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Dalian Ding - One of the best experts on this subject based on the ideXlab platform.
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Gap Detection Deficits in Chinchillas with Selective Carboplatin-Induced Inner Hair Cell Loss
Journal of the Association for Research in Otolaryngology, 2020Co-Authors: Edward Lobarinas, Richard Salvi, Dalian DingAbstract:Temporal resolution is essential for processing complex auditory information such as speech. In hearing impaired persons, temporal resolution, often assessed by detection of brief gaps in continuous sound stimuli, is typically poorer than in individuals with normal hearing. At low stimulus presentation levels, hearing impaired individuals perform poorly but the deficits are greatly reduced when the sensation level of the stimuli are adjusted to match their normal hearing peers. In the present study, we evaluated the effect of selective inner hair Cell Loss on gap detection in chinchillas treated with carboplatin, an anticancer drug that selectively damages inner hair Cells and afferents in this species. Treatment with carboplatin-induced inner hair Cell Loss of ~ 70 % but had little effect on audiometric thresholds in quiet and produced no evidence of outer hair Cell Loss. In contrast, selective inner hair Cell Loss had a significant effect on gap detection ability across a wide range of presentation levels. These results suggest that gap detection tasks are more sensitive to inner hair Cell pathology than audiometric thresholds.
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Chinchilla models of selective cochlear hair Cell Loss
Hearing Research, 2002Co-Authors: Sandra L. Mcfadden, Dalian Ding, Haiyan Jiang, Richard J. SalviAbstract:Although it is well known that ethacrynic acid (EA) can enhance gentamicin (GM) ototoxicity, there has been no systematic study of the relationship between dosing parameters and inner ear pathology. We examined the effects of two parameters, GM dose and time delay between GM and EA administration, on cochlear and vestibular hair Cell Loss in chinchillas. ‘No delay’ groups received one injection of GM (125, 40, 20, or 10 mg/kg i.m.) followed immediately by EA (40 mg/kg i.v.); ‘delay’ groups received GM (10 mg/kg i.m.) followed by EA 1 or 1.5 h later. Animals were sacrificed 7 days later for evaluation of hair Cell Loss in the cochlea and vestibular end organs (cristae, saccule and utricle). Vestibular function was assessed prior to sacrifice by measuring the duration of nystagmus induced by cold caloric stimulation. No delay groups had V100% Loss of outer hair Cells and dosedependent Losses of inner hair Cells, ranging from V100% to 58%. In 1 and 1.5 h delay groups, inner hair Cell Losses were V19% and 0%, outer hair Cell Losses were V74% and 47%, and outer hair Cell Loss followed a typical base to apex gradient. Two results were remarkable. First, the three groups with partial inner hair Cell Loss showed an atypical lesion pattern in which Losses were substantially greater in the apical half than in the basal half of the cochlea. Second, there was no vestibular pathology in any group. The results establish dosing parameters that can be used to produce animal models with defined patterns and magnitudes of cochlear hair Cell damage, but normal vestibular function and morphology. = 2002 Elsevier Science B.V. All rights reserved.
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Chinchilla models of selective cochlear hair Cell Loss.
Hearing Research, 2002Co-Authors: Sandra L. Mcfadden, Dalian Ding, Haiyan Jiang, Jenifer M Woo, Richard SalviAbstract:Abstract Although it is well known that ethacrynic acid (EA) can enhance gentamicin (GM) ototoxicity, there has been no systematic study of the relationship between dosing parameters and inner ear pathology. We examined the effects of two parameters, GM dose and time delay between GM and EA administration, on cochlear and vestibular hair Cell Loss in chinchillas. ‘No delay’ groups received one injection of GM (125, 40, 20, or 10 mg/kg i.m.) followed immediately by EA (40 mg/kg i.v.); ‘delay’ groups received GM (10 mg/kg i.m.) followed by EA 1 or 1.5 h later. Animals were sacrificed 7 days later for evaluation of hair Cell Loss in the cochlea and vestibular end organs (cristae, saccule and utricle). Vestibular function was assessed prior to sacrifice by measuring the duration of nystagmus induced by cold caloric stimulation. No delay groups had ∼100% Loss of outer hair Cells and dose-dependent Losses of inner hair Cells, ranging from ∼100% to 58%. In 1 and 1.5 h delay groups, inner hair Cell Losses were ∼19% and 0%, outer hair Cell Losses were ∼74% and 47%, and outer hair Cell Loss followed a typical base to apex gradient. Two results were remarkable. First, the three groups with partial inner hair Cell Loss showed an atypical lesion pattern in which Losses were substantially greater in the apical half than in the basal half of the cochlea. Second, there was no vestibular pathology in any group. The results establish dosing parameters that can be used to produce animal models with defined patterns and magnitudes of cochlear hair Cell damage, but normal vestibular function and morphology.
