Birdshot chorioretinopathy with steroid-responder glaucoma limiting standard uveitis therapy: A case report
Location
Moultrie, GA
Start Date
17-4-2026 12:00 PM
End Date
17-4-2026 1:00 PM
Description
Background: Birdshot chorioretinopathy (BSCR) is a chronic, rare, bilateral posterior uveitis characterized by lymphocytic choroiditis/retinitis that presents with progressive retinal dysfunction. This condition is strongly associated with HLA-A29 and typically affects older adults. Patients with BSCR often report blurred vision, floaters, photopsias, dyschromatopsia, and impaired night vision. BSCR can cause progressive damage through retinal vasculitis, macular edema, and outer retinal injury, making early recognition and durable immunosuppression essential to preserve vision. Long term treatment frequently requires corticosteroids plus steroid-sparing immunomodulatory therapy; however, steroid-induced ocular hypertension can significantly constrain management.
Case presentation: A 74-year-old female with a known diagnosis of birdshot chorioretinitis who is also HLA-A29 positive and has bilateral steroid responsiveness presented to the clinic with pseudo-bullous keratopathy. Her ocular history included bilateral cataract extraction with posterior capsulotomy, an OMNI glaucoma procedure in the right eye in 2020, and a right vitrectomy in 2023. Previously, she received an intravitreal dexamethasone implant (Ozurdex) in January 2024, and steroid-related intraocular pressure concerns were documented. At her current visit, intraocular pressure was 20 mmHg OD and 12 mmHg OS. Her problem list included steroid responder (OU) and BSCR. Given her steroid response, the clinical plan emphasized avoidance of additional corticosteroids and continuation of multi-agent glaucoma therapy (dorzolamide–timolol BID OU, tafluprost HS OU, and brimonidine TID OD). Furthermore, her systemic medication list included biologic immunomodulators such as adalimumab (Humira) and tocilizumab (Actemra), which are consistent with steroid-sparing control strategies for BSCR.
Conclusion: This complex case illustrates a management dilemma in BSCR, which often requires sustained anti-inflammatory control, yet steroid-induced ocular hypertension can limit first-line corticosteroid therapy. This may force earlier reliance on systemic steroid-sparing therapy and coordinated care between uveitis/retina and glaucoma specialists. Recognizing BSCR’s chronic, progressive nature along with its HLA-A29 association and the need for long-term monitoring for vasculitis and macular complications can help clinicians balance inflammation control against irreversible glaucomatous and retinal vision loss.
Embargo Period
5-27-2026
Birdshot chorioretinopathy with steroid-responder glaucoma limiting standard uveitis therapy: A case report
Moultrie, GA
Background: Birdshot chorioretinopathy (BSCR) is a chronic, rare, bilateral posterior uveitis characterized by lymphocytic choroiditis/retinitis that presents with progressive retinal dysfunction. This condition is strongly associated with HLA-A29 and typically affects older adults. Patients with BSCR often report blurred vision, floaters, photopsias, dyschromatopsia, and impaired night vision. BSCR can cause progressive damage through retinal vasculitis, macular edema, and outer retinal injury, making early recognition and durable immunosuppression essential to preserve vision. Long term treatment frequently requires corticosteroids plus steroid-sparing immunomodulatory therapy; however, steroid-induced ocular hypertension can significantly constrain management.
Case presentation: A 74-year-old female with a known diagnosis of birdshot chorioretinitis who is also HLA-A29 positive and has bilateral steroid responsiveness presented to the clinic with pseudo-bullous keratopathy. Her ocular history included bilateral cataract extraction with posterior capsulotomy, an OMNI glaucoma procedure in the right eye in 2020, and a right vitrectomy in 2023. Previously, she received an intravitreal dexamethasone implant (Ozurdex) in January 2024, and steroid-related intraocular pressure concerns were documented. At her current visit, intraocular pressure was 20 mmHg OD and 12 mmHg OS. Her problem list included steroid responder (OU) and BSCR. Given her steroid response, the clinical plan emphasized avoidance of additional corticosteroids and continuation of multi-agent glaucoma therapy (dorzolamide–timolol BID OU, tafluprost HS OU, and brimonidine TID OD). Furthermore, her systemic medication list included biologic immunomodulators such as adalimumab (Humira) and tocilizumab (Actemra), which are consistent with steroid-sparing control strategies for BSCR.
Conclusion: This complex case illustrates a management dilemma in BSCR, which often requires sustained anti-inflammatory control, yet steroid-induced ocular hypertension can limit first-line corticosteroid therapy. This may force earlier reliance on systemic steroid-sparing therapy and coordinated care between uveitis/retina and glaucoma specialists. Recognizing BSCR’s chronic, progressive nature along with its HLA-A29 association and the need for long-term monitoring for vasculitis and macular complications can help clinicians balance inflammation control against irreversible glaucomatous and retinal vision loss.