HLA class I/II matching and chronic endothelial cell loss in penetrating normal risk keratoplasty

OBJECTIVE: Chronic endothelial cell loss of the graft is very common after penetrating keratoplasty. The aetiology of this is unknown. Clinically, non-identifiable immune reactions have been suspected. Recently, we were able to demonstrate that proper human leucocyte antigen (HLA) matching is a suitable means to reduce classical immune reactions in normal risk keratoplasty patients. In this study, we therefore investigated whether HLA-matched grafts also experience less chronic endothelial cell loss. METHODS: A homogenous group of 223 normal risk keratoplasty patients was divided into six groups with different degrees of HLA matching (group 1 with unknown HLA data, group 2 with up to two mismatches, group 3 with three mismatches, group 4 with four mismatches, group 5 with five mismatches and group 6 with six mismatches on the HLA A, B, DR loci). All serological HLA A, B, C and all moleculargenetic HLA DRB, DRQB typings of donors and recipients were performed in a single laboratory accredited by the American Society for Histocompatibility and Immunogenetics. Only patients with at least three postoperative endothelial cell density values were included in the study. The slopes of the regression lines for each individual scatterplot of endothelial cell density values plotted against postoperative time (linear regression, lost cells/mm2/day), and after logarithmic transformation (exponential regression, annual relative loss of cells) were evaluated, respectively. RESULTS: There were no statistically significant differences between the six groups. CONCLUSION: Whereas proper HLA matching at present standards is already a suitable means to reduce identifiable immune reactions and to prolong graft survival even in normal risk keratoplasty patients, the same HLA matching procedures are not effective in reducing the extent of chronic endothelial cell loss. For several reasons this does not yet exclude, however, the possibility that the underlying cause of chronic endothelial cell loss is immunological.     

Endothelial cell density after deep anterior lamellar keratoplasty (Melles technique)

PURPOSE: To measure the recipient endothelial cell loss after the Melles technique for deep anterior lamellar keratoplasty. METHODS: In 21 eyes of 21 patients, a deep anterior lamellar keratoplasty procedure was performed. Before surgery and at 6, 12, and 24 months after surgery, specular microscopy was performed to evaluate the endothelial cell density. For each postoperative time interval, the mean endothelial cell loss relative to the preoperative value was calculated. RESULTS: Mean postoperative endothelial cell loss averaged 283 cells/mm(2) (+/- 293) at 6 months, 335 cells/mm(2) (+/- 309) at 12 months, and 421 cells/mm(2) (+/- 316) at 24 months. Estimate relative endothelial cell density losses obtained by mixed model analysis of variance were 11.1%, 2.0%, and 1.2%, respectively, each time compared with its previous measurement point. Second order comparisons showed that the loss within the first 6 months was significantly higher than after 6 months. CONCLUSION: In deep anterior lamellar keratoplasty, the recipient corneal endothelium showed a small initial drop in endothelial cell density followed by a physiologic rate of cell loss. Cell survival after lamellar keratoplasty may be expected to be better when compared with that following penetrating keratoplasty.     

Chronic endothelial cell loss of the graft after penetrating keratoplasty: influence of endothelial cell migration from graft to host

