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Diagnosis and Management of Corneal Allograft Rejection


Key Concepts

  • Of the approximately 50,000 corneal transplants performed annually in the United States, corneal allograft rejection is still the leading cause of corneal graft failure.

  • Young age, pre- or postoperative vascularization, preoperative inflammation, and iris synechiae to the graft-host junction are risk factors for graft failure after penetrating keratoplasty.

  • Deep anterior lamellar keratoplasty (DALK) avoids the risk for endothelial rejection, but stromal rejection can occur rarely.

  • Endothelial rejection can occur after Descemet stripping endothelial keratoplasty (DSEK) in approximately 10% of cases but may not present with a classic Khodadoust line.

  • Rejection rates after Descemet membrane endothelial keratoplasty (DMEK), where no stromal tissue is transplanted, are reported below 1%.

  • Most episodes of rejection are treatable with topical corticosteroids; however, early recognition and intervention is crucial to success.

Clinical Aspects of Corneal Allograft Rejection

Corneal transplantation is the most successful tissue transplantation procedure in humans. Increased success in corneal grafting is due to improved surgical technique, better donor tissue management, and the appreciation of the varied clinical manifestations. Improved medical management of corneal allograft rejection yields graft survival rates of up to 95% in some reported series of low-risk patients. , Of the approximately 50,000 corneal transplants performed annually in the United States, corneal allograft rejection is still the leading cause of corneal graft failure. The reported prevalence of corneal graft rejection events compared to prevalence of corneal graft failure due to rejection over the past few decades indicates improvement in our ability to manage allograft rejection but also reveals that we do not sufficiently understand the process to control it completely. , , The clinical challenge remains to recognize those patients who are at high risk of rejection, to communicate well with the patient the need for prompt recognition and therapy of rejection, to maintain a high level of suspicion for allograft rejection, to recognize the early and subtle signs of corneal allograft rejection, and to institute prompt and aggressive therapy. While developments in immunosuppression and immunomodulation promise to mitigate the effects of corneal allograft rejection, our most effective strategy presently in corneal transplantation is to recognize allograft rejection early and treat it aggressively.

Historical Perspective

A brief historical review of our understanding of corneal graft rejection not only increases appreciation of the mechanism of corneal graft rejection but also identifies some of the important clinical principles that apply to recognition and therapy of rejection. Paufique, Sourdille, and Offret first described graft failure (maladie du greffon) in 1948 as an opacification of the corneal graft occurring after an interval of clarity. They suggested that host sensitivity to the donor was the cause. In laboratory studies of allograft rejection, Maumenee confirmed in 1951 that sensitization of the host to the donor was the underlying basis of this graft failure. Maumenee’s subsequent clinical observations in the 1960s characterized the clinical features of corneal allograft failure and emphasized the importance of the endothelium as the cells damaged by the immunologic assault. Experimental studies in animals by Silverstein and Khodadoust in the late 1960s demonstrated the clinical and histopathologic events of corneal allograft rejection. These investigators observed that each layer of the cornea (epithelium, stroma, and endothelium) could induce host sensitization and undergo allograft rejection either individually or in concert. Polack showed that donor epithelial cells are replaced rapidly by host epithelial cells and, although susceptible to rejection when present, are not present for late immunologic assault. Conversely, stromal and endothelial cells persist and are subject to immunologic attack. With such supportive studies, it has been further asserted that allograft rejection is a form of delayed hypersensitivity. Studies, particularly by Streilein and associates, have raised the possibility that anterior chamber–associated immune deviation (ACAID) phenomena contributes to graft survival and that allograft rejection represents a breakdown in the protection afforded the graft by ACAID.

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