## Clinical Diagnosis **Key Point:** This patient has **wet (exudative) age-related macular degeneration (AMD)** with active choroidal neovascularization, evidenced by CNV, subretinal hemorrhage, lipid exudates, and metamorphopsia. ## Management of Wet AMD **High-Yield:** Wet AMD is a sight-threatening emergency requiring immediate anti-VEGF therapy. The standard of care is intravitreal anti-VEGF agents (bevacizumab, ranibizumab, or aflibercept) administered as monthly injections, with response assessed by optical coherence tomography (OCT). ### Why Bevacizumab is Correct 1. **Mechanism:** Bevacizumab is a monoclonal antibody against vascular endothelial growth factor (VEGF), which drives CNV formation and leakage in wet AMD. 2. **Efficacy:** Anti-VEGF therapy halts CNV progression, reduces macular edema, and stabilizes or improves vision in 90% of patients when initiated early. 3. **Timing:** Early intervention (within weeks of CNV detection) is critical to prevent irreversible photoreceptor loss and preserve central vision. **Clinical Pearl:** The presence of subretinal hemorrhage and exudates indicates active, progressive disease requiring urgent intervention—not observation. ## Why Other Options Are Suboptimal | Option | Why Incorrect | |--------|---------------| | **Oral zinc + antioxidants** | Appropriate for dry AMD or early-stage disease; ineffective for active CNV. These are preventive agents, not treatment for wet AMD. | | **Laser photocoagulation** | Historically used but now superseded by anti-VEGF therapy. Laser causes collateral photoreceptor damage and is reserved only for extrafoveal CNV (rare). | | **Observation** | Contraindicated in wet AMD. Active CNV will progress, causing rapid vision loss and irreversible macular scarring within weeks to months. | **Mnemonic:** **VEGF-driven wet AMD = Anti-VEGF therapy.** Bevacizumab, ranibizumab, aflibercept are first-line; laser and observation are obsolete for active CNV. [cite:Parson's Diseases of the Eye 22e Ch 9] 
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