BACKGROUND: Chronic endothelial cell loss of the graft is common after penetrating keratoplasty. Some kind of subclinical immunological reaction that is not visible at the slitlamp has been suspected as main cause for this phenomenon. Furthermore, migration of graft endothelial cells towards the host cornea has been discussed to add to this loss in special cases. In this study, 3 homogenous patient groups with similar risk of immunological reactions were examined. Main difference between these groups was the potential of graft endothelial cells to migrate towards the host cornea. PATIENTS AND METHODS: Patients with keratoconus without cataract surgery (group I with little migration potential, n = 273), patients with Fuchs endothelial dystrophy without/with cataract surgery (groups IIa/IIb with moderate migration potential, n = 89/n = 165) and patients with bullous keratopathy after cataract surgery (group III with potentially large migration tendency, n = 188) were included in the study. All patients had a first keratoplasty. Patients with glaucoma or further intraocular procedures after keratoplasty were excluded from the study. Clear graft survival and ratio of grafts without immune reactions were estimated according to Kaplan and Meier. Endothelial analysis concerned only patients without immune reactions and with at least 3 postoperative endothelial cell density values of the graft center (76 patients in I, 18 patients in IIa, 41 patients in IIb and 23 patients in III). RESULTS: Mean relative loss of endothelial cells per year was 14.0 +/- 19.0 % in group I, 17.0 +/- 19.1 % in group IIa, 20.8 +/- 18.2 % in group IIb and 29.4 +/- 17.6 % in group III (ANOVA, p < 0.01). Five years postoperatively in group I 99 %, in group IIa 98 %, in group IIb 93 % and in group III 69 % of the grafts were centrally clear (log rank test, p < 0.001). In the same period in group I 88 %, in group IIa 86 %, in group IIb 83 % and in group III 81 % of the grafts were free of immune reactions (log rank test, p < 0.05). Reasons for irreversible graft failure were immune reactions (0 in group I; 0 in group IIa; 1 in group IIb; 9 in group III, ), surface disorders (1 in group I; 0 in IIa; 1 in group IIb; 3 in group III) and endothelial failure (0 in group I; 1 in group IIa; 5 in group IIb; 6 in group III) (chi square test, p < 0.01). CONCLUSIONS: In patients with bullous keratopathy endothelial cell loss via migration seems to add significantly to the general chronic loss which is suspected to be immunological. Peripheral migration of endothelial cells, therefore, most probably contributes to limited prognosis of patients with bullous keratopathy in terms of clear graft survival. In consequence, corneal grafts for bullous keratopathy should be as large as immunologically tolerable, and endothelial cell density should be as high as possible in order to counteract this special endothelial loss factor.     

Corneal endothelium and postoperative outcomes 15 years after penetrating keratoplasty

PURPOSE: To determine changes in the central endothelium and thickness of grafted corneas and the cumulative probability of developing glaucoma, of graft rejection, and of graft failure 15 years after penetrating keratoplasty. DESIGN: Longitudinal cohort study of 500 consecutive penetrating keratoplasties by one surgeon. METHODS: Regrafted eyes, fellow eyes of bilateral cases, and patients not granting research authorization were excluded, leaving 388 grafts for analysis. At intervals after surgery, we photographed the endothelium and measured corneal thickness using specular microscopy. The presence of glaucoma, graft rejection, and graft failure were recorded. RESULTS: The 67 patients examined at 15 years represented 30% of the available clear grafts. Endothelial cell loss from preoperative donor levels was 71 +/- 12% (mean +/- standard deviation, n = 67), endothelial cell density was 872 +/- 348 cells/mm(2), and corneal thickness was 0.59 +/- 0.06 mm. Endothelial cell density was unchanged between 10 and 15 years, whereas corneal thickness increased (P = .001, n = 55). The mean annual rate of endothelial cell loss from 10 to 15 years after surgery was 0.2 +/- 5.7% (n = 54). The cumulative probability of developing glaucoma, graft rejection, or graft failure was 20%, 23%, and 28%, respectively, and 6 of the 8 graft failures after 10 years resulted from late endothelial failure. CONCLUSIONS: From 10 to 15 years after penetrating keratoplasty, the annual rate of endothelial cell loss was similar to that of normal corneas, corneal thickness increased, and late endothelial failure was the major cause of graft failure.     

Risk factors for endothelial cell loss post-keratoplasty

PURPOSE: Transplant survival following penetrating keratoplasty is determined to a large extent by the course of endothelial cell density loss. Different influencing factors such as organ culture conditions, surgical trauma, exchange between donor and recipient cells, cell ageing and immune reactions can contribute to endothelial cell loss. The aim of this study was to determine the rate of endothelial cell loss in our patients and to detect dependencies on donor-and recipient-related factors. METHODS: Using non-contact specular microscopy, endothelial cell counts were obtained every 6 months from 293 consecutive patients who underwent keratoplasty in our institution between 1996 and 2000. Follow-up time was 36 months. RESULTS: In comparison with the density of donor endothelial cells, the mean endothelial cell loss of patients was 28.8% after 6 months, 39.8% after 12 months and 49% after 24 months. Donor age and initial cell density did not have a significant influence on the course of endothelial cell loss. The lowest rate of endothelial cell loss was associated with patients diagnosed with keratoconus. Conversely, those with preoperative glaucoma had a significantly increased rate of endothelial cell loss (p < 0.05). CONCLUSIONS: This study shows that preoperative glaucoma is a major risk factor for increased endothelial cell loss following keratoplasty.     

