A 38-year-old immunocompetent man presents with sudden floaters, periocular pain, and progressive blurring of vision in the right eye over 7 days. Visual acuity is 6/24. Slit-lamp examination shows granulomatous anterior uveitis with mutton-fat keratic precipitates and intraocular pressure of 28 mmHg. Dilated fundoscopy reveals dense vitritis, occlusive retinal vasculitis with arteriolar sheathing, and confluent peripheral white necrotic retinal patches spreading circumferentially. Aqueous PCR confirms varicella-zoster virus. The management strategy marked **A** in the diagram is most appropriate for this patient. Which of the following BEST describes the rationale for the antiplatelet component of this regimen?
A. To address the occlusive vasculopathy and reduce optic-nerve ischemia in ARN
B. To suppress viral replication in the retina and vitreous
To reduce intraocular pressure and prevent secondary glaucoma
C.
D. To prevent thromboembolic complications of systemic corticosteroid therapy
Explanation
Why "To address the occlusive vasculopathy and reduce optic-nerve ischemia in ARN" is right
Acute retinal necrosis is characterized by occlusive retinal vasculopathy with prominent arteriolar involvement and sheathing. The management strategy marked A includes oral antiplatelet therapy (aspirin 75–150 mg/day) as an adjunctive measure specifically to counter the vasculitic component and reduce ischemic complications, particularly optic-nerve ischemia. This is a cornerstone of the multimodal approach outlined in the American Uveitis Society criteria and modern AAO Preferred Practice Patterns (AAO PPP Uveitis 2023). The antiplatelet agent works synergistically with systemic corticosteroids (started 24–48 hours after antivirals) to suppress both the inflammatory vasculitis and its ischemic sequelae.
Why each distractor is wrong
To prevent thromboembolic complications of systemic corticosteroid therapy: While corticosteroids can increase thrombotic risk in some contexts, this is not the primary indication for aspirin in ARN. The aspirin is specifically targeted at the viral vasculopathy, not at steroid-induced thromboembolism.
To reduce intraocular pressure and prevent secondary glaucoma: Aspirin has no direct effect on intraocular pressure. IOP elevation in ARN is managed with topical agents (prostaglandin analogues, beta-blockers, carbonic anhydrase inhibitors) and systemic corticosteroids; antiplatelet therapy does not address this.
To suppress viral replication in the retina and vitreous: Antiplatelet agents have no antiviral activity. Viral suppression is achieved by IV aciclovir (or oral valaciclovir) and intravitreal foscarnet; aspirin is purely anti-inflammatory and anti-thrombotic.
High-YieldNEET PG
ARN management is multimodal—antivirals (aciclovir/valaciclovir) kill the virus, corticosteroids suppress inflammation, and aspirin addresses the occlusive vasculopathy; prophylactic laser and vitrectomy prevent/manage retinal detachment.
Holland AUS Criteria, Am J Ophthalmol 1994; AAO Preferred Practice Pattern Uveitis 2023; Schoenberger Ophthalmology 2017
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