Trauma-Associated Glaucomas

Overview of Trauma-Associated Glaucoma

• Trauma-associated glaucoma encompasses a diverse range of mechanisms following injury.
• Trauma can induce an inflammatory reaction in the anterior chamber, leading to either an increase or a decrease in intraocular pressure (IOP).
• Multiple processes can cause IOP elevation, including lens-related injuries (covered separately in lens-induced glaucoma lectures):
  • Ectopia lentis.
  • Lens particle glaucoma.
  • Phacotoxic glaucoma.
• Primary topics of focus for this discussion: Angle recession, hyphema, ghost cell glaucoma, siderosis, and chemical burns.

Angle Recession Glaucoma

• Pathophysiology and Mechanism:

  • Occurs in the setting of blunt trauma.
  • Trauma is transmitted into the face of the ciliary body, causing a shearing injury through the ciliary body face.
  • The injury results in the ciliary body being torn and separated from the wall of the eye.
  • Histopathology reveals a tear in the ciliary body tissue; if a specific thin band of tissue is removed, the appearance is virtually identical to a cyclodialysis cleft.
  • Clinical importance: Angle recession is a marker or sign of severe blunt trauma near the trabecular meshwork (TM). The recession itself does not cause the pressure elevation; rather, it indicates the TM was subjected to significant trauma.
  • Analogy: Finding a "hand-grenade crater" in the living room floor is a clue as to why the television set is not working.

• Clinical Signs of Blunt Trauma (Slit Lamp Exam):

  • Sphincter tears in the iris.
  • Iridodialysis.
  • Traumatic aniridia (near-total loss of the iris).
  • Vossius ring: A ring of pigment deposited on the anterior capsule of the lens, acting as a "tattoo" from the iris hitting the lens during the traumatic event.

• Gonioscopic Findings in a Recessed Angle:

  • Ciliary body face appears abnormally wide.
  • Color: Typically lighter because the shearing of tissue leaves very little ciliary body between the examiner and the sclera. On occasion, it may appear dark.
  • Iris processes: If present, they may be broken or absent in the recessed area compared to normal areas.
  • Scleral spur: Often stands out as a distinct, bright white line due to the stripping away of overlying ciliary body tissue.
  • Comparison: It is essential to compare the affected eye to the fellow eye. Highly myopic patients may naturally have wide ciliary body faces.
  • Tangential tears: These may be visible in the ciliary body face, though they are not common.

• Epidemiology and Clinical Management:

  • Often presents as unilateral glaucoma, particularly in young men.
  • Development can be delayed by years or decades.
  • Risk: Approximately $6\%$ of eyes with $180^{\circ}$ of angle recession will develop glaucoma over a 10-year period (slightly under $10\%$ at 10 years).
  • Given the young age of typical patients, this is a significant long-term risk.
  • Fellow eye risk: There is a known increased risk of developing Primary Open-Angle Glaucoma (POAG) in the fellow eye, suggesting these patients may be genetically predisposed.

• Treatment:

  • Managed similarly to POAG.
  • Cholinergic Agonists (Pilocarpine): Used less frequently now; may cause a paradoxical elevation in pressure in recessed angles.
  • Trabeculoplasty: Less effective than in POAG.
  • Trabeculectomy: Generally effective, but caution is required regarding loose vitreous or broken zonules behind the iris if an iridectomy is performed.

Hyphema and Intraocular Pressure

• Definition and Composition:

  • Bleeding into the anterior chamber (AC).
  • The mixture contains blood, plasmin, fibrin, and debris, all of which can obstruct the trabecular meshwork.

• Mechanisms of IOP Elevation:

  • Direct obstruction of the TM by blood products.
  • Pupillary Block: In cases of total hyphema, the blood can mold to the pupil, causing block.

• Risk of Glaucoma Based on Hyphema Size:

  • Small hyphema ($<50\%$ volume): Low risk.
  • Large hyphema ($>50\%$ volume): Approximately $25\%$ risk.
  • Total hyphema ($100\%$ volume): Approximately $50\%$ risk.
  • 8-Ball Hyphema: A black, total hyphema indicating zero circulation within the blood. The risk of glaucoma is $100\%$.

