Chronic painless optic neuropathy with progressive visual field loss — leading cause of irreversible blindness worldwide.
Also known as: POAG, open-angle glaucoma, primary open-angle glaucoma, chronic glaucoma
Overview
Chronic, progressive, typically bilateral optic neuropathy characterized by retinal nerve fiber layer loss, characteristic optic disc cupping, and corresponding visual field defects, occurring in the presence of an open anterior chamber angle. Elevated intraocular pressure (IOP) is the most important modifiable risk factor, although normal-tension glaucoma occurs with IOP in the statistically normal range (<21 mmHg).
Epidemiology
Leading cause of irreversible blindness worldwide. Prevalence rises sharply with age — ~1% at age 40, ~10% by age 80. African ancestry: 3-4× risk and earlier onset; Hispanic ancestry also elevated. Approximately half of affected patients are undiagnosed.
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Imbalance between aqueous humor production by the ciliary body and outflow through the trabecular meshwork/Schlemm canal increases IOP, which damages retinal ganglion cell axons at the lamina cribrosa. Ischemic and mechanical factors contribute. The optic disc develops progressive cupping (loss of neuroretinal rim) and the visual field loses peripheral and arcuate function before central vision. In normal-tension glaucoma, vascular dysregulation and lower CSF pressure may produce the same end-organ damage at lower IOP.
Clinical presentation
Symptoms
Asymptomatic in early disease — vision loss is painless and gradual
Patients rarely notice peripheral field defects until advanced
Trouble with night driving, missing steps, or bumping into things
Central vision preserved until late
Frequently detected on screening exam or as 'large cup' on routine fundoscopy
Signs / physical exam
Elevated IOP on tonometry (most have IOP >21, but normal-tension subgroup does not)
Open angle on gonioscopy
Optic disc cupping: cup-to-disc ratio >0.6, asymmetric C/D between eyes >0.2, notching of the rim, disc hemorrhages (Drance hemorrhages)
Loss of retinal nerve fiber layer on OCT
Visual field defects: nasal step, paracentral or arcuate scotoma, eventually tunnel vision
Pupils equal with no RAPD until advanced asymmetric disease
Classic findings
Progressive optic disc cupping with corresponding nerve fiber bundle visual field defects in a patient with elevated IOP.
Differential diagnosis
Normal-tension glaucoma — POAG phenotype with IOP <21; consider vascular dysregulation; treat to lower IOP and address risk factors
Secondary glaucomas (pigmentary, pseudoexfoliative, steroid-induced, neovascular, uveitic, traumatic) — Findings on slit lamp/gonioscopy; treat underlying cause
Non-glaucomatous optic neuropathy (ischemic, compressive, inflammatory) — Pale rather than cupped disc, RAPD, sudden vision change, neuroimaging
Optic disc drusen / physiologic cupping — Stable disc and field over time; B-scan or OCT shows drusen
Retinal disease causing field loss — Macular or peripheral retinal pathology; normal disc
Diagnostic workup
Diagnostic criteria
Characteristic optic disc and/or nerve fiber layer damage with corresponding visual field defect in an eye with open angle, after exclusion of secondary causes.
POAG is painless and asymptomatic until advanced — screening of high-risk groups (African ancestry ≥40, family history) is essential.
Cup-to-disc ratio asymmetry >0.2 between eyes is suspicious for glaucoma even with normal IOP.
Disc (Drance) hemorrhages at the rim are a strong sign of progression.
Central corneal thickness influences applanation tonometry — thin corneas under-read IOP and confer independent risk (OHTS).
Prostaglandin analogs are the most powerful single-agent IOP lowerers and are once-daily — first-line pharmacotherapy.
Selective laser trabeculoplasty (SLT) is now considered a reasonable first-line option per the LiGHT trial — fewer drops, fewer side effects.
Normal-tension glaucoma still benefits from IOP lowering (CNTGS) — do not dismiss because IOP is 'normal.'
References
AAO 2020 — American Academy of Ophthalmology. Primary Open-Angle Glaucoma Preferred Practice Pattern. Ophthalmology 2021;128(1):P71-P150
OHTS — Kass MA et al. The Ocular Hypertension Treatment Study. Arch Ophthalmol 2002;120(6):701-713
EMGT — Heijl A et al. Reduction of intraocular pressure and glaucoma progression: Early Manifest Glaucoma Trial. Arch Ophthalmol 2002;120(10):1268-1279
LiGHT — Gazzard G et al. Selective laser trabeculoplasty versus eye drops for first-line treatment of ocular hypertension and glaucoma (LiGHT): a multicentre randomised controlled trial. Lancet 2019;393(10180):1505-1516
CNTGS — Collaborative Normal-Tension Glaucoma Study Group. Comparison of glaucomatous progression between untreated patients with normal-tension glaucoma and patients with therapeutically reduced intraocular pressures. Am J Ophthalmol 1998;126(4):487-497
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