Case Report: A rare case of ocular giant cell arteritis with bilateral orbital inflammation and diagnostic challenges.

Giant cell arteritis (GCA) is a systemic vasculitis of medium- and large-sized arteries, most commonly presenting with headache, scalp tenderness, and, if untreated, can lead to visual loss from ischemic optic neuropathy. Although the most common ophthalmic manifestations of Giant Cell Arteritis are related to ocular ischemia, orbital involvement can occur and remains underrecognized. Fewer than 10 cases in the literature describe perioptic or retrobulbar infiltration, underscoring the uniqueness and diagnostic challenge of such presentations. 75-year-old male with past medical history of hypertension, benign prostatic hyperplasia status post transurethral resection, traumatic subdural hematoma (SDH), who presented with episodic left eye vision loss (central and peripheral vision), followed by acute altitudinal vision loss in the right eye for 1 week. He also complained of right-sided headaches s/p SDH and chronic joint pain, but denied any other constitutional symptoms. The neurological exam revealed significantly decreased right eye visual acuity with an altitudinal field defect, color desaturation, and grade 2 + disc edema. Labs revealed an erythrocyte sedimentation rate (ESR) of 21 mm/h (normal age-adjusted), and a C-reactive protein (CRP) of 1.9 mg/dL(elevated). Magnetic resonance imaging of the brain and orbits, with and without contrast, showed bilateral retrobulbar/perioptic soft-tissue infiltration and enhancement, suggestive of an inflammatory, infectious, or autoimmune process. Blood work showed normal thyroid function and negative rheumatological work-up. Spinal fluid studies were within normal limits except for mildly elevated protein (white-blood cell 3, red-blood cell 1, Protein 52, and Glucose 54, while serum glucose was 94). Temporal artery biopsy was positive for temporal arteritis. His hospital course was complicated by left eye episodic vision loss. High-dose IV steroids led to initial improvement and stabilization of symptoms at discharge, requiring oral steroid taper. 10 months later, he had persistent vision loss in the right eye at the follow-up visit and also suffered complications from chronic steroid use. This case highlights the challenges in diagnosing and treating GCA. Diagnostic delay can occur from under-recognition of atypical presentations. Neuroimaging provided important diagnostic value in this case; however, its routine role in diagnostic criteria requires validation in larger studies.