Secondary Open-Angle Glaucomas

SOAGs Intro - Not Just POAG!

• Definition: SOAGs are glaucomas with ↑IOP from an identifiable secondary cause, despite an open, normal-appearing anterior chamber angle.
• SOAG vs. POAG:
  • POAG: Idiopathic trabecular meshwork (TM) dysfunction.
  • SOAG: Known cause for TM obstruction.
• Mechanisms of TM Obstruction:
  • Pre-trabecular: Membrane/tissue over TM (e.g., neovascularization, ICE syndrome).
  • Trabecular: Clogging within the TM itself.
    • Cells: RBCs (ghost cell glaucoma), inflammatory cells (uveitic glaucoma).
    • Material: Pigment (pigment dispersion), pseudoexfoliation (PXF) material, lens proteins (phacolytic).
    • Steroid-induced: Altered TM matrix/cellularity.

⭐ Exam Favourite: Steroid-induced glaucoma is a classic SOAG; risk varies with steroid potency, duration, route of administration (topical > periocular > systemic > inhaled), and individual susceptibility (e.g., POAG patients, diabetics).

Exfoliation & Pigmentary - Debris Drama Duo

• Common Theme: Trabecular meshwork (TM) obstruction by particulate debris leading to ↑IOP.

• Exfoliation Syndrome (XFS) & Glaucoma (PXG):

  • Debris: White "dandruff-like" pseudoexfoliative material (PXM) from abnormal basement membrane.
  • Key Signs:
    • PXM on pupil margin, anterior lens capsule ("bull's-eye" sign).
    • Sampaolesi's line.
    • Moth-eaten iris transillumination.
    • Zonular weakness (↑cataract sx risk).
  • Course: Often unilateral, aggressive.

• Pigment Dispersion Syndrome (PDS) & Glaucoma (PG):

  • Debris: Iris pigment granules from posterior iris epithelium rubbing against lens zonules.
  • Classic Triad:
    • Krukenberg spindle (vertical pigment on corneal endothelium).
    • Radial, mid-peripheral iris transillumination defects.
    • Dense TM pigmentation (often 360°).
  • Profile: Younger, myopic males.
  • Course: Bilateral; exercise/mydriasis → pigment showers, IOP spikes.

⭐ Pigmentary glaucoma often shows greater IOP fluctuations than POAG, with spikes after exercise or mydriasis, and may "burn out" in later life as pigment liberation decreases.

Steroid & Uveitic - Pressure & Passion Plays

• Steroid-Induced Glaucoma:
  • Patho: ↑Aqueous outflow resistance (Trabecular Meshwork - TM changes: ↑GAGs, ↓PGEs, altered ECM).
  • Risk factors: Route (topical > periocular > systemic), potency, duration, family Hx of POAG.
  • "Steroid responders": Genetically predisposed individuals.
  • Rx: Discontinue/taper steroid. IOP-lowering drugs (avoid Prostaglandin Analogs initially). Surgery if refractory.
• Uveitic Glaucoma (Open Angle):
  • Mechanism: TM inflammation/blockage by cells, fibrin, debris. Can be steroid-induced if steroids used for uveitis.
  • Fuchs' Heterochromic Iridocyclitis (FHI): Chronic, low-grade inflammation; stellate keratic precipitates (KPs), iris heterochromia, cataract, glaucoma (often late, difficult to control).
  • Posner-Schlossman Syndrome (PSS) / Glaucomatocyclitic Crisis: Recurrent, unilateral, acute ↑IOP; mild anterior chamber (AC) reaction, few KPs, open angle. 📌 "PSS - Painful, Seeing, Single eye".
  • Rx: Control inflammation (topical steroids, mydriatics). IOP-lowering drugs (aqueous suppressants preferred; miotics contraindicated in active inflammation).

⭐ In Posner-Schlossman Syndrome, IOP can rise very high (e.g., 40-60 mmHg) with minimal cells in AC and an open angle on gonioscopy.

Lens & Trauma - Crystal Clear Damage

• Lens-Induced Glaucomas (SOAG):
  • Phacolytic Glaucoma:
    • Hypermature cataract leaks lens proteins.
    • Macrophages engulf proteins, obstruct Trabecular Meshwork (TM).
    • Acute: ↑IOP, pain, cells/flare.
    • Tx: Medical, then cataract extraction.
  • Lens Particle Glaucoma:
    • Lens matter (post-trauma/surgery) obstructs TM.
    • Tx: Medical, surgical removal.
• Traumatic Glaucomas (SOAG):
  • Angle Recession Glaucoma:
    • Blunt trauma → ciliary body tear, TM damage/scarring.
    • Develops years later; gonioscopy: widened ciliary body band.
    • Risk: ~10% if >180° recession.
    • Tx: Medical, trabeculectomy.
  • Ghost Cell Glaucoma: 📌 "Old ghosts (RBCs) haunt the TM"
    • Degenerated RBCs (ghost cells) from vitreous hemorrhage block TM.
    • Khaki-colored cells in AC.
    • Tx: Medical, AC washout.

    ⭐ Ghost cell glaucoma typically occurs 2-3 weeks after vitreous hemorrhage, presenting with elevated IOP and khaki-colored cells.

High‑Yield Points - ⚡ Biggest Takeaways

• Pseudoexfoliation syndrome: Most common identifiable cause; white flaky deposits on anterior lens capsule, angle.
• Pigment dispersion syndrome: Features Krukenberg spindle, iris transillumination defects; common in young myopes.
• Lens-induced glaucoma: Includes phacolytic (leaked proteins from hypermature cataract) and lens particle types.
• Steroid-induced glaucoma: Results from prolonged steroid use, impairing trabecular meshwork outflow.
• Uveitic glaucoma: Arises from TM blockage by inflammatory cells/debris or trabeculitis.
• Traumatic glaucoma: Often due to angle recession or ghost cells post-vitreous hemorrhage.
• Glaucomatocyclitic crisis (Posner-Schlossman): Recurrent, unilateral ↑IOP with mild anterior uveitis; open angles maintained during attacks.