What Is Glaucoma?
Glaucoma is a group of optic neuropathies characterized by progressive damage to the optic nerve, resulting in characteristic visual field loss and, if untreated, blindness. It is the leading cause of irreversible blindness worldwide. While elevated intraocular pressure (IOP) is the primary modifiable risk factor, glaucoma can occur at normal IOP (normal-tension glaucoma), and not all patients with elevated IOP develop glaucoma (ocular hypertension).
Pathophysiology
The most widely accepted mechanism involves elevated IOP damaging the axons of retinal ganglion cells at the level of the optic nerve head. The optic nerve has limited regenerative capacity, so damage is permanent. IOP elevation typically results from impaired aqueous outflow through the trabecular meshwork. Over time, nerve fiber layer loss causes the characteristic enlargement of the optic cup and visual field defects.
Types of Glaucoma
Primary Open-Angle Glaucoma (POAG)
POAG is the most common form in the United States. The anterior chamber angle remains open (trabecular meshwork appears normal on gonioscopy), but outflow resistance is increased through the meshwork. Key features:
- Typically bilateral but often asymmetric
- Usually painless -- patients are unaware until significant damage occurs
- Peripheral vision lost first; central vision preserved until late
- IOP often elevated, but normal-tension glaucoma is also POAG
- Risk factors: age, African American descent, family history, elevated IOP, thin corneas, large cup-to-disc ratio
💡 Clinical Tip: POAG is the "silent thief of sight." Many patients have no symptoms until they have lost more than 40% of their retinal ganglion cells. This is why routine optic nerve evaluation and visual field testing are critical in screening programs.
Angle-Closure Glaucoma (ACG)
Angle-closure glaucoma occurs when the peripheral iris mechanically blocks the trabecular meshwork, preventing aqueous outflow. It can be:
- Acute: sudden, dramatic IOP spike causing severe eye pain, headache, nausea/vomiting, halos, and blurred vision. Cornea may appear hazy. This is an ocular emergency requiring immediate treatment.
- Subacute/chronic: intermittent episodes, often at night (when pupil is mid-dilated and blocks the angle)
Risk factors: hyperopic (farsighted) eyes with shallow anterior chambers, female sex, Asian descent, advancing age.
⚠️ Common Mistake: Never use mydriatic (dilating) drops in a patient with a known narrow angle without physician approval. Dilation mid-dilates the pupil and can trigger acute angle-closure. Always check the patient chart and ask the physician before dilating.
Secondary Glaucoma
Secondary glaucoma has an identifiable cause:
- Pseudoexfoliation glaucoma -- exfoliation material clogs trabecular meshwork; unilateral, higher IOP
- Pigmentary glaucoma -- pigment granules from the iris clog meshwork; common in myopic young men
- Neovascular glaucoma -- new blood vessels from retinal ischemia (diabetic retinopathy, CRVO) invade the angle
- Steroid-induced glaucoma -- topical, systemic, or injected steroids elevate IOP in susceptible individuals
Diagnosis
Glaucoma diagnosis integrates multiple findings:
- IOP measurement (Goldman applanation tonometry, target typically <21 mmHg)
- Optic disc evaluation (cup-to-disc ratio, rim notching, disc hemorrhages)
- Visual field testing (automated perimetry -- arcuate defects, nasal steps, paracentral scotomas)
- OCT (retinal nerve fiber layer and ganglion cell layer thickness)
- Gonioscopy (direct visualization of the angle)
- Central corneal thickness (pachymetry) -- thin corneas underestimate IOP
Treatment
The goal of glaucoma treatment is to lower IOP to a target level that prevents further damage. Treatment modalities:
Medications (First-Line)
| Drug Class | Mechanism | Example |
|---|---|---|
| Prostaglandin analogs | Increases uveoscleral outflow | Latanoprost (Xalatan) |
| Beta-blockers | Decreases aqueous production | Timolol |
| Alpha-2 agonists | Decreases production, increases outflow | Brimonidine |
| Carbonic anhydrase inhibitors | Decreases aqueous production | Dorzolamide, acetazolamide |
| Rho-kinase inhibitors | Increases trabecular outflow | Netarsudil (Rhopressa) |
Laser Treatment
- Laser trabeculoplasty (SLT or ALT) -- for open-angle glaucoma; improves outflow through trabecular meshwork
- Laser peripheral iridotomy (LPI) -- for narrow/closed angles; creates a hole in the iris to equalize pressure and open the angle
Surgery
- Trabeculectomy -- creates a new drainage pathway (bleb)
- Tube shunt (aqueous drainage device) -- silicone tube drains aqueous to a plate
- MIGS (minimally invasive glaucoma surgery) -- small devices or procedures to improve drainage with lower risk
CPOA Role in Glaucoma Management
- Performing accurate IOP measurements (tonometry) -- critical for monitoring treatment response
- Measuring and recording visual acuity
- Setting up and operating automated perimetry (visual field testing)
- Obtaining OCT nerve fiber layer scans
- Reviewing medication compliance and educating patients on proper drop instillation
- Checking for potential laser peripheral iridotomy in narrow-angle patients before dilation
🔑 Key Point: A patient with an acute angle-closure attack (severe eye pain, nausea, hazy cornea, elevated IOP) needs emergency intervention. Alert the physician immediately and do not delay care by performing routine testing.
Key Takeaways
- Glaucoma is progressive optic neuropathy causing irreversible vision loss; elevated IOP is the main modifiable risk factor
- POAG is the most common form -- painless, insidious, peripheral vision lost first
- Acute angle-closure is an emergency: severe pain, hazy cornea, dramatically elevated IOP
- Never dilate a narrow-angle patient without physician approval
- Prostaglandin analogs are first-line drops; beta-blockers, alpha agonists, and CAIs are also used
- The CPOA performs IOP checks, visual fields, and OCT to monitor glaucoma progression