What is glaucoma? Symptoms, causes & treatment

Glaucoma is a group of chronic, progressive optic neuropathies characterized by retinal ganglion cell loss, optic nerve head cupping, and corresponding visual field defects, most often associated with elevated intraocular pressure (IOP). Primary open-angle glaucoma is the most common subtype in the US; primary angle-closure glaucoma is less common but can present acutely with severe pain. Diagnosis is clinical based on optic nerve and angle examination, perimetry, and ocular imaging. Treatment lowers IOP with topical medications, laser trabeculoplasty or iridotomy, and incisional surgeries to slow or prevent further vision loss.

Key Points

• Glaucoma causes irreversible optic nerve damage and visual field loss; early detection and sustained IOP lowering reduce progression risk.
• Primary open-angle glaucoma is usually asymptomatic until advanced; primary angle-closure may present acutely with pain, halos, and nausea.
• Definitive diagnosis requires correlation of optic nerve structural changes with functional loss on visual field testing; IOP alone is insufficient.
• First-line therapies include prostaglandin analog eye drops and/or selective laser trabeculoplasty; angle-closure requires laser peripheral iridotomy.
• Risk factors include older age, family history, African American and Hispanic/Latino ancestry, thin central cornea, high IOP, myopia (open-angle), and hyperopia (angle-closure).
• Acute angle-closure is an ophthalmic emergency; prompt IOP reduction and laser iridotomy are required to prevent permanent vision loss.

Anatomy and Physiology

The anterior segment maintains IOP via aqueous humor production by the ciliary body and outflow through two routes:

• Trabecular (conventional) pathway: through the trabecular meshwork into Schlemm’s canal and the episcleral veins.
• Uveoscleral (unconventional) pathway: through the ciliary muscle and suprachoroidal space.

The optic nerve head (lamina cribrosa) transmits retinal ganglion cell axons. Mechanical strain and vascular factors at the lamina contribute to glaucomatous axonal injury.

Etiology

• Primary open-angle glaucoma (POAG): multifactorial; increased outflow resistance at the trabecular meshwork without angle closure.
• Primary angle-closure disease (PACD): pupillary block or plateau iris configuration causing iridotrabecular contact; risk increased by shallow anterior chamber and hyperopia.
• Normal-tension glaucoma (NTG): glaucomatous damage despite statistically normal IOP; often with vascular susceptibilities.
• Secondary glaucomas: pigment dispersion, pseudoexfoliation, neovascular (from retinal ischemia), uveitic, steroid-induced, lens-induced (phacomorphic/phacolytic), traumatic (angle recession), post-penetrating keratoplasty, and medication-related.

Pathophysiology

Elevated IOP and/or susceptibility of the optic nerve head lead to retinal ganglion cell apoptosis. Mechanical deformation of the lamina cribrosa and impaired axoplasmic flow, plus microvascular dysregulation and ischemia, contribute to damage. In angle closure, aqueous outflow is physically obstructed, causing intermittent or sustained IOP spikes with risk of peripheral anterior synechiae and rapid optic neuropathy.

Epidemiology

• About 3 million people in the United States have glaucoma; roughly half may be undiagnosed [1,2].
• POAG prevalence increases with age and is higher in African Americans and Hispanics/Latinos [1].
• PACD is more common in females and hyperopes and increases with age [3].
• Family history approximately doubles to triples risk for POAG [3].

Classification

• By mechanism:
  • Primary open-angle glaucoma
  • Primary angle-closure disease: suspect, intermittent (acute), chronic, and primary angle-closure glaucoma
  • Normal-tension glaucoma
  • Secondary open-angle or angle-closure glaucomas (e.g., pseudoexfoliation, pigmentary, neovascular, uveitic, steroid-induced, lens-related, traumatic)
• By age:
  • Primary congenital glaucoma (birth–3 years), infantile/juvenile glaucomas, secondary pediatric glaucomas
• By stage (ICD-10-CM staging for each laterality):
  • Mild (early), moderate, severe (advanced), indeterminate

Representative ICD-10-CM codes: H40.11X1–H40.11X4 (primary open-angle glaucoma, right eye, staged); H40.12X1–H40.12X4 (left eye); H40.21X1–H40.21X4 (primary angle-closure glaucoma); H40.03X (congenital glaucoma).

Symptoms and Signs

Primary open-angle glaucoma

• Usually asymptomatic until late. No pain or redness.
• Optic disc cupping with focal rim thinning/notching, RNFL defects.
• Visual field: arcuate scotomas, nasal steps, paracentral defects; central vision preserved until late.

Normal-tension glaucoma

• Similar optic disc and field patterns as POAG at lower IOP.
• Possible disc hemorrhages, peripapillary atrophy; often vascular comorbidities (e.g., migraine, Raynaud phenomenon) may coexist.