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Chinchilla models of selective cochlear hair Cell Loss.
Hearing research, 2002Co-Authors: Sandra L. Mcfadden, Dalian Ding, Haiyan Jiang, Jenifer M Woo, Richard J. SalviAbstract:Although it is well known that ethacrynic acid (EA) can enhance gentamicin (GM) ototoxicity, there has been no systematic study of the relationship between dosing parameters and inner ear pathology. We examined the effects of two parameters, GM dose and time delay between GM and EA administration, on cochlear and vestibular hair Cell Loss in chinchillas. 'No delay' groups received one injection of GM (125, 40, 20, or 10 mg/kg i.m.) followed immediately by EA (40 mg/kg i.v.); 'delay' groups received GM (10 mg/kg i.m.) followed by EA 1 or 1.5 h later. Animals were sacrificed 7 days later for evaluation of hair Cell Loss in the cochlea and vestibular end organs (cristae, saccule and utricle). Vestibular function was assessed prior to sacrifice by measuring the duration of nystagmus induced by cold caloric stimulation. No delay groups had approximately 100% Loss of outer hair Cells and dose-dependent Losses of inner hair Cells, ranging from approximately 100% to 58%. In 1 and 1.5 h delay groups, inner hair Cell Losses were approximately 19% and 0%, outer hair Cell Losses were approximately 74% and 47%, and outer hair Cell Loss followed a typical base to apex gradient. Two results were remarkable. First, the three groups with partial inner hair Cell Loss showed an atypical lesion pattern in which Losses were substantially greater in the apical half than in the basal half of the cochlea. Second, there was no vestibular pathology in any group. The results establish dosing parameters that can be used to produce animal models with defined patterns and magnitudes of cochlear hair Cell damage, but normal vestibular function and morphology.
Mark A. Terry - One of the best experts on this subject based on the ideXlab platform.
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Immediate endothelial Cell Loss after penetrating keratoplasty.
Cornea, 2013Co-Authors: Asem A. Alqudah, Mark A. Terry, Michael D. Straiko, Mark A. Greiner, David Davis-boozerAbstract:Purpose To report the pattern and the extent of corneal endothelial Cell Loss immediately after a penetrating keratoplasty (PK) is performed. Methods Ten donor corneal-scleral tissues with healthy endothelium were used to perform 10 PK surgeries on cadaver eyes. An 8.25-mm donor graft was placed into an 8.00-mm trephinated recipient bed of the cadaver eye. A 10-0 nylon suture was used with a 16-interrupted suture closure technique to secure each donor button. Viscoelastic was used to protect the endothelium in every case. The corneal donor buttons were removed and stained using trypan blue and alizarin red dyes. Digital high-definition photographs were obtained to record the pattern and quantity of stain resulting from endothelial damage and Cell Loss. Percent endothelial Loss was calculated using the digital planimetry of our previously described Adobe Photoshop technique. Results The immediate mean percent Cell Loss across the whole graft was 25.7% ± 7.5% (Range, 18-39). There was a distinct pattern of Loss, with 58.3% of the Loss in the peripheral 0.75 mm, and 12.4% of the Loss in the central 3.00 mm. Conclusions The immediate total endothelial Cell Loss after the PK was performed was about 25%. The immediate Cell Loss after the PK was consistent with areas of trephination and suture placement.