Impact of short-term versus longterm topical steroid treatment on 'idiopathic' endothelial cell loss after normal-risk penetrating keratoplasty

PURPOSE: Chronic endothelial cell loss after penetrating keratoplasty (PK) is suspected to result from a subclinical immune reaction. The aim of this study was to investigate whether the prolonged use of a topical steroid after normal-risk PK has a favourable impact on chronic endothelial cell loss. METHODS: The study included 305 eyes from the prospective Erlangen Normal-risk Keratoplasty Study, with a mean follow-up of 3.1 +/- 0.9 years. Postoperative treatment was initiated with prednisolone acetate 1% eyedrops five times a day and was tapered slowly over the first 6 months. Patients were then randomized into two treatment groups: a short-term group (n = 161), which stopped topical steroid treatment, and a longterm group (n = 144), which continued topical treatment with prednisolone acetate 1% eyedrops once a day until 12 months postoperatively. Endothelial cell counts were determined at each follow-up examination (after 6 weeks, then every 3 months until 2 years, then once a year). RESULTS: Endothelial cell density in the short-term and longterm groups decreased significantly from 1941 +/- 550 cells/mm(2) and 1957 +/- 568 cells/mm(2) to 1535 +/- 535 cells/mm(2) and 1472 +/- 549 cells/mm(2), respectively, from 6 weeks to 2 years postoperatively (p < 0.001). In a linear regression model, cell count in the short-term group decreased by 216 +/- 93 cells/mm(2) and in the longterm group by 206 +/- 111 cells/mm(2) per year. There was no significant difference in endothelial cell loss between the short-term and longterm groups (p = 0.5). CONCLUSIONS: Longterm, low-dose, topical steroid treatment does not seem to prohibit chronic endothelial cell loss after normal-risk penetrating keratoplasty, in contrast to its favourable effect on immunological graft reactions. Our results may indicate that the aetiology of chronic endothelial cell loss is not of inflammatory origin. Further studies are needed to investigate this phenomenon.     

Hinterkammerlinsenimplantation nach perforierender Keratoplastik

BACKGROUND: Posterior chamber lens implantation (PCL) after penetrating keratoplasty (pKp) might contribute to late endothelial graft failure due to intraoperative damage of graft endothelium or due to PCL-associated facilitation of chronic endothelial cell loss. PATIENTS AND METHODS: A total of 55 eyes were retrospectively selected. By means of exponential regression analysis, individual annual relative endothelial cell loss was calculated. Six patients were pseudophakic prior to pKp (group A). Due to advanced cataracts in 18 patients (group B) a combined operation (triple-procedure) had been initially performed. Of the remaining 31 eyes. 17 underwent PCL implantation after a mean of 1.5+/-1.2 years post pKp during follow-up (group C). The remaining 14 eyes remained phakic during follow-up (group D). RESULTS: A statistically significant difference between the groups was not observed for the follow-up period or duration of culture ( p=0.14; Kruskal-Wallis-Test). Graft failures during follow-up were also not observed. CONCLUSION: From these preliminary results, cataract surgery does not seem to promote late endothelial failure after pKp.     

