PURPOSE:To report a case of bilateral iridoschisis with cataracts and corneal decompensation in a patient who underwent cataract extraction and superficial iridectomy followed by Descemet membrane endothelial keratoplasty (DMEK).OBSERVATIONS:A 58-year-old man with previously diagnosed iridoschisis, cataracts, and diabetes mellitus experienced progressive vision loss bilaterally due to corneal decompensation. Slit lamp examination revealed iridoschisis with iris fibrils contacting the corneal endothelium, stromal edema, and mild guttate changes bilaterally. Corneal findings were more severe in the right eye, including the presence of bullous keratopathy at the time of presentation. Cataract extraction with intraocular lens implantation and superficial iridectomy were performed in the right eye, followed by DMEK. These same procedures were performed subsequently in the left eye. Postoperatively, the patient had significant improvement in visual acuity and corneal edema.CONCLUSIONS AND IMPORTANCE:DMEK can be performed safely and successfully after staged cataract surgery with superficial iridectomy in eyes with endothelial decompensation caused by iridoschisis.
Purpose: To compare the incidence of visually significant postoperative cystoid macular edema (CME) in pseudophakic eyes after Descemet membrane endothelial keratoplasty (DMEK) performed after recent versus remote cataract surgery.Methods: A retrospective chart review was performed of all consecutive eyes that underwent DMEK without concurrent cataract surgery at the University of Iowa between October 2012 and December 2014. The DMEK procedures were classified as staged if performed between 2 weeks and 6 months after cataract surgery and solitary if performed more than 6 months after cataract surgery. Possible confounders, including a history of diabetes in the recipient, were tracked. Macular optical coherence tomography was performed to detect CME 1 month after DMEK if the best-corrected visual acuity was <= 20/30 with a clear cornea with no other reason for visual compromise.Results: A total of 173 eyes from 140 patients were included in the statistical analysis. Staged DMEK was performed in 88 eyes (50.8%) and solitary DMEK in 85 eyes (49.2%). The incidence of CME was 8.0% (7 of 88 eyes) in the staged DMEK group and 7.1% (6 of 85 eyes) in the solitary DMEK group (P = 0.823). The incidence of CME did not differ significantly between the staged and solitary DMEK groups regardless of the recipient diabetic status. All cases of CME resolved within 6 months on topical therapy.Conclusions: The incidence of postoperative CME after DMEK is similar in the setting of recent or remote cataract surgery.
PURPOSE:To determine the incidence of positive corneoscleral donor rim fungal cultures after keratoplasty and to report clinical outcomes of grafts with culture-positive donor rims. DESIGN:Retrospective cohort study. PARTICIPANTS:Consecutive donor corneas and keratoplasty recipients at a single tertiary referral center over 20 years. METHODS:Patient charts were reviewed to determine the incidence of positive donor rim fungal cultures and clinical outcomes of all grafts using contaminated tissue. MAIN OUTCOME MEASURES:The primary outcome measures were positive donor rim fungal culture results and the development of postkeratoplasty fungal infection using corresponding corneal tissue. The secondary outcome measure was the impact of postoperative prophylaxis on donor tissue-associated infections. RESULTS:A total of 3414 keratoplasty cases were included in the statistical analysis. Seventy-one cases (2.1%) were associated with a fungal culture-positive donor rim. Candida species were cultured in 40 cases (56.3%). There was a higher incidence of positive rim cultures over the last 5 years of the analytic period compared with the first 15 years (P = 0.018). Fungal keratitis developed in 4 cases (5.6%), and all patients required further surgical intervention to achieve cure. There were no cases of fungal endophthalmitis. Empiric antimycotic prophylaxis initiated at the time of positive culture result reduced the incidence of keratitis from 15.8% in untreated cases to 1.9% in treated cases (P = 0.056). CONCLUSIONS:Positive donor rim fungal cultures are uncommon, but carry an unacceptably high risk of postoperative fungal infection. This risk may be reduced with prophylactic antimycotic therapy when culture-positive donor rims are identified.
