Glaucoma is a group of progressive optic neuropathies characterized by damage to the optic nerve, typically associated with elevated intraocular pressure (IOP). It is the leading cause of irreversible blindness worldwide and is often called the "silent thief of sight" because it causes painless, gradual vision loss that patients do not notice until significant damage has occurred. Glaucoma monitoring is a core CPO clinical task.
Types of Glaucoma
Primary Open-Angle Glaucoma (POAG)
Primary open-angle glaucoma (POAG) is the most common form in the developed world, accounting for approximately 70 to 75% of all glaucoma cases. The iridocorneal angle (where aqueous drains through the trabecular meshwork) remains anatomically open, but the trabecular meshwork offers increasing resistance to outflow over time, causing IOP to rise gradually. There is no acute attack, no pain, and no redness. Vision loss begins in the periphery and progresses centrally, often unnoticed until late in the disease.
Risk factors for POAG include:
- Elevated IOP (the primary modifiable risk factor)
- Advanced age
- African or Hispanic ancestry (higher prevalence and earlier onset)
- Family history of glaucoma
- Myopia (nearsightedness)
- Thin central corneal thickness
Primary Angle-Closure Glaucoma (PACG)
In angle-closure glaucoma, the peripheral iris physically blocks the trabecular meshwork, preventing aqueous drainage. This causes a rapid, dramatic rise in IOP. Acute angle-closure presents as a sudden, severe eye pain, blurry vision, halos around lights, headache, nausea and vomiting, and a fixed, mid-dilated pupil. The eye appears red and the cornea may be hazy. This is an ophthalmic emergency requiring immediate treatment to lower IOP and open the angle, typically with a laser peripheral iridotomy (LPI).
Intraocular Pressure (IOP)
Intraocular pressure is the fluid pressure inside the eye, determined by the balance between aqueous humor production and drainage. Normal IOP ranges from 10 to 21 mmHg. Elevated IOP above 21 mmHg is called ocular hypertension.
IOP is not the only determinant of glaucoma. Some patients develop glaucoma at normal IOP levels (normal-tension glaucoma), and some patients have elevated IOP without optic nerve damage (ocular hypertension). Glaucoma is diagnosed by optic nerve appearance and visual field changes, not IOP alone.
IOP measurement methods:
- Goldmann applanation tonometry (GAT): The gold standard. Requires a slit lamp and topical anesthetic. Measures the force required to flatten a standard area of the cornea.
- Non-contact tonometry (NCT): Uses an air puff; useful for screening, does not require anesthetic. Less accurate than GAT.
- Rebound tonometry (iCare): A probe-based device; no anesthetic required, good for children and non-cooperative patients.
Optic Nerve Assessment
Glaucoma damages the optic nerve by destroying retinal ganglion cell axons, enlarging the optic cup relative to the disc. Key observations during dilated fundus examination:
- Cup-to-disc (C/D) ratio: The ratio of the optic cup diameter to the total disc diameter. A C/D ratio above 0.6, or asymmetry of 0.2 or more between the two eyes, raises concern for glaucoma.
- ISNT rule: In a normal disc, the neuroretinal rim is thickest Inferiorly, then Superiorly, then Nasally, then Temporally. Glaucoma preferentially thins the inferior and superior poles first, violating this rule.
- Disc hemorrhage: Flame-shaped hemorrhages at the disc margin are a sign of active optic nerve damage and indicate progression risk.
Visual Field Testing
Visual field testing (perimetry) is essential for detecting and monitoring glaucomatous damage. Automated static perimetry (such as Humphrey Visual Field testing) maps the threshold sensitivity of the visual field at multiple test points. Glaucoma produces characteristic visual field defects including:
- Arcuate scotomas (curved defects following the nerve fiber layer pattern)
- Nasal steps (defects that do not cross the horizontal midline)
- Paracentral scotomas
- Altitudinal defects (loss of the upper or lower half of the visual field)
Treatment Overview
The only proven treatment for glaucoma is lowering IOP. Treatment options include:
- Topical medications: Prostaglandin analogs (first-line, increase uveoscleral outflow), beta-blockers (decrease production), alpha-2 agonists (decrease production, increase outflow), carbonic anhydrase inhibitors (decrease production), and ROCK inhibitors (newest class, increase trabecular outflow).
- Laser: SLT (selective laser trabeculoplasty) improves trabecular drainage; laser peripheral iridotomy (LPI) for angle closure.
- Surgery: Trabeculectomy (creates a new drainage bleb), tube shunt implantation, or minimally invasive glaucoma surgery (MIGS) for moderate cases.
Key Takeaways
- POAG is the most common type; it is painless with a gradual, peripheral-to-central vision loss pattern.
- Acute angle-closure glaucoma is a medical emergency presenting with sudden severe pain, fixed mid-dilated pupil, and elevated IOP.
- Normal IOP is 10 to 21 mmHg; Goldmann applanation tonometry is the gold standard measurement.
- Glaucoma diagnosis requires assessing optic nerve cupping (C/D ratio), visual fields, and IOP together, not IOP alone.
- Treatment targets IOP reduction through drops, laser, or surgery; prostaglandin analogs are first-line for POAG.