Glaucoma is a group of eye disorders that damage the optic nerve. This damage slowly reduces vision and, if untreated, can lead to permanent blindness. The main reason for optic nerve damage is usually high pressure inside the eye (intraocular pressure or IOP).
Classification
Major types of glaucoma include:
- Open-Angle (Chronic) Glaucoma: Slow and painless vision loss; most common type.
- Angle-Closure (Acute) Glaucoma: Sudden blockage of fluid outflow → severe eye pain and high IOP; a medical emergency.
- Congenital Glaucoma: Present at birth due to abnormal eye drainage; symptoms include cloudy cornea, tearing, and light sensitivity.
- Secondary Glaucoma: Caused by eye diseases, injuries, cataracts, tumors, steroids, or eye surgery.
- Normal-Tension Glaucoma: Optic nerve damage occurs even with normal IOP; cause unknown.
Etiology (Why Glaucoma Occurs)
The eye continuously produces a clear fluid called aqueous humor. This fluid must drain out through channels between the cornea and iris. If drainage is slowed or blocked, pressure builds up and damages the optic nerve.
Factors that increase the risk of high IOP include:
- Dilating eye drops
- Blocked drainage channels
- Use of corticosteroids
- Poor blood flow to the optic nerve
- High blood pressure
Simple Pathophysiology
Glaucoma mainly occurs when the balance between fluid inflow and outflow is disturbed. Increased IOP was once thought to be the only cause, but other factors also contribute:
- Reduced blood supply to the optic nerve
- Autoimmune damage
- Excitotoxicity (nerve cell overstimulation)
Drugs can influence fluid production and drainage: β-blockers, α2-agonists, carbonic anhydrase inhibitors decrease fluid production. Cholinergics and prostaglandin analogues increase fluid drainage.
Clinical Presentation
Open-Angle Glaucoma (Chronic)
- Slow, progressive loss of peripheral (side) vision
- Later stages → tunnel vision
- Usually no pain
Angle-Closure Glaucoma (Acute)
- Severe eye pain
- Headache, nausea, vomiting
- Blurred vision and halos around lights
- Eye redness
- Rapid rise in IOP → emergency
Other Types
- Congenital glaucoma: cloudy cornea, large eyes, tearing, light sensitivity
- Secondary glaucoma: symptoms depend on underlying cause
Diagnosis
- Tonometry (measures IOP)
- Optic nerve exam using dilation and imaging
- Visual field test (checks vision loss)
- Pachymetry (measures corneal thickness)
- Gonioscopy (examines drainage angle)
Treatment Overview
The goal of treatment is to reduce IOP and prevent further optic nerve damage.
Treatment of Open-Angle Glaucoma & Ocular Hypertension
Start treatment when IOP is significantly high or optic nerve damage is present.
Target IOP Reduction
- Ocular hypertension: reduce IOP by 20–30%
- POAG: initial target reduction of ~30%
First-Line Drugs
- Prostaglandin analogues: latanoprost, travoprost, bimatoprost
Increase outflow; once-daily dosing; highly effective. - Beta-blockers: timolol
Reduce inflow; avoid in asthma/COPD. - Alpha-2 agonists: brimonidine
Reduce inflow and increase outflow. - Topical carbonic anhydrase inhibitors (CAIs): dorzolamide, brinzolamide
Reduce inflow.
Second- or Third-Line Drugs
- Pilocarpine: increases outflow but causes vision blurring and eye pain.
- Dipivefrin: older drug; now rarely used.
- Oral CAIs (acetazolamide): short-term use for severe cases.
Laser or Surgical Options
- Laser trabeculoplasty
- Trabeculectomy (with mitomycin C or 5-FU to prevent scarring)
Treatment of Closed-Angle Glaucoma (Acute Emergency)
Requires fast reduction of IOP and immediate ophthalmology care.
- Osmotic agents: glycerin (oral) or mannitol (IV) to rapidly lower IOP
- Secretory inhibitors: timolol, brimonidine, latanoprost, CAIs
- Pilocarpine: used once IOP decreases
- Topical corticosteroids: reduce inflammation
- Definitive treatment: laser or surgical iridectomy to create a drainage hole in the iris
Detailed Notes:
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