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endothelial Cell Loss after descemet s stripping endothelial keratoplasty in a large prospective series
Ophthalmology, 2008Co-Authors: Mark A. Terry, Neda Shamie, Edwin S. Chen, Karen L. Hoar, Daniel J. FriendAbstract:PURPOSE: To report the donor endothelial Cell Loss in the first year after Descemet's stripping endothelial keratoplasty (DSEK) for the treatment of endothelial dysfunction. DESIGN: Prospective noncomparative interventional case series. PARTICIPANTS: Eighty eyes of 78 patients with corneal edema. METHODS: Eighty eyes with endothelial failure were entered into a prospective study of endothelial keratoplasty (EK). The donor central endothelial Cell density (ECD) was recorded postoperatively at 6 months (n = 80) and 12 months (n = 80) and then compared with the preoperative eye bank measurements. The subsets of eyes with the donor prepared manually (DSEK; n = 19) and the donor prepared with a microkeratome (Descemet's stripping automated EK [DSAEK]; n = 61) were also evaluated and compared. MAIN OUTCOME MEASURES: Preoperative and postoperative central ECDs were prospectively evaluated and the Cell Loss calculated for each postoperative time point. RESULTS: The average and standard deviation ECD at 6 months was 1908+/-354 Cells/mm(2), representing a mean Cell Loss from preoperative donor Cell measurements of 34+/-12%. At 12 months, ECD was 1856+/-371 Cells/mm(2) (35+/-13% Cell Loss). The 1% additional Cell Loss from 6 to 12 months was not significant (P = 0.233). In the subset of DSEK eyes (n = 19), the Cell Loss from preoperatively to 6 months was 34%, and at 12 months it was 39%. In the subset of DSAEK eyes (n = 61), the Cell Loss from preoperatively to 6 months was 34%, and at 12 months it was 34%. There was no statistical difference between the Cell Loss from DSEK and that from DSAEK at 6 months (P = 0.884) or at 12 months (P = 0.224). CONCLUSIONS: Descemet's stripping EK using our surgical technique has a mean donor endothelial Cell Loss of 34% at the 6-month postoperative examination, and this average Cell Loss remains relatively stable up to at least 1 year. We found no difference in Cell Loss between the DSEK and DSAEK techniques over this 1-year postoperative period.
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Endothelial Cell Loss after Descemet's stripping endothelial keratoplasty in a large prospective series.
Ophthalmology, 2007Co-Authors: Mark A. Terry, Neda Shamie, Edwin S. Chen, Karen L. Hoar, Daniel J. FriendAbstract:Purpose To report the donor endothelial Cell Loss in the first year after Descemet's stripping endothelial keratoplasty (DSEK) for the treatment of endothelial dysfunction. Design Prospective noncomparative interventional case series. Participants Eighty eyes of 78 patients with corneal edema. Methods Eighty eyes with endothelial failure were entered into a prospective study of endothelial keratoplasty (EK). The donor central endothelial Cell density (ECD) was recorded postoperatively at 6 months (n = 80) and 12 months (n = 80) and then compared with the preoperative eye bank measurements. The subsets of eyes with the donor prepared manually (DSEK; n=19) and the donor prepared with a microkeratome (Descemet's stripping automated EK [DSAEK]; n=61) were also evaluated and compared. Main Outcome Measures Preoperative and postoperative central ECDs were prospectively evaluated and the Cell Loss calculated for each postoperative time point. Results The average and standard deviation ECD at 6 months was 1908±354 Cells/mm 2 , representing a mean Cell Loss from preoperative donor Cell measurements of 34±12%. At 12 months, ECD was 1856±371 Cells/mm 2 (35±13% Cell Loss). The 1% additional Cell Loss from 6 to 12 months was not significant ( P = 0.233). In the subset of DSEK eyes (n = 19), the Cell Loss from preoperatively to 6 months was 34%, and at 12 months it was 39%. In the subset of DSAEK eyes (n = 61), the Cell Loss from preoperatively to 6 months was 34%, and at 12 months it was 34%. There was no statistical difference between the Cell Loss from DSEK and that from DSAEK at 6 months ( P = 0.884) or at 12 months ( P = 0.224). Conclusions Descemet's stripping EK using our surgical technique has a mean donor endothelial Cell Loss of 34% at the 6-month postoperative examination, and this average Cell Loss remains relatively stable up to at least 1 year. We found no difference in Cell Loss between the DSEK and DSAEK techniques over this 1-year postoperative period.
