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Secondary Angle-Closure Glaucomas

Secondary Angle-Closure Glaucomas

Secondary Angle-Closure Glaucomas

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Secondary Angle-Closure Glaucomas - Angle Antagonists

  • Definition: Trabecular meshwork (TM) obstruction; angle directly compromised by identifiable factors.
  • Mechanisms:
    • Anterior Pulling (Membranes):
      • Neovascular Glaucoma (NVG): Fibrovascular membrane (FVM) contracts, zippering angle. Causes: PDR, CRVO, OIS.
      • ICE Syndromes: Corneal endothelium membrane over angle.
      • Peripheral Anterior Synechiae (PAS): Chronic uveitis, post-op.
    • Posterior Pushing (Direct Obstruction):
      • Ciliary Body Swelling/Rotation: Topiramate, uveal effusion.
      • Phacomorphic Glaucoma: Large lens crowds angle.
      • Tumors/Cysts: Iris/ciliary body masses obstruct.

⭐ NVG: Rubeosis iridis precedes angle neovascularization. 90-day glaucoma classic post-CRVO.

Secondary Angle-Closure Glaucomas - Behind The Scenes Push

  • Posterior segment pathology or lens changes displace iris-lens diaphragm anteriorly, narrowing/closing the angle.
  • Key Mechanisms & Causes (Posterior Push):
    • Lens-induced (Phacomorphic):
      • Intumescent cataract (swollen lens).
      • Subluxated/dislocated lens.
    • Ciliary Body Swelling/Anterior Rotation:
      • Uveitis (e.g., Vogt-Koyanagi-Harada, posterior scleritis).
      • Drugs (e.g., topiramate, sulfonamides 📌 SulfaTop).
      • Choroidal effusion/hemorrhage.
      • Tumors (ciliary body/choroidal).
    • Aqueous Misdirection (Malignant Glaucoma):
      • Posterior aqueous diversion; often post-op.
    • Post-Retinal Surgery:
      • Scleral buckle, intravitreal gas/oil.
    • Nanophthalmos: Anatomical predisposition. UBM of posterior pushing mechanism in angle closure

⭐ Aqueous misdirection classically presents with a uniformly shallow anterior chamber and high IOP, often post-trabeculectomy.

Secondary Angle-Closure Glaucomas - Frontal Assault & Blockade

  • Anterior Pulling (No Pupillary Block): Iris pulled into TM, closing angle.
    • Neovascular Glaucoma (NVG): Membrane contraction (rubeosis iridis).
    • ICE Syndrome: Endothelial membrane contracts iris.
    • Epithelial/Fibrous downgrowth: Post-trauma/surgery.
    • PAS: Post-inflammation/trauma.
  • Pupillary Block: Aqueous flow obstructed at pupil.
    • Phacomorphic: Swollen lens (intumescent cataract).
    • Ectopia Lentis: Subluxated/dislocated lens.
    • Aphakic/Pseudophakic block: Vitreous/IOL.
    • Seclusio Pupillae: 360° posterior synechiae (uveitis).
    • Silicone oil. Pupillary Block in Glaucoma

⭐ NVG: rubeosis iridis & angle neovessels are key; linked to retinal ischemia (PDR, CRVO).

Secondary Angle-Closure Glaucomas - Spotting The Closure

  • Clinical Clues:
    • Symptoms: Acute pain, blurred vision, halos, N/V (if IOP ↑↑).
    • Signs: Corneal edema, shallow AC, mid-dilated pupil, ↑IOP.
  • Diagnostic Steps:
    • Gonioscopy: Essential to see Peripheral Anterior Synechiae (PAS) & angle status.
      • Indentation gonioscopy: Differentiates appositional vs. synechial closure.
    • Ultrasound Biomicroscopy (UBM): Visualizes angle structures if cornea hazy; ciliary body assessment.
    • Slit-lamp exam: Detailed anterior segment evaluation.

Gonioscopy of peripheral anterior synechiae

⭐ Gonioscopy is indispensable for diagnosing angle closure, revealing Peripheral Anterior Synechiae (PAS) which confirm synechial closure.

Secondary Angle-Closure Glaucomas - Unblocking The Path

  • Causes: Uveitis, neovascular (NVG), lens-induced (phacomorphic, phacolytic), trauma, tumors, drugs (e.g., topiramate).
  • Mechanisms:
    • Anterior pulling (e.g., peripheral anterior synechiae (PAS), membranes).
    • Posterior pushing (e.g., swollen lens, ciliary body edema/rotation).
  • Treatment Focus:
    • Crucially, treat the primary underlying pathology first.
    • Aggressively ↓IOP: Medical (aqueous suppressants; ⚠️ avoid miotics in pupillary block/phacomorphic), Laser (LPI if pupillary block present), Surgery (filtration, GDDs).

⭐ Neovascular glaucoma (NVG), often due to Proliferative Diabetic Retinopathy (PDR) or Central Retinal Vein Occlusion (CRVO), is a common, aggressive SACG.

High‑Yield Points - ⚡ Biggest Takeaways

  • Neovascular glaucoma (NVG): severe SACG, often from PDR/CRVO.
  • Uveitic glaucoma: inflammation causes synechiae (PAS/PS) or pupillary block.
  • Lens-induced: Phacomorphic (swollen lens), phacolytic (leaking proteins), lens subluxation/dislocation.
  • Aqueous misdirection (malignant glaucoma): posterior aqueous diversion, shallow AC.
  • ICE syndromes: progressive angle closure by abnormal corneal endothelium.
  • Epithelial/Fibrous downgrowth: post-surgery/trauma, obstructs angle.
  • Management: Treat underlying cause and aggressively lower IOP.

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