• Sickle Cell Disease and Trait:

  • Patients with sickle cell hemoglobinopathies have a harder time clearing blood from the AC.
  • Sickle cells do not deform and cannot pass through the TM easily.
  • These patients are at higher risk for sudden pressure rises and their optic nerves are more sensitive to elevated pressure.

• Corneal Blood Staining:

  • Occurs in long-standing, large hyphemas paired with high IOP.
  • Appearance: Perfectly round, yellowish-brown opacity in the cornea that can mimic a dislocated lens.
  • Children are higher risk because they have more permeable corneas, allowing staining even without markedly high pressure.
  • Clearance: Staining clears very slowly from the periphery inward; can take $12$ to $14$ months to resolve.
  • Amblyopia risk: A primary concern in children if the visual axis is obscured during amblyogenic years.

• Treatment of Hyphema:

  • Primary Goals: Control pressure and prevent re-bleeding.
  • Timing: The first $7$ days are most critical for re-bleeding risk.
  • Supportive Care: Avoid blood thinners (aspirin), use an eye shield, and elevate the head of the bed to allow blood to settle inferiorly. Rest is recommended, but strict bed rest may not be necessary for responsible patients.
  • Aminocaproic acid (Amicar): Can prevent re-bleeding by preventing clot contraction, but side effects include nausea and vomiting.
  • Medications:
    • Conflicting reports on the benefit of corticosteroids and cycloplegics (atropine).
    • Use aqueous suppressants.
    • Avoid cholinergic agonists (pilocarpine).
  • Sickle Cell Precautions:
    • Avoid oral Carbonic Anhydrase Inhibitors (CAIs) as they can cause acidosis and encourage sickling.
    • Avoid epinephrine and dipivefrin (generic adrenergic agonists) as they cause anterior segment vasoconstriction.
    • Bromonidine is the preferred adrenergic agonist if needed.

• Surgical Intervention (Clot Washout):

  • Ideal timing is around day $4$ when the clot begins to lyse.
  • Trabeculectomy is often preferred over simple washout as it provides a larger opening for the clot and the iridectomy relieves any pupillary block element.
  • Antimetabolites are generally not used in these cases.
  • Avoid gonioscopy for several weeks until the risk of re-bleeding has subsided.

Ghost Cell Glaucoma

• Definition: A secondary glaucoma resulting from a long-standing, large vitreous hemorrhage.
• Timeline: Red blood cells degenerate over $1$ to $3$ months into "ghost cells."
• Pathology: The cells denature and become rigid, inflexible, khaki-colored spheres. Unlike normal red blood cells, they cannot deform to pass through the TM into Schlemm's canal.
• Entry into Anterior Chamber: Ghost cells enter the AC if the anterior hyaloid is disrupted (via trauma, vitrectomy, or major surgery).
• Gonioscopic/Slit Lamp Signs:
  • Tiny, khaki-colored cells in the AC.
  • Pseudo-hypopyon: Khaki-colored settling of cells.
  • Candy-Striped Sign: Layers of fresh red blood mixed with khaki ghost cells.
• Treatment:
  • Pars plana vitrectomy to remove the source of cells.
  • Aqueous suppressants.

Siderosis and Chalkosis

• Siderosis:
  • Caused by a retained intraocular iron foreign body.
  • Iron is toxic to the photoreceptors, the lens (causing a "rusty cataract"), and the endothelium of the trabecular meshwork.
  • Slit lamp signs: Heterochromia (rusting of the iris) and a rusty-colored TM.
  • Treatment: Removal of the foreign body and management of IOP like POAG.
• Chalkosis:
  • A similar condition caused by retained intraocular copper.

Chemical Burns

• Nature of Injury: Alkali burns are significantly more destructive than acid burns (e.g., anhydrous ammonia used in farming).
• Phases of Pressure Elevation:
  • Immediate Phase: Massive shrinkage of the sclera, which decreases intraocular volume and causes a sudden, dramatic rise in IOP.
  • Late Phase: Inflammation and scarring lead to the loss of episcleral outflow channels.
• Treatment Challenges:
  • Standard medications are often ineffective because there is no functional aqueous outflow system.
  • Surgery is extremely difficult if the conjunctiva is severely damaged.
  • Cyclophotocoagulation (CPC): Often the only viable long-term surgical option for controlling pressure in these eyes.