How to deal with Neovascular glaucoma cases

How to deal with Neovascular glaucoma cases

1. Diagnosis & Management of Neovascular Glaucoma

2. History First described in association with iris rubeosis following CRVO (1906) “NVG” defined as elevated IOP in context of new blood vessel and connective tissue growth (1963) Also known as: Hemorrhagic glaucoma Congestive glaucoma Thrombotic glaucoma Rubeotic glaucoma

3. ● Normal eye : balance between pro- and anti-angiogenic growth factors Pro-angiogenic growth factors: Vascular endothelial growth factor (VEGF) & Angiopoietin-2 (Ang-2) Anti-angiogenic growth factors: Pigment epithelial derived growth factor (PDEF) ●Normal Blood vessel anatomy: non-fenestrated endothelial cells with tight intercellular junctions

4. Pathophysiology Ischemic eye : pro-angiogenic >> anti-angiogenic Retina ischemia/hypoxia → release of VEGF + Angiopoietin-2 → activation + proliferation + migration of endothelial cells → angiogenesis with fibrovascular membrane formation Neovascular vessels: Little/absent muscle layer and little adventitial structures → prone to leakage/breakage

5. Etiologies Diabetic Retinopathy Central Retinal Vein Occlusion Carotid Occlusive Disease : Ocular Ischemic Syndrome

6. Clinical Presentation Neovascularization of anterior segment: Iris Typically along pupillary border Irregular non-radial pattern (vs. normal iris vessels) c an bleed → hyphema Angle Reddish hue to SS (instead of white) Can lead to eventual synechial closure d/t leakage/scarring

7. Clinical Presentation Elevated IOP Open-angle Mechanical blockage of trabecular meshwork Angiogenic vessels, RBC’s, hemosiderin-laden macrophages, etc. Closed-angle Synechial closure

8. Diagnostic work-up Find the WHY to patient’s neovascularization History of DM? If yes, how is patient’s BG/BP control? Diabetes Control Complications Trial (DCCT): standard patients at 3x risk for developing NVD over 9 years vs. intensively treated group (24% vs. 8%) History of CRVO? If so, when was onset? 90-day glaucoma If no history or evidence of DM or CRVO → rule out ocular ischemia Obtain carotid ultrasound Check Blood glucose, A1c, BP

9. VF OCT: RNFL Macular edema associated with diabetic retinopathy or CRVO Pachymetry Fluorescein angiography: Look for hypoperfusion and/or neovascularization (may be occult) Diagnostic work-up

10. Management Lower IOP: Medications Surgery Reduce hypoxic stimulus: PRP Treat Macular edema (if present): anti-VEGF injections

11. Aqueous suppressants = theoretically more useful given compromised trabecular meshwork Typically I put this patients on max tolerated topicals May require systemic CAI’s for immediate IOP lowering (Acetazolamide) Severe cases often refractory to medical therapy Medication management

12. Surgical Management Glaucoma drainage device (GDD) > Trabeculectomy Risk of scarring of trabeculectomy flap from NV Valved GDD (Ahmed) > non-valved GDD ( Baerveldt ) Immediate IOP lowering Less risk of hypotony Cyclophotocoagulation (CPC) in refractory cases: I typically reserve this for patient’s have AGV already. Micropulse also option - less chance of hypotony than CPC

13. Which of the following is NOT considered a COMMON cause of Neovascular glaucoma? A.Ocular ischemic syndrome B.Diabetic retinopathy C.Central retinal artery occlusion D.Central retinal vein occlusion

14. Which of the following is NOT a clinical sign of neovascular glaucoma? A.Iris rubeosis B.Iris atrophy C.Angle vessels D.Optic Disc cupping

15. Which of the following is the optimal surgical intervention for neovascular glaucoma? A.Cataract surgery with goniotomy B.Trabeculectomy with Mitomycin C C.Non -valved glaucoma drainage device (i.e. Baerveldt ) D.Valved glaucoma drainage device (i.e. Ahmed)

16. Lecture Takeaways