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The goal of this study was to compare outcomes of Descemet stripping endothelial keratoplasty (DSEK) in eyes with glaucoma and abnormal anatomy to eyes with Fuchs endothelial corneal dystrophy (FECD).In a retrospective interventional series of all cases of DSEK between April 1, 2006, and November 30, 2015, recipient diagnosis, preoperative glaucoma status, concurrent surgical procedures, and graft outcomes were recorded. Graft survival, risk of rejection, and subsequent glaucoma surgery were estimated by using Kaplan-Meier analysis with risk factors determined by proportional hazard models.Of 703 DSEKs in 666 eyes (509 subjects), the main recipient diagnoses were FECD (n = 496), pseudophakic corneal edema (n = 112), and failed graft (n = 83). Glaucoma was present in 150 cases before DSEK. Overall graft survival was 85%, 75%, and 71% at 5, 10, and 12 years, respectively, and for FECD without glaucoma was 95%, 89%, and 87% at 5, 10, and 12 years, respectively. Independent risk factors for graft failure included recipient diagnoses of pseudophakic corneal edema (HR = 8.3, P0.001), failed graft (HR = 6.4, P0.001), and preoperative medical glaucoma (HR = 7.1, P0.001) or surgical glaucoma (HR = 12.3, P0.001). Preoperative glaucoma treated by previous surgery resulted in graft survival of 28% at 10 years. Preoperative glaucoma was associated with an increased risk of graft rejection (HR = 6.8, P0.001) and subsequent glaucoma surgery (HR17.4, P0.001).Preoperative glaucoma increases the risk of graft failure, graft rejection, and needing subsequent glaucoma surgery in the first decade after DSEK. With previous glaucoma surgery, DSEK graft survival was more favorable compared with published reports of Descemet membrane endothelial keratoplasty.

Oleander is a poisonous plant with extensively documented systemic side effects; however, oleander's ophthalmic side effects have not been detailed in the literature. We report a case of oleander-associated keratitis with subsequent corneal edema and anterior uveitis.This is a case report and review of relevant literature.A 58-year-old woman presented with large corneal epithelial defect after being struck in the eye with an oleander leaf. Despite treatment with topical moxifloxacin, she developed severe corneal edema and anterior uveitis. A diagnosis of oleander-associated ocular inflammation with secondary corneal edema was made, given the temporal relationship, and treatment was initiated with topical prednisolone and cyclopentolate. However, the corneal edema and inflammation continued to progress until oral prednisone and topical difluprednate were initiated. Visual acuity, anterior uveitis, and corneal edema significantly improved with aggressive immunomodulation. Follow-up at 1 month confirmed complete recovery of symptoms, corneal edema and anterior uveitis.Severe corneal edema and anterior uveitis can be associated with oleander exposure. Aggressive treatment with oral and topical steroids may be required without persistent sequelae at the 5-month follow-up. Ophthalmologists should consider this inflammatory reaction if patients experience ocular exposure to oleander.

Purpose To describe the management and outcome of an ocular surface alkali burn in the setting of previous laser in situ keratomileusis (LASIK). Methods This is a case report and review of relevant literature. Results A 25-year-old man with a history of LASIK presented 4 weeks after a sodium hydroxide splash to his left eye with visual acuity of 20/60 and a nonhealing epithelial defect adjacent to sectoral inferior limbal ischemia in the setting of trichiasis from upper eyelid cicatricial entropion. After topical corticosteroids were discontinued following the repair of the entropion, the patient returned 3 days later with worsening vision and severe diffuse lamellar keratitis with the melting of the LASIK flap. After promptly lifting the flap and debriding the interface, inflammation was managed with oral, instead of topical, corticosteroids. Over several weeks, the epithelium healed, and inflammation and interface edema resolved. At 10 years of follow-up, the patient had developed a localized pseudopterygium with mild corneal neovascularization but maintained 20/20 uncorrected visual acuity. Conclusions A chemical burn over a LASIK flap poses a challenge for managing corticosteroids, which are required to prevent diffuse lamellar keratitis but can also contribute to keratolysis beyond the first week after an alkali injury. Oral corticosteroid therapy may be beneficial in this situation, with a low threshold to lift the LASIK flap and debride the interface if inflammation occurs.

