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Graft failure through endothelial cell loss is a constant threat throughout the lifetime of a corneal graft. It can occur at various time points after transplantation. Primary graft failure has nowadays become increasingly rare owing to meticulous eye banking methods and improved surgical techniques. Corneal graft rejection is always held responsible for endothelial cell loss. However a rejection episode that is promptly and adequately treated does not necessarily lead to a higher than expected cell loss. A more smouldering danger to ultimate graft survival is late endothelial failure. This gradual graft decompensation is secondary to a decrease in cell density below that necessary to maintain corneal deturgesence. The process of transplantation itself seems to set off a series of events (possibly immunological) that greatly exacerbates the endothelial cell loss compared to virgin corneas. This accelerated cell loss persists for at least 10-15 years after transplantation, after which a more-stable situation is reached and cell attrition returns to normal rates. This provides a strong rationale for setting high donor standards of minimal cell density. Newer transplantation techniques such as deep anterior lamellar keratoplasty and deep lamellar endothelial keratoplasty could provide possible solutions to prevent this late endothelial failure. However they still have to prove themselves in the long run.

Purpose: A therapeutic penetrating keratoplasty (TPKP) technique that achieves satisfactory visual rehabilitation with a minimal risk of rejection is described., Methods: A patient presented with a central corneal perforation in the left eye extending to the temporal limbus. We performed a novel surgical procedure, in which a corneal allograft was combined with relocation of a crescent of autologous corneal tissue., Results: The TPKP placed the optical zone of the donor cornea over the center of the entrance pupil. The chances of an immunologic rejection were minimized by intercalating a crescent of autologous tissue between the allograft and the limbal vessels., Conclusion: The combination of an allograft with a crescent of autologous corneal tissue minimizes the disadvantages associated with eccentric or oversized trephination.

Background: The exact mechanism of human corneal allograft rejection, which is the major cause of corneal transplant failure, remains unclear. We investigated the role of natural killer (NK) cells in rat corneal allograft rejection by examining the aqueous humor (AH) cell infiltrate on different postoperative days., Methods: Flow cytometric analysis was performed on the AH and submandibular draining lymph node (DLN) cells before transplantation and at different time points thereafter. In addition, we performed functional cytotoxicity assays with cells present in the AH during corneal rejection., Results: We demonstrated a gradual increase in the absolute cell number of different hematopoietic subpopulations in the AH after allogeneic cornea transplantation. CD3CD4 cells, mainly monocytes and macrophages, were the predominant subpopulation 2 days after transplantation, followed by a successive relative increase of CD4 T cells, CD8 T cells, CD161 T cells, and NK cells. NK and CD161 T cells were present at a 10- to 15-fold higher percentage than in the DLN, suggestive of local expansion of these cells. A higher percentage of NK cells were CD8-negative compared with DLN NK cells. AH cells specifically lysed allogeneic cells, and this cytotoxicity was mainly attributable to NK cells but not to CD4 or CD8 T lymphocytes., Conclusion: These results confirm the crucial role of CD4 cells in the allogeneic corneal graft rejection process and implicate NK cells as possible mediators of the rejection.

Purpose: To compare the results in our patient series after penetrating keratoplasty (PKP) for syphilitic interstitial keratitis (IK) with those described in the literature., Methods: Retrospective case series in which visual acuity (VA), graft clarity, rejection episodes, intraocular pressure and endothelial cell density (ECD) were examined postoperatively., Results: Postoperative VA improved in all cases. There was no evidence of wound dehiscense or occurrence of retrocorneal membrane formation in any case. Postoperative inflammation was not more severe in our patients with syphilitic IK compared to patients undergoing PKP for other reasons. A normal decline in ECD proved that there was no subclinical inflammation as well., Conclusion: PKP for syphilitic IK has a good prognosis in our case series as far as graft survival is concerned. Improvement in VA was present in all cases, though sometimes limited. In our case series, we experienced less postoperative complications than described in the older literature, which is probably due to better microsurgical techniques used nowadays.

Purpose: Corneal allograft rejection is one of the major causes of transplant failure. The purpose of the current study was to examine the decline in endothelial cell density (ECD) in patients experiencing allograft rejection, by comparing this decline with the normal evolution in patients who undergo penetrating keratoplasty (PKP) and to identify possible factors predictive of this endothelial cell loss after corneal allograft rejection., Methods: In a case-control study of 45 corneas that underwent corneal allograft rejection, specular microscopy photographs taken within the shortest time preceding the onset of rejection and after the resolution of the rejection were analyzed., Results: The observed percentage loss of ECD in 21 (47%) corneas was not significantly greater than expected. A second group of 13 (29%) corneas showed a decline in ECD that was significantly greater than expected. Finally there were 11 corneas (24%) in which endothelial cells were no longer observable. The only two risk factors that reached statistical significance after multiple logistic regression analysis were a delay in diagnosis (a delay of >1 day yielded an odds ratio of 10.40; P=0.02) and a recipient age of more than 60 years (odds ratio, 6.95; P=0.04)., Conclusions: Corneal allograft rejection does not necessarily cause a higher than expected endothelial cell loss; almost half of the patients in this study showed a decline in ECD that is comparable to the decline in patients who undergo PKP and have an uneventful follow-up. The most important variable influencing the extent of endothelial cells loss is a delay in diagnosis and treatment.