穿透性角膜移植术后角膜植片内皮慢性失功的临床分析

目的探讨圆锥角膜行穿透性角膜移植（PK）术后角膜植片内皮慢性失功的临床特点。设计回顾性病例系列。研究对象圆锥角膜患者PK术后角膜植片内皮慢性失功148例（163眼）。方法所有患者实施PK术,采用非接触式角膜内皮显微镜、A型超声测厚仪和眼前节OCT扫描系统对角膜植片进行评价。主要指标中央角膜内皮细胞密度（ECD）、六边形细胞百分率、内皮细胞丢失率、内皮细胞形态、中央角膜厚度（CCT）及最佳矫正视力。结果PK术后3年内患者植片ECD呈下降趋势,内皮细胞年丢失率为14．2％±10．9％。术后1．5年较术后1年的ECD有明显下降（舟O．002）。术后不同时间点的植片内皮六边形细胞百分率均在50％以上,CCT在500μm以上,各组间比较无统计学差异（辟10．869）。PK术后5年以上复查,患者角膜植片ECD仍呈下降趋势,但个体差异性较大,多数患者的六边形细胞百分率仍在50％以上,内皮细胞面积增大是局部性的,CCT保持在500μm以上。150例未发生排斥的角膜植片除2例发生植片混浊外,其余均保持透明,患者术后最佳矫正视力提高。结论ECD的超生理下降和局部内皮细胞面积增大是PK术后角膜植片内皮慢性失功的主要临床表现。内皮慢性失功的发展存在个体差异性,且在同一个体不同时期发展程度亦有不同。     

Autologous ipsilateral rotating penetrating keratoplasty

PURPOSE: To evaluate visual outcome after autologous ipsilateral rotating penetrating keratoplasty. METHODS: The study included nine patients who consecutively underwent autologous ipsilateral rotating penetrating keratoplasty for treatment of traumatic central corneal avascular scars. These patients were compared with 105 patients who consecutively underwent homologous central penetrating keratoplasty in the same study period for treatment of avascular corneal scars extending to the corneal periphery. All operations were performed by the same surgeon. Mean follow-up time for both study groups was 31.27 +/- 21.54 and 32.0 +/- 19.4 months, respectively. RESULTS: In the autologous rotating keratoplasty group, visual acuity increased significantly (P = 0.03; Wilcoxon test) from 0.13 +/- 0.11 preoperatively to 0.29 +/- 0.16 postoperatively. Refractive astigmatism and keratometric astigmatism, respectively, increased (P = 0.02) from 3.19 +/- 2.53 diopters and 3.20 +/- 2.24 diopters, respectively, preoperatively to 6.9 +/- 1.82 diopters and 9.55 +/- 4.32 diopters, respectively, postoperatively. Comparing the study groups, postoperative visual acuity was significantly lower (P = 0.01), and keratometric astigmatism (P = 0.003) and refractive astigmatism (P = 0.01) were significantly higher in the autologous rotating keratoplasty group than in the control group. CONCLUSIONS: Autologous ipsilateral rotating penetrating keratoplasty compared with homologous central penetrating keratoplasty is associated with a high postoperative refractive and keratometric astigmatism leading to a relatively low postoperative visual acuity. It suggests that, in normal clinical conditions when donor material is available and postoperative follow-up examinations can be performed, homologous central penetrating keratoplasty may be superior to autologous ipsilateral rotating keratoplasty.     

Verlauf der Endothelzelldichte nach perforierender Keratoplastik Einfluss von spender- und empfängerabhängigen Faktoren

PURPOSE: Endothelial cell loss can be observed after keratoplasty, therefore in a retrospective study we analysed whether there is a correlation between donor age, recipient age, time post-mortem, preoperative cell density, diagnosis of the recipient and postoperative endothelial cell density. METHODS: The endothelial cell densities of 120 patients who had undergone penetrating keratoplasty were examined over a period of 2 years. We divided the patients into four groups based on the endothelial cell density over 2 years. We examined the groups with regard to the parameters given above. RESULTS: The lowest postoperative cell densities 2 years after keratoplasty showed a high correlation with the highest donor and recipient age. Even the lowest preoperative cell density was found in this group. Patients who underwent keratoplasty because of keratoconus had the highest cell densities after 2 years and also the lowest donor and recipient age. The preoperative cell density was also highest in this group. DISCUSSION: The results indicate a correlation between increasing donor and recipient age, decreasing preoperative cell density and loss of endothelial cells 2 years after penetrating keratoplasty. Patients with the diagnosis keratoconus should also receive transplants with higher donor age.     