PURPOSE: To evaluate agreement between eye banks (EBs) and a reading center on endothelial cell density (ECD) determinations in the Cornea Preservation Time Study. METHODS: The Cornea Image Analysis Reading Center (CIARC) performed variable frame image analysis on EB-obtained–preoperative central endothelial images (after lamellar dissection for Descemet stripping automated endothelial keratoplasty by the EBs or before shipping, if surgeon prepared) to determine ECD. The EBs performed their usual method of ECD determination. The CIARC and EBs also provided ECD determinations from screening central endothelial images taken by the EBs during donor evaluation. Two independent masked CIARC readers determined ECD with measurements averaged. RESULTS: The mean preoperative ECD was 15 cells/mm(2) greater by the EBs than by CIARC (N = 1286, P < 0.001) with 95% limits of agreement of (−644, 675 cells/mm(2)). The limits of agreement in preoperative ECD were wider in the After-Lamellar-Dissection Group (−687, 683 cells/mm(2)) than in the Before Shipping Group [(−505, 633 cells/mm(2)); P = 0.03]. The EBs-determined preoperative ECD was within 10% of the CIARC-determined ECD for 886 (69%) image sets, with 236 (18%) higher by >10% and 164 (13%) lower by >10%. Excellent agreement appeared between the EBs and CIARC when 100–300 cells could be analyzed in contrast to

Corneal tomography has an emerging role in the assessment of Fuchs endothelial corneal dystrophy (FECD) in clinical practice and potentially for future clinical trials. Posterior elevation and pachymetry maps derived from elevation based Scheimpflug tomography can detect early corneal edema, even at a subclinical stage, enabling clinicians to better counsel patients about their vision and the risk of disease progression with and without cataract surgery. Tomographic imaging provides a functional assessment of corneal endothelial health, and could enable objective assessment of FECD progression, or regression, in response to novel therapeutic interventions. Clinicians and investigators should adopt Scheimpflug imaging for the assessment of FECD over traditional morphologic imaging modalities.

PURPOSE To investigate the association of body mass index (BMI) with Fuchs endothelial corneal dystrophy (FECD) severity and TCF4 CTG18.1 expansion. METHODS A total of 343 patients with FECD were enrolled from the Mayo Clinic. FECD severity was graded by slit-lamp biomicroscopy. BMI values were obtained from the electronic medical records. DNA extracted from leukocytes was analyzed for CTG18.1 expansion length, with ≥40 repeats considered expanded. Wilcoxon signed-rank tests were used to compare FECD grade and CTG18.1 expansion length in patients by BMI (

PURPOSE To investigate the key factors associated with eyes with an endothelial cell density (ECD) of ≥2000 cells/mm at 5 years after corneal transplantation. METHODS This retrospective cohort study included 174 eyes that underwent penetrating keratoplasty by 1 corneal specialist surgeon at the Baptist Eye Institute, Kyoto, Japan, from 1998 through 2011 and that were carefully followed for over 5 years postoperative. In all operated eyes, corneal ECD was measured at 1, 2, 3, 4, and 5 years postoperative. Multivariate analysis with adjustment for preoperative donor ECD was performed between eyes with an ECD of ≥2000 cells/mm and those with an ECD of

PURPOSE Patients with Fuchs endothelial corneal dystrophy (FECD) often notice poor vision in the morning that improves as the day progresses. In this study, we determined changes in corneal optical properties associated with induced corneal edema. METHODS Twenty-three phakic eyes (23 participants) with FECD (grades 1-6, modified Krachmer scale) and 8 normal eyes (8 participants) were examined by Scheimpflug photography. Central corneal thickness, high-order aberrations from anterior and posterior corneal surfaces, and backscatter from the anterior, mid-, and posterior cornea were determined from the Scheimpflug images. A low-oxygen permeable contact lens was placed on the eye, and eyes were closed for 2 hours, after which the lens was removed and Scheimpflug photography was repeated for up to 5 hours to determine changes in backscatter and high-order aberrations. RESULTS Corneas swelled by 10% [95% confidence interval (CI), 9-10]. Backscatter from the anterior cornea increased by 416 scatter units (SU, 95% CI, 344-488; P < 0.001), independent of the presence and severity of FECD. Recovery of anterior backscatter was slower in advanced FECD (81 SU/h, 95% CI, 60-120) compared with normal (123 SU/h, 95% CI, 95-150; P = 0.019). Anterior and posterior corneal high-order aberrations, and mid and posterior backscatter, did not increase with induced swelling. CONCLUSIONS Inducing corneal edema increases anterior corneal backscatter but not high-order aberrations. Subjective poor vision in the morning in FECD is probably caused by scattered light rather than by high-order aberrations, suggesting that these patients experience more disability glare than decreased visual acuity.