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a prospective study of endothelial Cell Loss during the 2 years after deep lamellar endothelial keratoplasty
Ophthalmology, 2007Co-Authors: Mark A. Terry, Karen L. Hoar, Jennifer Wall, Paula J OusleyAbstract:Purpose To report the endothelial survival over a 2-year period after 2 techniques of deep lamellar endothelial keratoplasty (DLEK) in the treatment of endothelial dysfunction. Design Prospective, noncomparative, interventional case series. Participants One hundred eyes of 88 patients with corneal edema. Methods One hundred consecutive eyes with endothelial failure were entered into a prospective study of endothelial keratoplasty, and the donor central endothelial Cell density (ECD) was recorded postoperatively at 6 months (n = 98), 12 months (n = 96), and 24 months (n = 85) and then compared with the preoperative eye bank measurements. The subsets of eyes with large-incision DLEK (n = 36) and small-incision DLEK (n = 62) were also evaluated and compared. Main Outcome Measures Preoperative and postoperative central ECDs were prospectively evaluated and the Cell Loss calculated for each postoperative time point. Results The average (and standard deviation) ECD at 6 months was 2140±426 Cells/mm 2 , representing a mean Cell Loss from preoperative donor Cell measurements of 25±15%. At 12 months, ECD was 2090±448 Cells/mm 2 (26±16% Cell Loss), and at 24 months, it was 1794±588 Cells/mm 2 (37±27% Cell Loss). The additional Cell Loss from 1 to 2 years was significant ( P P = 0.013) and 24-month ( P Conclusions Although the initial Cell Loss from DLEK surgery is minimally changed from 6 to 12 months postoperatively, there is an acceleration of Cell Loss from 1 year to 2 years postoperatively. The small-incision DLEK technique, which involves folding of the donor tissue, results in a significantly higher endothelial Cell Loss at 1 and 2 years than that found after large-incision DLEK surgery, wherein the tissue is not folded.
Richard J. Salvi - One of the best experts on this subject based on the ideXlab platform.
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Chinchilla models of selective cochlear hair Cell Loss
Hearing Research, 2002Co-Authors: Sandra L. Mcfadden, Dalian Ding, Haiyan Jiang, Richard J. SalviAbstract:Although it is well known that ethacrynic acid (EA) can enhance gentamicin (GM) ototoxicity, there has been no systematic study of the relationship between dosing parameters and inner ear pathology. We examined the effects of two parameters, GM dose and time delay between GM and EA administration, on cochlear and vestibular hair Cell Loss in chinchillas. ‘No delay’ groups received one injection of GM (125, 40, 20, or 10 mg/kg i.m.) followed immediately by EA (40 mg/kg i.v.); ‘delay’ groups received GM (10 mg/kg i.m.) followed by EA 1 or 1.5 h later. Animals were sacrificed 7 days later for evaluation of hair Cell Loss in the cochlea and vestibular end organs (cristae, saccule and utricle). Vestibular function was assessed prior to sacrifice by measuring the duration of nystagmus induced by cold caloric stimulation. No delay groups had V100% Loss of outer hair Cells and dosedependent Losses of inner hair Cells, ranging from V100% to 58%. In 1 and 1.5 h delay groups, inner hair Cell Losses were V19% and 0%, outer hair Cell Losses were V74% and 47%, and outer hair Cell Loss followed a typical base to apex gradient. Two results were remarkable. First, the three groups with partial inner hair Cell Loss showed an atypical lesion pattern in which Losses were substantially greater in the apical half than in the basal half of the cochlea. Second, there was no vestibular pathology in any group. The results establish dosing parameters that can be used to produce animal models with defined patterns and magnitudes of cochlear hair Cell damage, but normal vestibular function and morphology. = 2002 Elsevier Science B.V. All rights reserved.
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Chinchilla models of selective cochlear hair Cell Loss.