Entwicklung der Endothelzellzahl der Wirtshornhaut Situation nach Blockexzision und exzentrischer Korneoskleralplastik

PURPOSE: Block excision of anterior uveal tumors and cystic epithelial ingrowth to the anterior chamber is a curative treatment for morphological rehabilitation of the globe. This study quantified the course of the host corneal endothelium after this peripheral corneoscleral graft. PATIENTS AND METHODS: This retrospective cross-sectional study examined 53 specular microscopic photographs of the central host cornea in 30 patients. The diameter of the block excision was 8.5 +/- 1.9 mm (6.0-11.0 mm). Follow-up after surgery averaged 37.9 +/- 47.6 months (1-216). RESULTS: The corneal endothelial cell count decreased with the duration of follow-up after block excision. The cell count was not related to indication for surgery or to diameter of block excision. Mean visual acuity was 16/20 before block excision and 6/20 at the end of follow-up. CONCLUSION: There is a significant loss of endothelial cells of the host after block excision, requiring a second central penetrating keratoplasty in some patients. Loss of endothelial cells may be due to the surgical trauma, chronic immunological reaction against the donor endothelium, or migration of the host endothelial cells onto the corneoscleral graft.     

Predicting endothelial cell loss and long-term corneal graft survival

PURPOSE: To evaluate a biexponential decay model for describing the loss of corneal endothelial cells with age as well as the increased loss of cells after cataract surgery and penetrating keratoplasty. METHODS: Data from previous studies were identified and the sum of two exponentials, d = p. exp(-at) + q. exp(-bt) (where d is cell density at time t, p and q are constants the sum of which is equal to the initial cell density, and a and b are exponential rate constants), fitted to each data set by a nonlinear least-squares algorithm. Goodness of fit was indicated by the residual standard deviation. Half times were calculated from the exponential rate constants. RESULTS: The model identified in each instance a rapid and a slow component to the cell loss. The half time for the slow component of the loss with age was 224 years, underlining the excess endothelial capacity in normal eyes. After surgery, the rapid component of the cell loss was probably due to surgical trauma and, after penetrating keratoplasty, cell-mediated rejection and other complications. The half times of the slow component were only 26 years after cataract surgery and 21 years after penetrating keratoplasty. DISCUSSION: The loss of endothelial cells followed a biexponential decay and could thus be described by a single equation. The half times of the slow component of the cell loss after surgery were substantially less than for the loss with age, indicating a markedly increased rate of cell loss that persisted for many years after surgery. A mechanism for this accelerated cell loss is suggested that involves a nonspecific, innate response initiated by the breakdown of the blood-ocular barrier. The model was used to calculate endothelial cell loss in the long term after penetrating keratoplasty and to predict when cell density would reach levels that are incompatible with maintenance of transparency and graft function. Thus, a rationale is presented for the setting of minimum donor cell densities by eye banks.     

The effect of allograft rejection after penetrating keratoplasty on central endothelial cell density

We identified all patients who had undergone penetrating keratoplasty for keratoconus and were being observed longitudinally (N = 174). During the follow-up period, 57 of 174 patients (33%) showed evidence of an allograft rejection episode, which occurred at an average of eight months after the operation. We analyzed specular photographs of the corneal endothelium, taken before and after the first allograft rejection episode. A significant decrease in endothelial cell density was observed (11.8%, P less than .0001). As a control, we analyzed all available specular photographs from patients with keratoconus who showed no evidence of allograft rejection after penetrating keratoplasty. The observed endothelial cell density decrease (11.8%) in patients with keratoconus undergoing allograft rejection exceeded that found in the control subjects (6.8%) during a comparable time period (P = .06). Severe allograft rejection episodes resulted in a decrease in endothelial cell density that exceeded expected loss significantly (14.8% compared with 6.9%, P = .01), whereas mild allograft rejection episodes were not associated with a loss in endothelial cell density exceeding that expected (1.8% compared with 6.5%, P = .34).     

