Glaucoma Classification & Types

Primary Open-Angle Glaucoma: The Baseline Definition

Glaucoma is defined by its optic nerve findings, not by a pressure threshold. Primary open-angle glaucoma (POAG) is a chronic, progressive optic neuropathy occurring with an open drainage angle: progressive cupping of the optic disc and a matching pattern of visual field loss, classically arcuate scotomas, are what define the disease. The underlying process is loss of retinal ganglion cell axons, and elevated intraocular pressure (IOP) is the single most important risk factor for that loss, but IOP is not the definition itself. A reading above 21 mmHg is considered statistically elevated, yet glaucomatous damage can develop at pressures within the normal range too. That pattern is normal-tension glaucoma, covered on its own page.

A patient with an IOP of 24 mmHg and a completely normal optic nerve and visual field does not have glaucoma. That combination is ocular hypertension: elevated IOP without glaucomatous optic neuropathy or field loss. It is a risk state, not a diagnosis of glaucoma, though the OHTS trial (see Landmark Glaucoma Clinical Trials) showed that treating it lowers the rate of conversion to actual glaucoma.

How IOP-Lowering Therapy Actually Works

Every IOP-lowering intervention, whether a drop, a laser procedure, or surgery, works through one of two routes: reducing aqueous production, or increasing its outflow through either the conventional trabecular pathway or the uveoscleral pathway. Most agents act mainly through one of these. A given treatment either turns down production or opens a drainage route, though a few (brimonidine, netarsudil) do both.

Angle-Closure Glaucoma

Acute angle-closure looks nothing like POAG. It presents with a sudden, painful red eye, reduced vision, and a fixed, mid-dilated pupil that fails to react to light, a finding driven by pressure-induced ischemia of the iris sphincter. Halos around lights often accompany the pain: acutely elevated IOP waterlogs the cornea, and the edematous stroma scatters incoming light. POAG almost never produces either finding. The risk factor for angle-closure is anatomic rather than epidemiologic: a hyperopic, short-axial-length eye has a crowded anterior segment and a shallow anterior chamber, which predisposes to pupillary block. POAG's risk factors run the opposite direction, tracking instead with high myopia, thin corneas, and African ancestry. For the full presentation, mechanism, and management, see the dedicated Angle-Closure Glaucoma page.

Emergency management has two parts. Pilocarpine constricts the pupil and pulls the peripheral iris away from the trabecular meshwork, reopening the angle acutely. Definitive treatment is a laser peripheral iridotomy (LPI), which creates a permanent hole in the peripheral iris so pressure can equalize between the anterior and posterior chambers, relieving the block for good.

Secondary Glaucomas: A Preview

Both open- and closed-angle glaucoma can also arise secondary to an identifiable cause rather than as a primary disease. Pigment dispersion, pseudoexfoliation, phacolytic and phacomorphic glaucoma, and neovascular glaucoma are the mechanisms tested most often, and each has a genuinely distinct pathophysiology worth learning on its own terms. The Secondary Glaucomas page covers all four in full.

High-Yield Pearls

• Ocular hypertension = elevated IOP, normal nerve, normal field. Not glaucoma.
• Angle-closure risk factor: hyperopia (short eye, shallow AC), the opposite of POAG's myopia association.
• Halos around lights are characteristic of acute angle-closure (corneal edema scattering light), not seen in POAG.
• Malignant glaucoma is the classic presentation where a patent LPI doesn't fix a flat anterior chamber.