Traumatic Glaucoma

Traumatic glaucoma is raised intraocular pressure following ocular injury, either early (in the first weeks) or late (months to decades later).

• Early mechanisms: hyphaema with trabecular obstruction by red cells, inflammation (traumatic iritis), lens induced mechanisms (dislocated, swollen or ruptured lens), steroid response, trabecular oedema or disruption, and pupillary block.
• Late mechanisms: angle recession glaucoma (tear between the longitudinal and circular ciliary muscle fibres causing scarring of the trabecular meshwork), ghost cell glaucoma (degenerated red cells after vitreous haemorrhage), chronic inflammation with peripheral anterior synechiae, hemosiderotic glaucoma (iron from retained blood), siderosis from iron foreign body, chemical burns with trabecular damage, and cyclodialysis closure.
• Angle recession of 180 degrees or more carries about 4 to 9 percent risk of glaucoma; onset can be decades after injury, and the fellow eye has a higher risk of primary open angle glaucoma.

• Early: eye pain, blurred vision, hyphaema (microscopic or layered), raised pressure, corneal blood staining in severe hyphaema with high pressure, iris sphincter tears, traumatic mydriasis.
• Late (angle recession): usually asymptomatic until field loss; unilateral raised pressure, widened ciliary body band on gonioscopy, torn iris processes, whitened scleral spur, deep anterior chamber, iridodialysis.
• Sickle cell trait or disease: more susceptible to pressure rise with hyphaema because sickled cells obstruct meshwork and optic nerve is vulnerable.

• History and documentation of injury; slit lamp examination (hyphaema grade, iris damage, lens status, corneal blood staining).
• Gonioscopy once the eye is quiet (after 4 weeks for angle recession), comparing with the fellow eye.
• Tonometry (avoid in suspected open globe), disc examination and perimetry; ultrasound biomicroscopy to show cyclodialysis clefts and angle recession.
• B-scan for posterior segment injury; CT orbits for foreign body; sickle cell screening in at risk patients.

• Hyphaema: bed rest with head elevation, shield, avoid aspirin and NSAIDs, topical prednisolone acetate 1 percent four to six times daily and cycloplegic (atropine 1 percent twice daily), tranexamic acid 25 mg/kg three times daily orally for 5 days where used, and pressure control (timolol 0.5 percent, dorzolamide 2 percent, brimonidine 0.2 percent; acetazolamide 250 to 500 mg orally twice daily and methazolamide are avoided in sickle cell disease, and mannitol is likewise avoided). Surgical washout when pressure remains above 35 mmHg for 7 days, above 50 mmHg for 4 days, corneal blood staining, or total hyphaema for 5 days.
• Angle recession glaucoma: prostaglandin analogues (increase uveoscleral outflow, preferred), beta blockers, alpha agonists, carbonic anhydrase inhibitors; avoid miotics (reduce uveoscleral outflow and may increase pressure). Laser trabeculoplasty has poor effect. Trabeculectomy with mitomycin C (0.4 mg/mL) or glaucoma drainage devices for refractory cases.
• Ghost cell glaucoma: observation with aqueous suppressants, anterior chamber washout, vitrectomy when blood persists.
• Lens related: remove a swollen, ruptured or dislocated lens once pressure and inflammation are controlled (phacoemulsification, or vitrectomy for lens fragments in the vitreous), with acetazolamide 250 mg four times daily, timolol 0.5 percent twice daily and prednisolone acetate 1 percent every 1 to 2 hours in the meantime.
• Cyclodialysis cleft with hypotony: atropine, argon laser or cryotherapy, or surgical closure.
• Lifelong monitoring: pressure and optic disc every 6 months for at least 10 to 20 years after injury with recession over 180 degrees, and surveillance of the fellow eye.