Specular and scanning electron microscopy in diffuse silicone keratopathy

In a 50-year-old man, penetrating keratoplasty was carried out to treat a diffuse silicone keratopathy that developed 2 years after a pars plana vitrectomy combined with an intravitreal silicone injection for a complicated retinal detachment in the only aphakic eye. At 2 weeks after the intravitreal silicone injection, specular microscopy revealed a mild pleomorphism in the corneal endothelium and an endothelial cell loss of 26%. After 5 months, a small silicone drop floated in the anterior chamber and the first signs of diffuse keratopathy were observed. At the same time, specular microscopy revealed severe damage to the endothelial cells and a cell loss of 69%. After the keratoplasty, scanning electron microscopy of the corneal button showed a filamentous structure of the posterior surface of the cornea, with fibroblast-like cells; the endothelial cells were absent.     

Immune cells in the anterior chamber of patients with immune reactions after penetrating keratoplasty.

PURPOSE: Lymphocytes, monocytes, and macrophages are the predominating immune cells in graft rejection after keratoplasty in animal models. This study focuses on the isolation of immune cells from the anterior chamber of patients with slight, moderate, and severe endothelial immune reactions after penetrating keratoplasty. METHODS: Anterior chamber puncture was performed in five patients with cataract without inflammation and without penetrating keratoplasty (C1), in three patients undergoing penetrating keratoplasty without immune reactions (C2), in four patients undergoing penetrating keratoplasty after complete resolution of endothelial immune reactions (C3), in seven patients undergoing penetrating keratoplasty with slight endothelial immune reactions (IMI), in 10 patients undergoing penetrating keratoplasty with moderate endothelial immune reactions (IM2), and in eight patients undergoing penetrating keratoplasty with severe endothelial immune reactions (IM3). In each patient, approximately 0.1 mL of aqueous humor was examined. Cells in suspension were directly centrifuged on glass slides using a Cytospin centrifuge, stained, and evaluated under the light microscope. RESULTS: Groups C1, C2, and C3 did not contain cells. Immune cells were identified in three of seven patients in IM1, in eight of 10 patients in IM2, and in eight of eight patients in IM3. Predominating cells were macrophages and monocytes followed by lymphocytes. Regarding all patients in IMI, IM2, and IM3, a statistically significant correlation between detected cells and patient age, period between penetrating keratoplasty and anterior chamber puncture, or period between first symptoms and anterior chamber puncture could not be revealed. Granulocytes were found statistically significantly less often in patients with high-risk indications, in patients with a history of immune reactions and under immunosuppression. Lymphocytes were found statistically significantly less often in patients with a history of immune reactions. CONCLUSIONS: The probability to isolate immune cells from the anterior chamber of patients undergoing penetrating keratoplasty correlates with the severity of the endothelial immune reactions. This study is a first step to evaluate how detailed immunologic findings from animal keratoplasty models fit to clinical reality in patients undergoing keratoplasty. In the next step, cells found in the aqueous humor of patients with endothelial immune reactions should be further characterized directly (determination of molecules on the surface of the cells) or indirectly (determination of cytokine levels in the aqueous humor).     

Long-term Evaluation of Endothelial Cell Changes in Fuchs Corneal Dystrophy: The Influence of Phacoemulsification and Penetrating Keratoplasty

Purpose

To evaluate the natural course of the long-term endothelial cell changes in Fuchs corneal dystrophy (FCD) patients and investigate the effects of phacoemulsification on the annual rate of change in endothelial indices in FCD patients.

Methods

Thirty-four patients diagnosed with FCD at Seoul National University Hospital from 1994 to 2010 were retrospectively reviewed. Sixteen patients who had been followed up for more than 1 year were selected and classified into 3 groups: group A, patients with no ocular surgery; group B, patients who had undergone phacoemulsification only; and group C, patients who had undergone penetrating keratoplasty with cataract surgery. Endothelial cell density, polymegethism, pleomorphism, and pachymetry were measured and the exponential rates of endothelial cell and pachymetry change were analyzed.

