A 62-year-old woman with a 15-year history of rheumatoid arthritis presents with gradual onset of pain, redness, and blurred vision in both eyes over 3 months. On slit-lamp examination, she has fine keratic precipitates, anterior chamber cells (2+ in both eyes), and posterior synechiae. Gonioscopy shows angle closure with iris-angle apposition and neovascularization of the angle. Intraocular pressure is 38 mmHg bilaterally. B-scan ultrasonography reveals no retinal detachment. What is the most likely mechanism of glaucoma in this patient?

Explanation

## Neovascular Glaucoma (NVG) in the Setting of Chronic Uveitis **Key Point:** When gonioscopy explicitly demonstrates **neovascularization of the angle with iris-angle apposition**, the mechanism of angle closure is neovascular glaucoma — fibrovascular membrane contraction closes the angle, regardless of coexisting uveitic features. ### Pathophysiology of Neovascular Angle Closure Neovascular glaucoma (NVG) follows a well-defined sequence: 1. **Ischemic or inflammatory stimulus** → release of VEGF and other angiogenic factors 2. **Rubeosis iridis** → new vessels appear on iris surface and angle 3. **Fibrovascular membrane formation** → membrane bridges the angle 4. **Membrane contraction** → pulls peripheral iris over trabecular meshwork 5. **Synechial angle closure** → progressive, irreversible obstruction of outflow 6. **IOP elevation** → markedly elevated (often >35 mmHg), refractory ### Why Option A Is Correct in This Stem The gonioscopy finding is the decisive clue: **neovascularization of the angle with iris-angle apposition**. This is the hallmark of NVG. The fibrovascular membrane — not iris bombé from posterior synechiae — is the structural mechanism closing the angle. Chronic uveitis (including that associated with rheumatoid arthritis) can drive intraocular ischemia and VEGF release, secondarily producing angle neovascularization. The coexisting keratic precipitates and posterior synechiae reflect the underlying uveitic process but are not the proximate cause of angle closure in this case. ### Distinguishing Features | Feature | Neovascular Angle Closure (NVG) | Uveitic Iris Bombé | Open-Angle Uveitic | Phacomorphic | |---------|--------------------------------|-------------------|-------------------|--------------| | **Gonioscopy** | NV + membrane, closed | Closed by iris | Open | Open | | **Neovascularization** | **Prominent, defining** | Absent/minimal | Absent | Absent | | **Posterior synechiae** | May coexist | Prominent, causative | May be present | Absent | | **Keratic precipitates** | May coexist | Present | Present | Absent | | **IOP** | Very high, refractory | Elevated | Mildly elevated | Elevated | | **Lens** | Normal | Normal | Normal | Intumescent | ### Why Option C Is Incorrect Here Iris bombé from posterior synechiae (Option C) causes angle closure by aqueous accumulating behind the iris, bowing it forward. However, this mechanism does **not** produce neovascularization of the angle. The stem explicitly states gonioscopy shows **neovascularization of the angle** — this finding cannot be explained by iris bombé alone and mandates the diagnosis of NVG as the primary mechanism. **Clinical Pearl (Harrison's / Kanski):** In any patient with angle closure and gonioscopic neovascularization, NVG must be diagnosed as the mechanism. Treatment targets both the underlying cause (anti-VEGF, laser photocoagulation if ischemia-driven) and IOP control. Coexisting uveitis requires concurrent anti-inflammatory management. **High-Yield:** Gonioscopic neovascularization + angle closure + high IOP = Neovascular Glaucoma. This triad overrides other coexisting findings when determining the mechanism of glaucoma. ### Why This Is Secondary Glaucoma NVG here is secondary to chronic uveitis-driven intraocular ischemia/VEGF release. The rheumatoid uveitis is the inciting event; the neovascular membrane formation and angle closure are the consequence.