Patients with progressive supranuclear palsy (PSP) and patients with Parkinson disease frequently manifest signs of dry eyes, yet many remain asymptomatic. In this study, we established the relationships between blink rate, corneal sensitivity, and corneal nerve density in patients with ocular surface disease associated with PSP and Parkinson disease.Fourteen eyes of 7 patients with PSP, 8 eyes of 4 patients with Parkinson disease, and 10 eyes of 5 age-matched controls were examined for meibomian dysfunction, ocular surface staining, and blink rate. Corneal sensitivity was measured with a Cochet-Bonnet esthesiometer, and corneal subbasal nerve density was measured by using confocal microscopy in vivo. Comparisons between variables were assessed by using generalized estimating equation models to account for possible correlation between fellow eyes of the same subject.Abnormal ocular surface staining and meibomian disease were present in most subjects with PSP and Parkinson disease, but in none of the controls. Patients with PSP and Parkinson disease had lower blink rates (P0.001) and decreased corneal sensitivity (P0.001) compared with controls, whereas subbasal nerve density did not differ between groups. Blink rate was correlated with corneal sensitivity (r = 0.83, P0.001), but corneal sensitivity was not correlated with subbasal nerve density (r = -0.16, P = 0.78).Patients with ocular surface disease associated with PSP and Parkinson disease might be asymptomatic because of decreased corneal sensitivity. Decreased corneal sensitivity was not explained by loss of corneal nerves but was associated with decreased blink rate.

To determine corneal sensitivity and evaluate corneal nerves before and after keratoplasty for Fuchs endothelial dystrophy.Central corneal sensitivity, measured by using a Cochet-Bonnet esthesiometer in 69 eyes before and after different keratoplasty procedures for Fuchs dystrophy, was compared with that of 35 age-matched normal corneas. Corneal nerves were qualitatively examined by confocal microscopy in 42 eyes before and after Descemet stripping endothelial keratoplasty (DSEK).Corneal sensitivity in Fuchs dystrophy (4.61 ± 1.42 cm) was lower than that of age-matched controls (5.74 ± 0.48 cm, P0.001). Sensitivity decreased by 1 month after DSEK (2.98 ± 2.01 cm, P0.001), returned to preoperative sensitivity by 24 months (4.50 ± 1.63 cm, n = 33, P = 0.99), but remained lower than controls at 36 months (4.50 ± 1.48 cm, n = 15, P0.001). Sensitivity at 36 months after penetrating keratoplasty (1.46 ± 1.98 cm) remained decreased compared with preoperative sensitivity (P0.001). Subbasal nerves appeared sparse with abnormal branching before and through 36 months after DSEK. Sensitivity was lower in corneas without visible subbasal nerves by confocal microscopy at 12 months after DSEK (P0.005) than in corneas with visible nerves. Stromal nerves were frequently tortuous and formed loops in Fuchs dystrophy, and this appearance persisted in some eyes at 36 months after DSEK.Corneal sensitivity is decreased in Fuchs dystrophy compared with normal and remains subnormal even at 3 years after endothelial keratoplasty. Decreased sensitivity is likely to be related to loss of subbasal nerves and abnormal nerve morphology, which persist after endothelial keratoplasty.