Results

A non-linear mixed model of non-operated FCD patients showed that only pachymetric data tended to increase with statistical significance (p = 0.001) with a mean follow-up period of 4.15 years. Using an exponential regression analysis fitting curve, the mean rates of annual endothelial cell loss were 0.82%/yr, 20.39%/yr, and 29.27%/yr in groups A, B, and C respectively, and statistical significance was seen only in group C (p < 0.05).

Conclusions

Retrospective long-term follow-up data showed that changes in endothelial density did not significantly decrease over at least 4 years in middle-aged FCD patients. The changes in pachymetric corneal thickness appeared to increase over the same period. Considering that no exponential changes were aggravated after performing cataract surgery alone, cataract surgery would be a preferable option in FCD patients compared to an approach of "wait-and-do" penetrating keratoplasty combined with cataract surgery.     

角膜移植术后行白内障摘出人工晶状体植入对角膜植片的影响

目的探讨穿透性角膜移植术后白内障行白内障摘出联合人工晶状体植入术对角膜植片的影响。方法穿透性角膜移植术6个月后行白内障摘出联合人工晶状体植入术17例（17眼）,随访3～18个月,平均11个月,观察术后角膜水肿情况、角膜内皮细胞计数变化、眼压变化、免疫排斥反应和术后并发症,并进行分析。结果术后所有患眼裸眼视力≥0．3,最佳矫正视力≥0．5者8眼。术后角膜水肿3～7d内消退,角膜恢复透明。术前角膜内皮计数平均为（1547±111）个／mm2。术后3月内皮细胞数量稳定,平均为（1275±106）个／mm2,内皮细胞丧失率平均为4．92％。无其它不良反应。结论对穿透性角膜移植术后行白内障摘出联合人工晶状体植入术对角膜植片是安全的。     

Pathology of late endothelial failure: late endothelial failure of penetrating keratoplasty: study with light and electron microscopy

PURPOSE: Late endothelial failure of penetrating keratoplasty can be defined as gradual decompensation (increasing thickness with loss of clarity) of a previously clear graft without apparent cause. This study examined the possibility that a chronic subclinical rejection process may be occurring in grafts that fail from late endothelial failure. METHOD: Six patients fulfilling the diagnostic criteria for late endothelial failure who underwent repeated keratoplasty were studied. The clinical course and results of specular microscopy were reviewed. The failed corneal graft for each patient was examined by light and electron microscopy. RESULTS: Sequential specular microscopy demonstrated low initial postoperative endothelial cell density with continued decrease in density and increase in corneal thickness over the first 5 postoperative years. Electron microscopy revealed irregular-shaped cells of varying size with many abnormal features, lying on abnormal Descemet's membrane. Degenerating endothelial cells were commonly seen. There was no sign of acute or chronic inflammation. CONCLUSIONS: The pathologic findings are suggestive of an unstable and highly stressed endothelial cell population in late endothelial failure but are nonspecific. There was no evidence of acute or chronic rejection at the time of graft failure.     

穿透性角膜移植术后低密度角膜内皮细胞白内障手术的临床观察

目的探讨穿透性角膜移植术(PKP)后角膜植片低内皮细胞密度的白内障患者行白内障摘除联合人工晶状体植入术的安全性。方法 PKP术后角膜内皮细胞计数<1500个/mm2行白内障摘除联合人工晶状体植入术治疗的患者15例(15只眼),根据晶状体核硬度分别选择不同的手术方式,行相应的围手术期处理,分别记录术前及术后3个月患者裸眼视力、角膜内皮细胞计数及裂隙灯观察角膜植片情况。结果术前内皮细胞计数为(1195±315)个/mm2,术后3个月内皮细胞计数为(1044±301)个/mm2,差异有统计学意义(P=0),内皮损失率为12.6%。术前及术后3个月的裸眼视力分别为0.06±0.09和0.35±0.22,两者差异有统计学意义,平均提高>5行标准视力表。白内障术后6个月之内无一例角膜内皮功能失代偿及角膜植片免疫排斥反应,角膜植片均保持透明。结论 PKP术后角膜植片内皮细胞计数<1500个/mm2的患者,只要注意围手术期治疗,选择合适的手术方法,和注意术中保护角膜内皮细胞,白内障摘除联合人工晶状体植入术是安全有效的。