- Clinical science
Glaucoma is a group of eye diseases associated with acute or chronic destruction of the optic nerve with or without concomitant increased intraocular pressure (IOP). In the US, glaucoma is the second leading cause of blindness in adults following age-related macular degeneration (AMD). The two main types are open-angle glaucoma and angle-closure glaucoma. Open-angle glaucoma accounts for 90% of all cases of glaucoma, is slowly progressive, and is initially often asymptomatic, but leads to bilateral peripheral vision loss over time. With appropriate screening (e.g., fundoscopy, gonioscopy, and tonometry) and treatment that lowers IOP (e.g. topical prostaglandins), progression can be stopped before severe damage occurs. Angle-closure glaucoma, on the other hand, is sudden onset and characterized by a painful, red, and hard eye in combination with frontal headache, blurry vision, and halos appearing around lights. Immediate initiation of medical therapy (e.g. timolol eye drops and IV acetazolamide) is crucial to rapidly decrease IOP and prevent vision loss.
- : (also primary or chronic glaucoma): generally bilateral, progressive loss of optic nerve fibers with open chamber angles (often with increased IOP), not caused by another systemic or local condition
- : (also narrow-angle or acute glaucoma): sudden and sharp increase in intraocular pressure caused by an obstruction of aqueous outflow (most commonly as a result of an occlusion of the chamber angle)
|Important types of glaucoma|
|Clinical features|| |
Basic physiological principles
- Aqueous humor is produced by the ciliary body on the iris, flows from the posterior chamber through the pupil into the anterior chamber, and then drains back into the venous system via the trabecular meshwork in the angle of the anterior chamber.
- Physiologically, the flow of aqueous humor against resistance generates an average intraocular pressure (IOP) between 10–21 mm Hg.
- Any process that disrupts the flow of aqueous humor (e.g., adhesion of the iris to the lens) may raise intraocular pressure and lead to optic nerve damage and visual impairment. (See the pathophysiology of “” and “” below.)
- Primary cause unclear
- Risk factors
- Secondary clogging of the trabecular meshwork or reduced drainage → gradual ↑ in IOP → vascular compression → ischemia to the optic nerve → progressive visual impairment.
- Initially often asymptomatic
- Over time, nonspecific symptoms such as mild headaches, impaired adaptation to darkness
- Generally bilateral, progressive visual field loss (from peripheral to central)
- Halos around lights may occur.
- Slit lamp examination of the anterior segment: normal appearing anterior chamber angle
- Tonometry: measure IOP (standard values range between 10–21 mm Hg)
- Gonioscopy : to rule out angle-closure glaucoma
- Fundoscopy: cupping and pallor of optic disc
- Conservative (first-line): topical prostaglandins are most effective and usually used initially; other drugs (with a different mechanism) may be added if unsuccessful
- Alternative first-line treatment: laser trabeculoplasty
- Refractory cases: surgical trabeculectomy
For all individuals > 40 years, a regular eye examination by an ophthalmologist or optometrist is recommended. This should include:
- Inspection of the disc
- Intraocular pressure measurements
- Anatomic features predisposing to angle closure: shallow anterior chamber (e.g., hyperopia, short eye)
- Advanced age
- Female gender
- Inuit and Asian ethnicity
- Eye injury with scarring and adhesions
Blocked trabecular meshwork → ↓ drainage of aqueous humor from the eye → sudden ↑ IOP
- Primary: : the chamber angle is narrowed due to the peripheral iris obstructing the trabecular meshwork. Certain anatomic features, such as shallow chamber depth (enhanced in mydriasis) and small anterior segments, predispose to developing angle-closure.
- Secondary : : scarring, lens luxation, or rubeosis iridis (neovascular glaucoma)
- Sudden onset of symptoms
- Unilaterally inflamed, reddened, and severely painful eye (hard on palpation)
- Frontal headaches, vomiting, nausea
- Blurred vision and halos seen around light
- Cloudy cornea (opacification)
- Mid-dilated, irregular, unresponsive pupil
- Complications: rapid permanent vision loss due to ischemia and atrophy of the optic nerve
- Rock-hard globe on palpation
- Slit lamp examination of the anterior segment: narrow anterior chamber angle, shallow anterior chamber
- Gonioscopy (gold-standard)
- Tonometry (if gonioscopy is unavailable): ↑ IOP
Do not use mydriatic drugs (e.g., atropine and epinephrine) during ophthalmologic examination in patients with suspected angle-closure glaucoma! Also don't cover the eye, since darkness induces mydriasis and worsens the condition!
- First-line: drugs can be used alone but are usually given in combination
- Topical cholinergics (e.g., pilocarpine) can be added once IOP is < 40 mm Hg (contraindicated in cases of lens-induced glaucoma, e.g., in lens luxation)
- Analgesics and antiemetics
- Definitive surgical treatment
Blood supply to the optic nerve may be impaired by lowering blood pressure. → No systemic blood pressure reduction in acute glaucoma patients.
Immediate ophthalmic treatment is necessary, as the eye is at risk of being irreversibly damaged!