Purpose: To compare corneal graft survival using tissue from diabetic and nondiabetic donors in patients undergoing initial Descemet stripping automated endothelial keratoplasty (DSAEK) or penetrating keratoplasty (PKP).Methods: A retrospective chart review of pseudophakic eyes that underwent DSAEK or PKP was performed. The primary outcome measure was graft failure. Cox proportional hazard regression and Kaplan-Meier survival analyses were used to compare diabetic versus nondiabetic donor tissue for all keratoplasty cases.Results: A total of 183 eyes (136 DSAEK, 47 PKP) were included in the statistical analysis. Among 24 procedures performed using diabetic donor tissue, there were 4 cases (16.7%) of graft failure (3 DSAEK, 1 PKP), and among 159 procedures performed using nondiabetic donor tissue, there were 18 cases (11.3%) of graft failure (12 DSAEK, 6 PKP). Cox proportional hazard ratio of graft failure for all cases comparing diabetic with nondiabetic donor tissue was 1.69, but this difference was not statistically significant (95% confidence interval, 0.56-5.06; P = 0.348). There were no significant differences in Kaplan-Meier curves comparing diabetic with nondiabetic donor tissue for all cases (P = 0.380). Statistical analysis of graft failure by donor diabetes status within each procedure type was not possible because of the small number of graft failure events involving diabetic tissue.Conclusions: We found similar rates of graft failure in all keratoplasty cases when comparing tissue from diabetic and nondiabetic donors, but further investigation is needed to determine whether diabetic donor tissue results in different graft failure rates after DSAEK compared with PKP.
We read with great interest the excellent summary and historical perspective regarding Foster Kennedy syndrome by Lai et al (1). We recently saw another fascinating case of Foster Kennedy syndrome secondary to a suprasellar pilocytic astrocytoma, which showed a characteristic fundus pattern of hemiretinal atrophy respecting the vertical meridian in association with optic disc edema in the right eye and optic atrophy in the fellow eye, which localized the site of the lesion to the chiasm, left optic nerve, and third ventricle. A 13-year-old girl with an unremarkable medical history complained of headaches accompanied by nausea and vomiting over 4 weeks. She also had been experiencing intermittent crossing of the eyes for 1 week with associated diplopia. Visual acuity was 20/40 in right eye and 20/60 in left eye. There was a 1.2-log unit left relative afferent pupillary defect. Ocular motility showed normal versions and ductions. She had a 20-25 prism diopter comitant esotropia. The anterior segment examination was normal. Funduscopy revealed right optic disc edema and left optic disc pallor (Fig. 1). There was visible dropout of the retinal nerve fiber layer (RNFL) in the nasal macula of the right eye, which respected the vertical meridian and edema of the RNFL temporal to the vertical meridian. Optical coherence tomography (OCT) revealed RNFL edema in the right eye and RNFL thinning in the left eye (Fig. 2). There was nasal hemiretinal thinning of the macular ganglion cell–inner plexiform layer complex in the right eye and diffuse thinning of the macular ganglion cell layer in the left eye (Fig. 3). Results of kinetic perimetry are shown in Figure 4. Magnetic resonance imaging demonstrated a suprasellar mass and obstructive hydrocephalus (Fig. 5). Biopsy of the mass showed Grade 1 pilocytic astrocytoma.FIG. 1: In the right eye, there is optic disc edema of the superior, inferior and nasal sectors but no temporal edema. The left optic disc is pale. There is thinning of the retinal nerve fiber layer in the nasal macula of each eye with delineation along the vertical meridian of the right eye (arrows), most visible superior to the fovea.FIG. 2: OCT reveals RNFL edema in a “twin peaks” distribution in the right eye and RNFL atrophy in the left eye (see quadrant and clock hour sector probability plot, right eye) that was not as obvious in the fundus photographs of the optic nerve shown in Figure 1 (comparisons are made with the normative database for 18-year-old individuals for illustrative purposes). OCT, optical coherence tomography; RNFL, retinal nerve fiber layer.FIG. 3: Macular ganglion cell–inner plexiform layer analysis shows thinning of the ganglion cell layer nasal to the fovea of the right eye, corresponding to temporal field loss. The pattern of retinal ganglion cell layer thinning respects the vertical meridian, especially in the superior retina. The retinal ganglion cell layer is diffusely