Trauma-Associated Glaucomas

Overview of Trauma-Associated Glaucoma

• Trauma-associated glaucoma is a diverse topic encompassing various mechanisms where physical injury leads to an elevation in intraocular pressure ($IOP$).
• Initial Inflammatory Reaction: Trauma can trigger an immediate inflammatory response in the anterior chamber, which may either increase or decrease the $IOP$.
• Lens-Induced Mechanisms: Several trauma-related glaucomas are secondary to lens injury and are categorized under lens-induced glaucoma. Specific conditions mentioned include:
  • Ectopia lentis (lens dislocation).
  • Lens particle glaucoma.
  • Phacotoxic glaucoma.
• Key Primary Topics: The focus of this discussion is on angle recession, hyphema, ghost cell glaucoma, siderosis, and chemical 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 ($CB$), causing a shearing injury through the ciliary body face.
• Pathology:
  • The ciliary body is torn and separated from the wall of the eye.
  • Histopathologically, angle recession is very similar to a cyclodialysis cleft; if a small band of tissue is removed from an image of angle recession, it appears identical to a cleft, though clinical management differs significantly.
• Clinical Significance:
  • Angle recession itself is not the direct cause of the damage to the drainage system; rather, it is a sign of severe blunt trauma in the vicinity of the trabecular meshwork ($TM$).
  • Analogy: Like finding a "hand-grenade crater" in a living room; it provides a clue as to why the television ($TM$ function) isn't working.
• Slit Lamp Findings of Blunt Trauma:
  • Sphincter tears in the iris.
  • Iridodialysis (detachment of the iris from the ciliary body).
  • Traumatic aniridia (near total loss of the iris).
  • Vossius Ring: A "tattoo" or ring of pigment deposited on the anterior capsule of the lens. This occurs when the iris "slaps" back against the lens during the traumatic event.
• Gonioscopic Examination:
  • Ciliary Body Face: Appears wider and usually lighter in color. The light color is due to the shearing away of tissue, leaving very little ciliary body between the observer and the sclera. Occasionally, it may appear dark.
  • Iris Processes: If present, they may be broken. Observing where iris processes disappear helps identify the precise extent of the recession.
  • Scleral Spur: May stand out as a distinct, bright white line due to the stripping away of overlying ciliary body tissue.
  • Old Blood: Remnants of past hyphema may appear as small dots in the inferior angle.
• Clinical Course and Risk Factors:
  • Often the differential diagnosis for unilateral glaucoma, particularly in young men.
  • Glaucoma can develop years after the initial injury; patients require lifelong follow-up.
  • Incidence: Approximately $6\%$ of eyes with $180^{\circ}$ of angle recession will develop glaucoma over a period of $10\,\text{years}$.
  • Fellow Eye Risk: There is an increased risk of developing primary open-angle glaucoma ($POAG$) in the fellow, uninjured eye. This suggests these patients may have a baseline predisposition to glaucoma.
• Management:
  • Treated similarly to $POAG$.
  • Cholinergic Agonists: Drugs like pilocarpine can paradoxically elevate $IOP$ in these cases and are generally avoided.
  • Trabeculoplasty: Generally less effective than in cases of standard $POAG$.
  • Trabeculectomy: Effective, but surgeons must be cautious of loose vitreous or broken zonules behind the iris when performing an iridectomy.