Purpose: To compare the results in our patient series after penetrating keratoplasty (PKP) for syphilitic interstitial keratitis (IK) with those described in the literature., Methods: Retrospective case series in which visual acuity (VA), graft clarity, rejection episodes, intraocular pressure and endothelial cell density (ECD) were examined postoperatively., Results: Postoperative VA improved in all cases. There was no evidence of wound dehiscense or occurrence of retrocorneal membrane formation in any case. Postoperative inflammation was not more severe in our patients with syphilitic IK compared to patients undergoing PKP for other reasons. A normal decline in ECD proved that there was no subclinical inflammation as well., Conclusion: PKP for syphilitic IK has a good prognosis in our case series as far as graft survival is concerned. Improvement in VA was present in all cases, though sometimes limited. In our case series, we experienced less postoperative complications than described in the older literature, which is probably due to better microsurgical techniques used nowadays.

Purpose: To identify the influence of the underlying etiology on the outcome of therapeutic penetrating keratoplasty (PKP) in the management of corneal perforation, impending perforation or refractory corneal disease., Methods: A retrospective observational case series with 28 patients (28 eyes) was performed. Patients were divided in two subgroups, based on the underlying ocular disease leading to the therapeutic PKP. Group I consisted of 15 patients (54%) with an infectious etiology, the other 13 patients (46%) with a noninfectious condition belonged to group II. Mean follow up was 23.2 months (median 21 months)., Results: An enucleation could be avoided in all but two cases. In group I, 12 of 15 (80%) grafts remained clear, compared with only 3 of 13 (23%) in group II (p = 0.0004). Visual acuity (VA) amelioration was achieved in 20 of 28 patients (71%). In group I the postoperative VA was significantly better than preoperatively (p = 0.002); however, in group II the improvement was only borderline significant (p = 0.05). Overall five out of ten (50%) patients with a therapeutic PKP in group I had an endothelial cell density >or= 1900 cells/mm2 at the time of their last specular microscopy., Conclusion: Our study demonstrates the importance of underlying etiology on the outcome of therapeutic PKP. Graft survival and postoperative visual acuity varied widely depending on the underlying ocular disease, and it was clear that therapeutic PKP has a much better prognosis in infectious conditions when compared with noninfectious conditions. We believe that these good results can justify the use of therapeutic PKP in selected cases of infectious keratitis.

Background: Systemic cyclosporine A (CsA) remains a valuable treatment option in the prevention of corneal graft rejection, but the question of timing and duration of this systemic therapy remains unresolved. The effect of a pre- and postoperative dosing schedule, related to the expected moment of rejection, was examined in a rat model., Methods: All AO (strain) recipients of PVG grafts were assigned to the following treatment groups: Group 1 (controls), groups 2-5 (a postoperative treatment regimen of CsA for 5, 10, 15 and 30 days respectively) and groups 6 and 7 (CsA preoperatively for 5 days and postoperatively for another 5 or 10 days respectively). Corneal allografts were clinically evaluated and blood CsA levels were measured at various time points., Results: Untreated controls rejected their allografts after 13 days. Regression analysis showed a strongly significant positive correlation between graft survival time and duration of cyclosporine therapy. There was no difference in graft survival between groups 3 (CsA 10 days) and 4 (CsA 15 days). A pre-operative dosing schedule of CsA followed by postoperative treatment had no advantage over a solely postoperative treatment regimen. The moment of rejection was characterized by a low to undetectable CsA concentration., Conclusion: The present study demonstrates a significant influence of the duration of systemic CsA administration on allograft survival time. However, preoperative administration of CsA does not seem to have an additional influence on graft survival, which is in line with the biological evidence of the mechanism of action of CsA on the efferent arm of graft rejection.

An 80-year-old man, with a solid abdominal tumor and multiple skin lesions, was admitted to the hospital because of a perforated right cornea and an impending perforation of the left. The clinical, histological, immunohistological and immunoprecipitation findings of the skin lesions were consistent with Anhalt's criteria for paraneoplastic pemphigus (PNP). The underlying malignancy proved to be an incurable peripheral neuronal shaft tumor. Both conjunctivae appeared normal. The right eye revealed a flat anterior chamber, due to a spontaneous, central corneal perforation. The central part of the left cornea had severely thinned, resulting in a descemetocele, which eventually perforated. Multiple surgical interventions were needed to restore the anterior chamber in both eyes. Although a causative association between PNP and corneal perforation could not be demonstrated, we think that corneal melting should be added to the list of ocular complications in patients with PNP., (Copyright 2001 S. Karger AG, Basel.)

Acanthamoeba keratitis is caused by protozoa and characterised by a protracted course. All patients presenting with a therapy-resistant keratitis, even non-contact lens wearers, should be examined for the presence of Acanthamoeba by means of specific cultures, histopathological stainings and--if necessary--a corneal biopsy. The combination of clinical signs, such as excessive pain, a radial keratoneuritis and in a later phase a stromal ring infiltrate, together with a suggestive history (contact lenses, polluted water) is an important factor for the early diagnosis. Because of improved clinical detection and earlier diagnosis, the infection can often be controlled with a combination therapy of polyhexamethylene biguanide or chlorhexidine with propamidine and neomycine. This results in a better visual prognosis and a decreased need for therapeutic keratoplasty.