection was 0% for patients who continued using topical steroids through the second year but increased to 6% in the second year in patients who stopped the steroids after 1 year. The graft rejections experienced were mild and asymptomatic, and all but one reversed with resumption of steroid therapy.

    Anshu A, Price MO, Price FW Jr. Risk of corneal transplant rejection significantly reduced with Descemet’s membrane endothelial keratoplasty. Ophthalmology. 2012;119(3):536–540.

    Dapena I, Ham L, Netuková M, van der Wees J, Melles GR. Incidence of early allograft rejection after Descemet membrane endothelial keratoplasty. Cornea. 2011;30(12):1341–1345.

    Price MO, Feng MT, Scanameo A, Price FW Jr. Loteprednol etabonate 0.5% gel vs prednisolone acetate 1% solution after Descemet membrane endothelial keratoplasty: prospective randomized trial. Cornea. 2015;34(8):853–858.

    Price MO, Scanameo A, Feng MT, Price FW Jr. Descemet’s membrane endothelial keratoplasty: risk of immunologic rejection episodes after discontinuing topical corticosteroids. Ophthalmology. 2016;123(6):1232–1236.

    Ratanasit A, Gorovoy MS. Long-term results of Descemet stripping automated endothelial keratoplasty. Cornea. 2011;30(12):1414–1418.

    Wu EI, Ritterband DC, Yu G, Shields RA, Seedor JA. Graft rejection following Descemet stripping automated endothelial keratoplasty: features, risk factors, and outcomes. Am J Ophthalmol. 2012;153(5):949–957.

    Endothelial cell loss

    Several maneuvers potentially contribute to early endothelial cell loss in EK patients, including the manipulation of tissue entailed in the preparation of donor tissue, placement and orientation of the tissue within the anterior chamber, primary injection of air to facilitate graft adherence, and rebubbling and tissue manipulation to treat dislocated grafts. Endothelial cell loss at 1 year for both DSEK and DMEK is reported to be approximately 32%–37%. In a follow-up study of 95 eyes by Price and colleagues, the median endothelial cell loss was 53% at 5 years and 71% at 10 years, which compares favorably to results for PK in the Cornea Donor Study, which showed a mean cell loss of 70% at 5 years and 76% at 10 years. Long-term viability of the endothelial cells is influenced by ocular comorbidity such as previous filtering surgery and, in particular, tube shunts. Long-term prospective trials on DMEK and DSEK are necessary to better understand the clinical biology of the corneal endothelium and the impact of endothelial cell loss on graft viability.

    Li JY, Terry MA, Goshe J, Shamie N, Davis-Boozer D. Graft rejection after Descemet’s stripping automated endothelial keratoplasty: graft survival and endothelial cell loss. Ophthalmology. 2012;119(1):90–94.

    Ni N, Sperling BJ, Dai Y, Hannush SB. Outcomes after Descemet stripping automated endothelial keratoplasty in patients with glaucoma drainage devices. Cornea. 2015;34(8): 870–875.

    Price FW Jr, Feng MT, Price MO. Evolution of endothelial keratoplasty: where are we headed? Cornea. 2015;34(Suppl 10):S41–S47.

    Price MO, Calhoun P, Kollman C, Price FW Jr, Lass JH. Descemet stripping endothelial keratoplasty: ten-year endothelial cell loss compared with penetrating keratoplasty. Ophthalmology. 2016;123(7):1421–1427.

    Price MO, Fairchild KM, Price DA, Price FW Jr. Descemet’s stripping endothelial keratoplasty: five-year graft survival and endothelial cell loss. Ophthalmology. 2011;118(4):725–729.

    Ratanasit A, Gorovoy MS. Long-term results of Descemet stripping automated endothelial keratoplasty. Cornea. 2011;30(12):1414–1418.

    Sugar A. The importance of corneal endothelial cell survival after endothelial keratoplasty. JAMA Ophthalmol. 2015;133(11):1285–1286.

    Excerpted from BCSC 2020-2021 series: Section 10 - Glaucoma. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.

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