Hyphema-Induced Glaucoma

• Pathophysiology: Bleeding into the anterior chamber ($AC$) leads to $IOP$ elevation via two primary mechanisms:
  1. Obstruction of the trabecular meshwork by blood, plasmon, fibrin, and cellular debris.
  2. Pupillary block: In cases of total hyphema, the blood can mold through the pupil, obstructing the flow of aqueous humor.
• Risk of Glaucoma based on Hyphema Size:
  • $< 50\%$ volume: Small risk.
  • $> 50\%$ volume: Approximately $25\%$ risk.
  • $100\%$ volume (Total Hyphema): Approximately $50/50$ or $50\%$ risk.
  • Eight-Ball Hyphema: A black, deoxygenated hyphema with no circulation; the risk of glaucoma is nearly $100\%$.
• Sickle Cell Disease/Trait:
  • Patients have a much harder time clearing blood from the $AC$ because sickled red cells cannot deform to pass through the $TM$.
  • They are at a significantly higher risk for pressure rise, and their optic nerves are more sensitive to elevated pressure.
• Corneal Blood Staining:
  • Occurs with long-standing, large hyphemas and high $IOP$.
  • Appearance: Perfectly round, orange-brown discoloration that looks almost like a dislocated lens within the cornea, usually with a clear peripheral zone.
  • Exceptions: Children may develop blood staining even with normal pressures because their corneas are relatively more permeable.
  • Resolution: Blood staining clears from the periphery inward with a crisp margin; this process can take up to $14\,\text{months}$.
  • Amblyopia Risk: In children of amblyogenic age, corneal blood staining can cause permanent vision loss if it obscures the visual axis.
• Treatment and Management:
  • Activity and Protection: First $7\,\text{days}$ are critical for preventing re-bleeding. Use an eye shield, elevate the head of the bed to allow blood to settle inferiorly, and ensure "taking it easy" or bed rest.
  • Medications to Avoid: Blood thinners like aspirin.
  • Aminocaproic Acid (Amicar): Can prevent re-bleeding by inhibiting clot contraction, but side effects include nausea and vomiting.
  • Glaucoma Medications: Use aqueous suppressants. Avoid cholinergic agonists (pilocarpine).
  • Sickle Cell Specific Precautions:
    • Avoid oral carbonic anhydrase inhibitors ($CAIs$) due to risks of systemic acidosis and increased sickling.
    • Avoid older adrenergic agonists like epinephrine or dipivefrin due to anterior segment vasoconstriction. Use brimonidine if an adrenergic agonist is required.
• Surgical Intervention:
  • Clot washout is ideally performed around $\text{day } 4$ when the clot begins to lyse.
  • Trabeculectomy (often without antimetabolites) may be preferred over simple washout to provide a larger opening for the clot to exit.
  • Iridectomy during surgery can relieve the pupillary block caused by "dumbbell-shaped" clots.
  • Note: Perform gonioscopy only after several weeks when the risk of re-bleeding has passed.

Ghost Cell Glaucoma

• Etiology: Results from a long-standing ($1-3\,\text{months}$) large vitreous hemorrhage.
• Pathogenesis:
  • Red blood cells in the vitreous degenerate over time, denaturing into "ghost cells."
  • Ghost cells are rigid, inflexible, khaki-colored, and cannot deform to pass through the $TM$ into the Canal of Schlemm.
  • If the anterior hyaloid face is disrupted (via trauma, vitrectomy, or major surgery), these cells migrate into the $AC$ and clog the drainage system.
• Clinical Presentation:
  • Khaki-colored cells in the anterior chamber.
  • Pseudo-hypopyon: Accrual of these cells in the inferior angle.
  • Candy-Striped Sign: A layering effect seen when fresh red blood is mixed with khaki ghost cells.
• Treatment:
  • Pars plana vitrectomy ($PPV$) to remove the source of the cells in the vitreous.
  • Aqueous suppressants to manage $IOP$.

Siderosis and Chalcosis

• 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.
  • Characteristic sign: Rusty color to the trabecular meshwork and heterochromia (the iris may change color as it "rusts").
• Chalcosis: A similar toxic condition caused by a retained intraocular copper foreign body.
• Management: Surgical removal of the foreign body and treatment of the resulting $IOP$ elevation as open-angle glaucoma.

Chemical Burns and Intraocular Pressure

• Alkali Burns: Generally much worse than acid burns. Anhydrous ammonia (common in farming states like Iowa) is a frequent cause of severe alkali injury.
• Phases of $IOP$ Elevation:
  1. Immediate Phase: Sudden, marked rise in $IOP$ due to immediate shrinkage of the sclera, which decreases intraocular volume.
  2. Late Phase: Elevation due to chronic inflammation and the destruction of episcleral outflow channels.
• Treatment Challenges:
  • Traditional medications are often ineffective if the episcleral venous system and outflow channels are lost.
  • Surgical management is difficult due to extensive conjunctival and tissue damage.
  • Cyclophotocoagulation ($CPC$): Often the only viable surgical option for controlling pressure in these severely damaged eyes.