Hearing research, 2002Co-Authors: Sandra L. Mcfadden, Dalian Ding, Haiyan Jiang, Jenifer M Woo, Richard J. SalviAbstract:Although it is well known that ethacrynic acid (EA) can enhance gentamicin (GM) ototoxicity, there has been no systematic study of the relationship between dosing parameters and inner ear pathology. We examined the effects of two parameters, GM dose and time delay between GM and EA administration, on cochlear and vestibular hair Cell Loss in chinchillas. 'No delay' groups received one injection of GM (125, 40, 20, or 10 mg/kg i.m.) followed immediately by EA (40 mg/kg i.v.); 'delay' groups received GM (10 mg/kg i.m.) followed by EA 1 or 1.5 h later. Animals were sacrificed 7 days later for evaluation of hair Cell Loss in the cochlea and vestibular end organs (cristae, saccule and utricle). Vestibular function was assessed prior to sacrifice by measuring the duration of nystagmus induced by cold caloric stimulation. No delay groups had approximately 100% Loss of outer hair Cells and dose-dependent Losses of inner hair Cells, ranging from approximately 100% to 58%. In 1 and 1.5 h delay groups, inner hair Cell Losses were approximately 19% and 0%, outer hair Cell Losses were approximately 74% and 47%, and outer hair Cell Loss followed a typical base to apex gradient. Two results were remarkable. First, the three groups with partial inner hair Cell Loss showed an atypical lesion pattern in which Losses were substantially greater in the apical half than in the basal half of the cochlea. Second, there was no vestibular pathology in any group. The results establish dosing parameters that can be used to produce animal models with defined patterns and magnitudes of cochlear hair Cell damage, but normal vestibular function and morphology.
Sandra L. Mcfadden - One of the best experts on this subject based on the ideXlab platform.
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Chinchilla models of selective cochlear hair Cell Loss
Hearing Research, 2002Co-Authors: Sandra L. Mcfadden, Dalian Ding, Haiyan Jiang, Richard J. SalviAbstract:Although it is well known that ethacrynic acid (EA) can enhance gentamicin (GM) ototoxicity, there has been no systematic study of the relationship between dosing parameters and inner ear pathology. We examined the effects of two parameters, GM dose and time delay between GM and EA administration, on cochlear and vestibular hair Cell Loss in chinchillas. ‘No delay’ groups received one injection of GM (125, 40, 20, or 10 mg/kg i.m.) followed immediately by EA (40 mg/kg i.v.); ‘delay’ groups received GM (10 mg/kg i.m.) followed by EA 1 or 1.5 h later. Animals were sacrificed 7 days later for evaluation of hair Cell Loss in the cochlea and vestibular end organs (cristae, saccule and utricle). Vestibular function was assessed prior to sacrifice by measuring the duration of nystagmus induced by cold caloric stimulation. No delay groups had V100% Loss of outer hair Cells and dosedependent Losses of inner hair Cells, ranging from V100% to 58%. In 1 and 1.5 h delay groups, inner hair Cell Losses were V19% and 0%, outer hair Cell Losses were V74% and 47%, and outer hair Cell Loss followed a typical base to apex gradient. Two results were remarkable. First, the three groups with partial inner hair Cell Loss showed an atypical lesion pattern in which Losses were substantially greater in the apical half than in the basal half of the cochlea. Second, there was no vestibular pathology in any group. The results establish dosing parameters that can be used to produce animal models with defined patterns and magnitudes of cochlear hair Cell damage, but normal vestibular function and morphology. = 2002 Elsevier Science B.V. All rights reserved.
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Chinchilla models of selective cochlear hair Cell Loss.
Hearing Research, 2002Co-Authors: Sandra L. Mcfadden, Dalian Ding, Haiyan Jiang, Jenifer M Woo, Richard SalviAbstract:Abstract Although it is well known that ethacrynic acid (EA) can enhance gentamicin (GM) ototoxicity, there has been no systematic study of the relationship between dosing parameters and inner ear pathology. We examined the effects of two parameters, GM dose and time delay between GM and EA administration, on cochlear and vestibular hair Cell Loss in chinchillas. ‘No delay’ groups received one injection of GM (125, 40, 20, or 10 mg/kg i.m.) followed immediately by EA (40 mg/kg i.v.); ‘delay’ groups received GM (10 mg/kg i.m.) followed by EA 1 or 1.5 h later. Animals were sacrificed 7 days later for evaluation of hair Cell Loss in the cochlea and vestibular end organs (cristae, saccule and utricle). Vestibular function was assessed prior to sacrifice by measuring the duration of nystagmus induced by cold caloric stimulation. No delay groups had ∼100% Loss of outer hair Cells and dose-dependent Losses of inner hair Cells, ranging from ∼100% to 58%. In 1 and 1.5 h delay groups, inner hair Cell Losses were ∼19% and 0%, outer hair Cell Losses were ∼74% and 47%, and outer hair Cell Loss followed a typical base to apex gradient. Two results were remarkable. First, the three groups with partial inner hair Cell Loss showed an atypical lesion pattern in which Losses were substantially greater in the apical half than in the basal half of the cochlea. Second, there was no vestibular pathology in any group. The results establish dosing parameters that can be used to produce animal models with defined patterns and magnitudes of cochlear hair Cell damage, but normal vestibular function and morphology.
