Supplemental Material for: Surgically Induced Sclerokeratitis after Excision of Conjunctival Squamous Cell Carcinoma: A Case Report
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Introduction: Ocular surface squamous neoplasia (OSSN) encompasses a spectrum of conjunctival and corneal epithelial neoplasms, including invasive squamous cell carcinoma (SCC). Although postoperative complications following OSSN excision have been reported, progressive non-infectious, non-necrotizing interstitial sclerokeratitis after surgical management remains poorly characterized.Case Presentation: A 77-year-old white male presented with progressive right eye pain, irritation, redness, and tearing after conjunctival trauma in an eye with a longstanding presumed temporal pterygium. Examination demonstrated a temporal fibrovascular lesion in the right eye with posterior stromal neovascularization and focal ulceration. Despite topical corticosteroids and antibiotics, the lesion enlarged, prompting excisional biopsy with adjunctive cauterization, cryotherapy,and amniotic membrane transplantation. Pathology confirmed invasive conjunctival SCC. Six months postoperatively, the patient developed progressive corneal haze, stromal neovascularization, lipid keratopathy, and declining visual acuity despite topical corticosteroid therapy. Evaluation for recurrent OSSN, infectious keratitis, surgically induced necrotizing scleritis, peripheral ulcerative keratitis, ocular cicatricial pemphigoid, and systemic autoimmune disease was unremarkable. Topical 5-fluorouracil, antiviral therapy, and subconjunctival bevacizumab/triamcinolone injections produced partial regression of neovascularization; however, stromal haze, scarring, and lipid keratopathy progressed, leading to endothelial decompensation and hand motion visual acuity.Conclusion: This case describes surgically induced, non-infectious, non-necrotizing fibrovascularsclerokeratitis, a rare, vision-threatening postoperative complication after OSSN excision characterized by progressive stromal haze, lipid keratopathy, neovascularization, and reactive scar formation. The clinical course suggests a multifactorial pathogenesis involving limbal stem cell dysfunction, localized immune dysregulation, exaggerated fibrovascular healing, and possible endothelial compromise. Clinicians should be aware of this vision-threatening postoperative complication after OSSN excision and adjunctive cryotherapy, particularly in patients with a predisposition to immune dysregulation.
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