Necrotizing Infectious Anterior Scleritis With Scleral Abscess On Adalimumab Requiring Surgical Reconstruction
Published 2026 - 44th Congress of the ESCRS
Reference: POCOR078 | Type: Case Report | DOI: 10.82333/9mct-pq61
Authors: Dr Josip Knežević 1 , Dr Dejan Ilišković* 1 , Dr Sanja Masnec 1 , Dr Ivan Škegro 1 , Dr Nenad Vukojević 1
1Ophthalmology,University Hospital Centre Zagreb,Zagreb,Croatia
Purpose
Infectious necrotizing scleritis may closely mimic immune-mediated inflammation, particularly in patients receiving anti-TNF therapy, where new-onset ocular symptoms are often attributed to paradoxical autoimmune phenomena. This diagnostic overlap may delay microbiological confirmation and lead to inappropriate immunosuppression, accelerating scleral necrosis. We report a case of necrotizing infectious anterior scleritis caused by Staphylococcus aureus, complicated by scleral abscess formation and adjacent peripheral corneal ulceration in a patient receiving long-term adalimumab therapy. Due to rapid progression and impending globe perforation, urgent tectonic scleral reconstruction was required to preserve ocular integrity.
Setting
This case was managed at a tertiary referral university hospital with a dedicated anterior segment and ocular surface service, providing access to microbiological diagnostics and surgical management of complex infectious scleral disease. A multidisciplinary approach involving ophthalmology and infectious disease specialists enabled prompt diagnosis and coordinated care.
Report of case
A 50-year-old man receiving adalimumab for hidradenitis suppurativa for 2 years presented with a painful, red left eye and inferotemporal nodular scleral thickening. There was no history of trauma or prior ocular surgery, and uncorrected visual acuity was 20/20. In the context of ongoing anti-TNF therapy, immune-mediated scleritis was initially presumed, and systemic methylprednisolone (64 mg/day) was commenced. Within 7 days, rapid progression to scleral necrosis with suspected abscess formation was observed, and ultrasound biomicroscopy demonstrated intrascleral involvement supporting abscess formation. An infectious etiology was suspected, prompting discontinuation of adalimumab and tapering of corticosteroids, with initiation of empirical systemic and topical antibiotics. Despite treatment, peripheral marginal corneal ulceration developed adjacent to the affected sclera, with progressive scleral necrosis and impending globe perforation. Urgent surgery was performed, including debridement of necrotic tissue, drainage of the scleral abscess, and tectonic scleral patch graft with conjunctival advancement. Intraoperative direct microscopy of debrided necrotic tissue showed no fungal elements prior to scleral patch graft placement. Cultures obtained from the scleral abscess grew Staphylococcus aureus, while blood cultures remained negative. The infection resolved with preservation of globe integrity, and visual acuity remained 20/20.
Conclusion/Take home message
In patients receiving anti-TNF therapy, new-onset scleritis may mimic paradoxical immune-mediated inflammation, delaying recognition of an underlying infection and leading to inappropriate immunosuppression. Rapid progression despite corticosteroid therapy should prompt urgent microbiological evaluation. Infectious necrotizing scleritis may require early surgical intervention, including tectonic scleral reconstruction despite active infection, to prevent perforation and preserve globe integrity and visual function.