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Chinchilla models of selective cochlear hair Cell Loss.
Hearing research, 2002Co-Authors: Sandra L. Mcfadden, Dalian Ding, Haiyan Jiang, Jenifer M Woo, Richard J. SalviAbstract:Although it is well known that ethacrynic acid (EA) can enhance gentamicin (GM) ototoxicity, there has been no systematic study of the relationship between dosing parameters and inner ear pathology. We examined the effects of two parameters, GM dose and time delay between GM and EA administration, on cochlear and vestibular hair Cell Loss in chinchillas. 'No delay' groups received one injection of GM (125, 40, 20, or 10 mg/kg i.m.) followed immediately by EA (40 mg/kg i.v.); 'delay' groups received GM (10 mg/kg i.m.) followed by EA 1 or 1.5 h later. Animals were sacrificed 7 days later for evaluation of hair Cell Loss in the cochlea and vestibular end organs (cristae, saccule and utricle). Vestibular function was assessed prior to sacrifice by measuring the duration of nystagmus induced by cold caloric stimulation. No delay groups had approximately 100% Loss of outer hair Cells and dose-dependent Losses of inner hair Cells, ranging from approximately 100% to 58%. In 1 and 1.5 h delay groups, inner hair Cell Losses were approximately 19% and 0%, outer hair Cell Losses were approximately 74% and 47%, and outer hair Cell Loss followed a typical base to apex gradient. Two results were remarkable. First, the three groups with partial inner hair Cell Loss showed an atypical lesion pattern in which Losses were substantially greater in the apical half than in the basal half of the cochlea. Second, there was no vestibular pathology in any group. The results establish dosing parameters that can be used to produce animal models with defined patterns and magnitudes of cochlear hair Cell damage, but normal vestibular function and morphology.
Francis W. Price - One of the best experts on this subject based on the ideXlab platform.
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Clinical Factors for Early and Late Endothelial Cell Loss After Corneal Transplantation
Current Ophthalmology Reports, 2018Co-Authors: Marianne O. Price, Jonathan H. Lass, Francis W. PriceAbstract:Purpose of Review To consider the relative importance of factors associated with post-keratoplasty endothelial Cell Loss. Recent Findings Lamellar keratoplasty continues to supplant penetrating keratoplasty. When host endothelium is healthy, retaining it with deep anterior lamellar keratoplasty significantly reduces long-term endothelial Cell Loss. Endothelial keratoplasty and penetrating keratoplasty differ fundamentally in relative rates of early and late central endothelial Cell Loss, yet at 10 years, their cumulative Cell Loss is similarly substantial. The greatest risk factor for post-keratoplasty endothelial decompensation is prior glaucoma filtration surgery, particularly an aqueous shunt. Interestingly, vital dye staining and sophisticated imaging software suggest that the actual viable endothelial Cell density of donor corneas is often overestimated by specular microscopy, inflating estimates of early Cell Loss. Summary Corneal graft longevity is often determined by endothelial Cell survival. Adoption of new surgical techniques has improved graft survival, and new imaging techniques allow more accurate preoperative endothelial Cell evaluation.
