Trauma-Associated Glaucoma

Overview of Trauma-Associated Glaucomas

• General Pathophysiology: Trauma is a diverse topic in ophthalmology. It can stimulate an inflammatory reaction in the anterior chamber, which may lead to either an increase or a decrease in intraocular pressure ($IOP$).
• Relationship to Lens-Induced Glaucomas: Several trauma-related processes involve lens injury, such as ectopia lentis, lens particle glaucoma, or phacotoxic glaucoma. However, these are strictly categorized under lens-induced glaucoma lectures.
• Primary Focus Areas:
  • Angle recession.
  • Hyphema.
  • Ghost cell glaucoma.
  • Siderosis.
  • Burns.

Angle Recession Glaucoma

• Mechanism of Injury: Occurs in the setting of blunt trauma. The traumatic force is transmitted into the face of the ciliary body, creating a shearing injury. This results in the ciliary body face tearing and separating from the wall of the eye.
• Histopathology: Histopathologically, an angle recession is nearly identical to a cyclodialysis cleft. If the band of tissue connecting the ciliary body to the sclera were removed, it would be a cleft. However, while similar histologically, they are managed very differently clinically.
• Clinical Significance: Angle recession is a sign of severe blunt trauma in the vicinity of the trabecular meshwork ($TM$).
  • Metaphor/Analogy: The speaker compares it to walking into a living room with a broken television: seeing a "hand-grenade crater" in the floor in front of it is a clue as to why the TV isn't working. The recession itself isn't the damage causing the glaucoma; it is an indicator that the nearby $TM$ has suffered significant traumatic impact.
• Associated Signs of Blunt Trauma (Slit Lamp Exam):
  • Sphincter Tears: Visible in the iris.
  • Iridodialysis: Separation of the iris from the ciliary body.
  • Traumatic Aniridia: In extreme cases, near-total loss of the iris.
  • Vossius Ring: A ring of pigment deposited on the anterior lens capsule. This occurs when the iris "slaps back" against the lens during trauma, leaving a pigment "tattoo."
• Gonioscopy Findings in Angle Recession:
  • Ciliary Body Face: Appears widened and is typically lighter in color because the shearing has left very little tissue between the examiner and the sclera. (Note: Occasionally, it may appear dark).
  • Iris Processes: If present, they may be broken. This can create a distinct boundary where recessed angle meets non-recessed angle.
  • Scleral Spur: May stand out as a very distinct, bright white line due to the stripping away of ciliary body tissue.
  • Old Blood: May present as small dots or remnants of a previous hyphema in the inferior angle.
• Epidemiology and Risk:
  • Typical Patient: Often young men (unilateral glaucoma differential diagnosis).
  • Latency: Glaucoma can develop years after the initial injury.
  • Statistics: Approximately $6\%$ of eyes with $180^{\circ}$ of angle recession will develop glaucoma within $10$ years.
  • Fellow Eye Risk: There is an increased risk of developing Primary Open-Angle Glaucoma ($POAG$) in the fellow, non-traumatized eye. This suggests the patient may have been genetically or structurally predisposed to glaucoma.
• Management:
  • Standard Treatment: Generally treated like $POAG$.
  • Cholinergic Agonists (e.g., Pilocarpine): Should be used with caution as they can cause a paradoxical elevation in $IOP$.
  • Trabeculoplasty: Generally less effective than in $POAG$ cases.
  • Trabeculectomy: Effective, but surgeons must be wary of loose vitreous or broken zonules behind the iris if an iridectomy is performed.

