Keratolimbal Transplantation For Limbal Ischemia And Peripheral Corneal Perforation In Severe Ocular Graft-Versus-Host Disease

To report the surgical management of peripheral corneal perforation secondary to severe limbal ischemia in chronic ocular graft-versus-host disease (GVHD) complicated by the development of recurrent ocular surface squamous neoplasia (OSSN), which was treated with no-touch lesion excision and topical interferon alpha-2b (IFN-a2b), highlighting the role of keratolimbal transplantation as a structural rescue procedure in advanced ocular surface disease complicated by recurrent ocular surface neoplasia and progressive limbal stem cell deficiency.

Department of Ophthalmology of ULS São João (Porto, Portugal), a tertiary referral center for complex anterior segment pathology. The procedure was performed by a cornea and ocular surface surgeon within a high-volume surgical unit performing over 150 corneal transplants annually, including penetrating, lamellar and endothelial keratoplasties, intrastromal ring implantation for ectatic disorders, and advanced ocular surface reconstruction procedures.

A 58-year-old male with B-cell acute lymphoblastic leukemia underwent allogeneic bone marrow transplantation and subsequently developed severe chronic ocular GVHD with inflammation and limbal dysfunction. Inital management consisted of topical cyclosporine and lubricants, with intermittent courses of antibiotics-steroids therapy during exacerbations.

The left eye followed a complex course. In the setting of ocular surface inflammation, the patient developed OSSN, requiring repeated no-touch surgical excisions with adjunctive cryotherapy, topical 5-fluorouracil and IFN therapy, as well as amniotic membrane transplantation. This culminated in symblepharon formation and persistent inferior limbal ischemia involving approximately 180°.

Earlier this year, he presented to the emergency department with acute visual deterioration (hand motion), inferior corneal melting, shallow anterior chamber, and peripheral perforation sealed by iris prolapse. Despite intensive antimicrobial and anti-inflammatory therapy, structural decompensation progressed. A keratolimbal graft was performed to restore tectonic integrity of the compromised corneal–limbal unit. Early postoperative assessment demonstrated stable graft positioning without acute rejection; however, inferior corneoscleral exposure and partial scleral suture exposure required secondary autologous oral mucosal grafting. Current management includes topical cyclosporine, steroid–antibiotic therapy, and optimization of immunosuppression.

Severe chronic ocular GVHD may culminate in progressive limbal ischemia, stem cell deficiency, corneal melting, and perforation. OSSN development and subsequent treatment may aggravate these ocular surface complications. Keratolimbal transplantation can provide tectonic stabilization in advanced cases of peripheral corneal perforation, but stepwise reconstruction - including mucosal grafting - may be required to achieve durable anatomical preservation. In end-stage ocular surface disease, structural rescue may precede and outweigh visual rehabilitation as the primary therapeutic objective.