thin in the left eye (comparisons are made with the normative database for 18-year-old individuals for illustrative purposes).FIG. 4: Kinetic perimetry demonstrates generalized visual field depression in each eye with temporal loss in the right eye, respecting the vertical meridian.FIG. 5: Contrasted axial (A) and coronal (B) magnetic resonance imaging reveals a 3 × 5 cm suprasellar mass involving the optic chiasm and left optic nerve and causing obstructive hydrocephalus.In our patient, one could predict the chiasmal location of the mass based on the fundus pattern of hemi-RNFL edema and atrophy in the same eye. The OCT findings further substantiated chiasmal involvement. It is known that chiasmal compressive lesions can produce a “bow-tie” pattern of optic nerve atrophy secondary to retrograde degeneration of the ganglion cells and axons supplying the temporal visual field (2). Our patient's right optic nerve appearance showed only a “half bow-tie” with edema superiorly, inferiorly, and nasally along with atrophy of the temporal sector. A pattern of superior and inferior disc edema separated by a nasal and temporal band of atrophy has been described previously as “twin peaks” papilledema (3–6). Although this was not readily visualized on funduscopic examination, the OCT plot of peripapillary RNFL in the right eye showed a twin peaks pattern of edema. Our patient's fundus pattern of hemiretinal nerve fiber atrophy respecting the vertical meridian through the fovea helped to localize the lesion to the chiasm and constitutes a diagnostic retinal feature. Although Sanders (1) ends his historical commentary on Foster Kennedy syndrome with a humorous comment “In Gowers' day, the clinician localized the lesion. Today, the neuroradiologist does it for him.” Our case demonstrates the ability of the ophthalmologist to localize a lesion with accuracy that rivals the best neuroimaging.
Purpose. To compare test-retest variability in rarebit perimetry (RBP) and conventional standard automated perimetry (SAP) using Goldmann size I and III stimuli. Methods. Seventeen normal subjects underwent RBP, size I SAP, and size III SAP on five separate visits within a 5-week period. Test-retest variability could not be directly compared because of differences in units. Instead, data were transformed to lie on the same scale by calculating a percentile range to mean ratio for each test. Results. Percentile range to mean ratio was highest for size I (3.42 ± 0.62), followed by size III (2.29 ± 0.55), and RBP (0.29 ± 0.10). Results for all three tests were significantly different from each other. Conclusions. Comparison of tests with different scales is problematic, but RBP's retest variability appears to be significantly less than both sizes I and III SAP in the measurement of normal subjects.
We have developed a rapid, inexpensive, and reliable assay for the determination of ascorbate using a plate reader. In this assay, ascorbic acid is oxidized to dehydroascorbic acid using Tempol (4-hydroxy-2,2,6,6-tetramethylpiperidinyloxy) and then reacted with o-phenylenediamine to form the condensation product, 3-(dihydroxyethyl)furo[3,4-b]quinoxaline-1-one. The rate of appearance of this product is monitored over time using fluorescence. With this method, it is possible to analyze 96 wells in less than 10min. This permits the analysis of 20 samples with a full set of standards and blanks, all in triplicate. The assay is robust for a variety of samples, including orange juice, swine plasma, dog plasma, and cultured cells. To demonstrate the usefulness of the assay for the rapid determination of experimental parameters, we investigated the uptake of ascorbate and two different ascorbate derivatives in U937 cells. We found similar plateau levels of intracellular ascorbate at 24h for ascorbate and ascorbate phosphate. However, the intracellular accumulation of ascorbate via the phosphate ester had an initial rate that was three to five times slower than that via the palmitate ester. Only lower concentrations of the palmitate ester could be examined because the ethanol needed as solvent decreased cell viability; it behaved similarly to the other two compounds at lower concentrations. To come to these conclusions, only nine plates needed to be analyzed to provide us with the end result after only 7h of analysis. This clearly demonstrates the strength of the plate reader assay, which allows the analysis of large-sample sets in a fraction of the time required for the methods that are most commonly used today. The assay is quick, is very economical, and provides results with uncertainties on the order of only 5%.