Hyphema and Pressure Elevation

• Definition: Bleeding into the anterior chamber.
• Mechanisms of Intraocular Pressure ($IOP$) Elevation:
  1. Obstruction: Blood, plasma, fibrin, and cellular debris can physically clog the trabecular meshwork.
  2. Pupillary Block: In cases of total hyphema, the blood can "mold" through the pupil, blocking flow and leading to pupillary block glaucoma.
• Risk of Glaucoma based on Hyphema Size:
  • < 50% Hyphema: Low risk of pressure elevation.
  • > 50% Hyphema: Approximately a $25\%$ risk.
  • 100% (Total) Hyphema: Approximately a $50\%$ risk.
  • Eight-Ball Hyphema: A black, deoxygenated clot indicating no circulation. The risk of glaucoma is $100\%$.
• Sickle Cell Disease/Trait Considerations:
  • Sickle cells do not deform well enough to pass through the $TM$ pores, making it much harder to clear blood.
  • These patients are at a higher risk of pressure spikes, and their optic nerves are more sensitive to high pressure.
• Corneal Blood Staining:
  • Occurs with long-standing, large hyphemas and high pressure ($IOP$).
  • Appearance: Looks like a dislocated lens within the cornea; it is usually perfectly round with a clear peripheral zone.
  • Vulnerability: Children are more susceptible due to higher corneal permeability and can develop staining even without markedly high pressure.
  • Duration: Can take a long time to clear (e.g., up to $14$ months). It clears from the periphery inward.
  • Pediatric Risk: Risk of amblyopia if the blood staining occurs during amblyogenic ages.
• Management of Hyphema:
  • Acute Phase: The first $7$ days are critical for preventing rebleeding.
  • General Measures: Eye shield for protection, elevating the head of the bed to allow blood to settle inferiorly, and avoidance of blood thinners (e.g., aspirin).
  • Medications:
    • Aminocaproic Acid (Amicar): Prevents clot contraction to reduce rebleed risk, but causes significant side effects like nausea and vomiting.
    • Standard Glaucoma Meds: Aqueous suppressants.
    • Avoid: Cholinergic agonists (pilocarpine).
    • Sickle Cell Warnings: Avoid oral Carbonic Anhydrase Inhibitors ($CAIs$) due to risks of systemic acidosis and sickling. Avoid adrenergic agonists like epinephrine/dipivefrin (no longer commonly used) due to vasoconstriction; use brimonidine instead.
  • Surgical Intervention:
    • The ideal time for clot washout is around day $4$ when the clot begins to lyse.
    • Speaker's Preference: Trabeculectomy without antimetabolites. This allows a larger opening to flush the "dumbbell-shaped" clot and includes an iridectomy to relieve pupillary block.
    • Note: Do not perform gonioscopy for several weeks until the risk of rebleeding has passed.

Ghost Cell Glaucoma

• Definition: A secondary open-angle glaucoma resulting from long-standing, large vitreous hemorrhage.
• Pathophysiology:
  • Timeline: Red cells in the vitreous degenerate and denature over $1$ to $3$ months, turning into "ghost cells."
  • Entry: If the anterior hyaloid is disrupted (due to trauma, vitrectomy, or major surgery), these cells enter the anterior chamber.
  • Obstruction: Ghost cells are rigid and inflexible; unlike healthy red blood cells, they cannot deform to pass through the trabecular meshwork and Schlemm’s canal, leading to obstruction.
• Clinical Presentation:
  • Color: Khaki-colored cells in the anterior chamber.
  • Pseudo-hypopyon: A collection of these khaki cells settling.
  • Candy-Striped Sign: Bands of fresh red blood mixed with khaki-colored ghost cells.
• Treatment:
  • Often requires a pars plana vitrectomy ($PPV$) to remove the source of the cells in the vitreous.
  • Standard aqueous suppressants are used for pressure management.

Siderosis and Chalkosis

• Siderosis: Caused by a retained intraocular iron foreign body.
  • Toxicity: Iron is toxic to the photoreceptors, the lens (causing a "rusty cataract"), and the endothelium of the trabecular meshwork.
  • Signs: Heterochromia (rusting iris), and a "rusty" appearance of the angle/TM.
• Chalkosis: A similar condition caused by a retained copper foreign body.
• Treatment: Surgical removal of the foreign body and management of pressure as one would for open-angle glaucoma.

Chemical and Thermal Burns

• Chemical Burns: Alkali burns are significantly more destructive than acid burns (e.g., anhydrous ammonia injuries in farming).
• Two Phases of Pressure Elevation:
  1. Immediate Phase: Shrunken sclera decreases intraocular volume, causing a sudden, marked rise in $IOP$.
  2. Late Phase: Inflammation and loss of episcleral outflow channels.
• Management Challenges:
  • Standard medications are often ineffective because there is no remaining aqueous outflow functionality through the episcleral venous system.
  • If the conjunctiva is too damaged, standard filtration surgery is impossible.
  • Surgical Option: Often, the only viable option is Cyclophotocoagulation ($CPC$) to reduce aqueous production at the source.