Case Report: Concurrent retinal vasculitis and optic neuritis in systemic lupus erythematosus

Abstract

Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease that can affect the ocular system, with retinal vasculitis and optic neuritis being rare but serious manifestations. We present a case of a 26-year-old female with newly diagnosed SLE who developed both retinal vasculitis and optic neuritis, leading to progressive visual impairment. She was successfully treated with methylprednisolone and rituximab, achieving significant visual recovery. A review of existing literature highlights the diagnostic challenges, pathophysiology, and optimal treatment strategies for such cases. Our findings emphasize the importance of early recognition and aggressive immunosuppressive therapy in improving patient outcomes.

Keywords: autoimmune ocular disease; immunosuppressive therapy; optic neuritis; retinal vasculitis; systemic lupus erythematosus.

Figure 1

(a-c) Comparison of fundus photographs before and after treatment. (a) Fundus photographs obtained on admission. Bilateral optic disc edema with blurred margins. Posterior pole retinal white exudates. Right eye demonstrates enhanced superior temporal vascular reflex and hemorrhagic spots. (b) Fundus photographs obtained on 12 days after admission. Persistent bilateral disc edema and retinal exudates. (c) Fundus photographs at three-month post-treatment follow-up. Marked reduction of exudates in both eyes, with residual disc margin blurring. Compared with before treatment, the patient’s retinal vasculitis lesions showed significant improvement after treatment.

Figure 2

Bilateral retinal nerve fiber layer (RNFL) OCT scan reveals: thinning of nasal RNFL thickness and thickening of temporal RNFL thickness, indicating bilateral optic neuritis-induced RNFL damage. In this patient, the nasal RNFL is significantly thinned, being the first to be affected and suffering the most severe damage. The relative thickening of the temporal RNFL may be attributed to inflammation-induced axonal swelling and optic disc edema, leading to increased RNFL thickness.

Figure 3

Cranial MRA demonstrated vascular abnormalities consistent with secondary cerebral vasculitis. Cranial MRA demonstrated patent bilateral anterior cerebral arteries, middle cerebral arteries, and posterior cerebral arteries with diminished distal branching, diffuse luminal caliber irregularities, and multiple foci of severe stenosis.