PURPOSE The center method of corneal endothelial cell analysis is rapid but excludes the outermost digitized cells of a contiguous group from analysis; the flex-center method (Konan, Inc) is a modification that includes analysis of the outermost cells, which is advantageous in images with few cells. In this study, we examined agreement among the flex-center, center, and corner (standard) methods of endothelial analysis. METHODS Identical cells in endothelial images of 10 normal corneas and 10 corneas after penetrating keratoplasty (PK) were analyzed by each method. Agreement among methods for endothelial cell density (ECD), coefficient of variation of cell area (CV), and the percentage of hexagonal cells (HEX) was assessed by using a Student-Newman-Keuls procedure. RESULTS In normal corneas, there were small (clinically insignificant) differences among methods for ECD (P < 0.001) (mean +/- SD: flex center, 2846 +/- 248 cells/mm; center, 2870 +/- 253 cells/mm; and corner, 2892 +/- 254 cells/mm), CV (P < 0.001) (flex center, 33% +/- 3%; center, 30% +/- 3%; and corner, 30% +/- 3%), and HEX (P = 0.004) (flex center, 60% +/- 6%; center, 60% +/- 8%; and corner, 58% +/- 7%). In PK corneas, the methods agreed for ECD (P = 0.06) (flex center, 908 +/- 319 cells/mm; center, 912 +/- 307 cells/mm; and corner, 929 +/- 333 cells/mm) but disagreed for CV (P = 0.02) (flex center, 35% +/- 13%; center, 30% +/- 10%; and corner, 35% +/- 15%) and HEX (P = 0.02) (flex center, 56% +/- 19%; center, 54% +/- 17%; and corner, 43% +/- 23%). CONCLUSION ECD agreed among methods in normal and PK corneas, whereas morphometric data agreed poorly in PK corneas.

PURPOSE: To develop a rabbit model for femtosecond laser-assisted posterior lamellar keratoplasty. METHODS: The femtosecond laser was used to make the posterior corneal lamellar interface and trephine (side) cut in 12 eyes of 11 rabbits. Laser parameters were energy 6.0 to 8.7 (lamellar cut) and 6.0 to 8.8 microJ (trephination cut), spot size 2.4 microm, firing rate 15 kHz, and trephination diameter 6.0 to 7.0 mm. In all eyes, the posterior corneal disc was removed from the eye after laser treatment through a blade incision in the peripheral cornea. The same excised corneal disc was repositioned into the posterior stromal bed to simulate posterior lamellar transplantation. Four eyes of 3 rabbits were enucleated immediately after surgery, and 8 eyes of 8 rabbits were enucleated after a mean follow-up of 17.9 +/- 6.5 weeks. The corneal cut surfaces were examined by light microscopy and scanning electron microscopy. RESULTS: The femtosecond laser was successful in producing posterior lamellar and trephination cuts in rabbit eyes. The thickness of the posterior corneal discs was 204.3 +/- 21 microm (56.9% of central corneal thickness), and postoperative keratometry was 49.1 +/- 5.8 D. Clinical appearance consistent with corneal ectasia was noted in 3 eyes. CONCLUSION: The femtosecond laser can make nonmechanical cuts for posterior lamellar keratoplasty with relative ease and reliability in rabbit eyes. A minimum residual anterior corneal thickness may need to be maintained to prevent ectasia.

PURPOSE: To report a case of aberrant corneal nerve regeneration after myopic photorefractive keratectomy (PRK). METHODS: One patient underwent bilateral PRK to correct a refractive error of -5.50 D in each eye. Thirteen months after the original PRK, the left eye underwent an uncomplicated PRK reoperation to correct a regression of -1.00 D. The central corneas were examined by confocal microscopy preoperatively in both eyes, at 1 and 2 years after the original PRK in the right eye, and before and 1 and 2 years after the PRK reoperation in the left eye. RESULTS: Aberrant anterior stromal nerves with a coiled course and irregular branching pattern were identified 22 micro m deep to the most anterior keratocyte layer at 1 year after the PRK reoperation in the left eye and remained unchanged 2 years after reoperation. No abnormal stromal nerves were identified in the left eye before the reoperation or at any time in the right eye. CONCLUSION: Aberrant regeneration of corneal stromal nerves may occur after myopic PRK reoperation.