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descemet stripping endothelial keratoplasty ten year endothelial Cell Loss compared with penetrating keratoplasty
Ophthalmology, 2016Co-Authors: Marianne O. Price, Francis W. Price, Peter Calhoun, Craig Kollman, Jonathan H. LassAbstract:Purpose To assess endothelial Cell density (ECD) and model 10-year Cell Loss after Descemet stripping endothelial keratoplasty (DSEK), and to compare with results after penetrating keratoplasty (PK) performed for the same indications in the Cornea Donor Study (CDS). Design Retrospective, longitudinal study. Participants Five hundred ninety DSEK recipients, 21 to 96 years of age, treated for Fuchs' dystrophy (n = 498; 84%), pseudophakic or aphakic corneal edema (n = 89; 15%), or other endothelial dysfunction (n = 3; Methods Review of 1005 consecutive primary DSEK procedures by 6 surgeons identified 752 grafts (75%) in 590 recipients with ECD measurements at 1 or more postoperative examinations between 6 months and 10 years. Four statistical models applied previously to the CDS PK data were considered. The preferred model (Bayesian Markov chain Monte Carlo) accounted for missing data, selective dropout from graft failure, correlations between fellow eyes, and correlations between longitudinal repeated measures. Main Outcome Measures Central corneal ECD. Results The median donor corneal ECD (25th–75th percentiles) was 3005 Cells/mm 2 (2852–3203 Cells/mm 2 ) at baseline, 2077 Cells/mm 2 (1660–2411 Cells/mm 2 ) at 6 months, and 926 Cells/mm 2 (617–1433 Cells/mm 2 ), with a range from 408 to 2538 Cells/mm 2 at 10 years. After median Cell Loss of 32% in the perioperative period, ECD declined at a linear rate of approximately 110 Cells/mm 2 per year between 6 months and 10 years after DSEK. At 10 years, the median Cell Loss was 71% (53%–80%) relative to the baseline donor ECD, comparable with the 76% (70%–82%) median Cell Loss after PK by 68 surgeons in the CDS. The 10-year ECD correlated with the 6-month postoperative ECD ( r = 0.56; P r = −0.04; P = 0.78). Selective dropout from graft failure did not affect the Cell Loss model significantly. Conclusions The linear decline in ECD after DSEK was consistent with shorter-term endothelial keratoplasty studies and was distinct from the biexponential Cell Loss trend characteristic of PK. By 10 years, Cell Loss was comparable in surviving clear grafts for both DSEK and PK.
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endothelial Cell Loss after descemet stripping with endothelial keratoplasty influencing factors and 2 year trend
Ophthalmology, 2008Co-Authors: Marianne O. Price, Francis W. PriceAbstract:Purpose To identify factors correlated with early endothelial Cell Loss after Descemet stripping with endothelial keratoplasty (DSEK) and to document Cell Loss over a 2-year period. Design Cross-sectional and longitudinal retrospective analyses. Participants A series of 263 eyes in 216 patients who were treated with DSEK and were examined at the same center after surgery. Methods Six-month endothelial Cell density (ECD) measurements were analyzed by multivariate analysis of variance to identify preoperative, operative, and postoperative factors that significantly influenced early Cell Loss. In addition, ECD measurements were compared longitudinally at 6, 12, and 24 months after grafting. Main Outcome Measures Central ECD after transplantation. Results Mean ECD was 2000±550 Cells/mm 2 6 months after DSEK, representing Cell Loss of 34±18%. Factors associated with lower 6-month Cell Loss were use of single-point fixation forceps that compressed the donor tissue only at the tip during graft insertion ( P = 0.025) and absence of any secondary donor reattachment procedure ( P = 0.035). Six-month Cell Loss also was significantly less when DSEK was performed as a combined procedure; in combined cases, the graft was inserted through a clear corneal incision, whereas in standard cases, it was inserted through a scleral tunnel incision, which likely exerted more compression. Cell Loss was comparable with manual and microkeratome donor dissection techniques ( P = 0.91). Postoperative ECD was correlated positively with donor ECD ( P P P = 0.45), donor death-to-use time (range, 2–8 days; P = 0.86), and recipient demographics. In 34 DSEK eyes analyzed longitudinally, mean ECD was 3100±250 Cells/mm 2 before surgery, 2000±540 Cells/mm 2 at 6 months, 1900±480 Cells/mm 2 at 1 year, and 1800±490 Cells/mm 2 at 2 years. Conclusions Cell Loss 6 months and 1 year after DSEK was higher than in a recent penetrating keratoplasty series performed at the same center, consistent with more donor tissue manipulation in DSEK. Cell Loss was reduced with certain variations in surgical technique.