Primary angle-closure disease

• Acute attack: severe ocular pain, headache, halos around lights, decreased vision, nausea/vomiting.
• Findings: conjunctival injection, corneal edema, mid-dilated poorly reactive pupil, shallow anterior chamber, markedly elevated IOP.
• Chronic angle closure: peripheral anterior synechiae, progressive IOP elevation, optic neuropathy with or without intermittent symptoms.

Secondary glaucomas

• Pseudoexfoliation: flaky material on the lens/angle, high IOP fluctuation, rapid progression.
• Pigmentary: midperipheral iris transillumination defects, Krukenberg spindle (corneal pigment), open angle with dense trabecular pigmentation.
• Neovascular: rubeosis iridis, fibrovascular angle membranes; often from proliferative diabetic retinopathy or ischemic CRVO.
• Uveitic: anterior chamber cells/flare with IOP elevation from trabeculitis or steroid use.
• Steroid-induced: IOP rise after corticosteroid exposure (topical, periocular, intravitreal, systemic).

Pediatric glaucomas

• Primary congenital glaucoma: epiphora, photophobia, blepharospasm, enlarged cornea (buphthalmos), corneal haze/Haab striae, elevated IOP.

Complications

• Progressive, irreversible visual field loss; potential legal blindness.
• Acute angle-closure complications: corneal edema, synechiae, cataract, sustained optic nerve damage.
• Medication adverse effects:
  • Prostaglandins: conjunctival hyperemia, iris and periocular hyperpigmentation, eyelash growth, periocular fat atrophy.
  • Beta blockers: bradycardia, hypotension, bronchospasm, fatigue, depression (systemic absorption).
  • Alpha-2 agonists: dry mouth, fatigue, allergic follicular conjunctivitis; avoid in infants.
  • Carbonic anhydrase inhibitors: paresthesias, GI upset, kidney stones, metabolic acidosis (systemic); sulfonamide allergy cross-reactivity possible.
  • Rho-kinase inhibitor: conjunctival hyperemia, corneal verticillata, instillation site pain.

Diagnosis

Clinical evaluation

• History: family history, steroid exposure, trauma, migraines/vascular disease, sleep apnea; symptoms of angle-closure.
• Examination:
  • IOP measurement (Goldmann applanation preferred).
  • Gonioscopy to assess angle width, pigmentation, synechiae, neovascularization.
  • Central corneal thickness (pachymetry) to interpret IOP and as a risk factor.
  • Dilated fundus examination for optic nerve head: cup-to-disc ratio, rim integrity, disc hemorrhages, RNFL defects; stereophotography for baseline.

Imaging and laboratory testing

• Optical coherence tomography (OCT) of RNFL and macular ganglion cell complex for structural loss.
• Standard automated perimetry (e.g., 24-2, 10-2) for functional loss and staging.
• Anterior segment OCT or ultrasound biomicroscopy to evaluate narrow angles/plateau iris.
• Ancillary: diurnal IOP curve, corneal hysteresis (optional risk metric). No routine laboratory testing unless secondary causes suspected.

Differential diagnosis

Treatment

Target IOP reduction is individualized based on disease stage and risk; many patients with POAG benefit from an initial 20% to 30% IOP reduction from baseline with subsequent adjustment based on progression [3,4].

Medical management

• Prostaglandin analogs (first-line for POAG/NTG):
  • latanoprost 0.005%, travoprost 0.004%, bimatoprost 0.01%, tafluprost 0.0015%: 1 drop qhs (once nightly).
• Beta blockers:
  • timolol 0.25%–0.5%: 1 drop bid (twice daily); consider qam (morning) if adequate.
  • Avoid or use caution in asthma/COPD, bradycardia, heart block.
• Alpha-2 agonist:
  • brimonidine 0.1%–0.2%: 1 drop tid (three times daily) or bid; allergy is common.
• Topical carbonic anhydrase inhibitors:
  • dorzolamide 2% or brinzolamide 1%: 1 drop tid or bid.
• Rho-kinase inhibitor:
  • netarsudil 0.02%: 1 drop qhs; hyperemia common.
• Miotics (limited use):
  • pilocarpine 1%–4%: dosing varies; used in certain mechanisms (e.g., post-LPI plateau iris).
• Fixed-combination drops (lower drop burden):
  • Examples: timolol/dorzolamide bid; brimonidine/timolol bid; netarsudil/latanoprost qhs; brimonidine/brinzolamide tid-bid.

Acute primary angle-closure (emergent)

• Immediate IOP reduction:
  • acetazolamide 500 mg PO or IV, then 250 mg PO q6h (or 500 mg ER PO bid) short term.
  • Topical: timolol 0.5% 1 drop; brimonidine 0.2% 1 drop.
  • Once IOP is lowered and pupil begins to respond: pilocarpine 1%–2%, 1 drop q15 minutes for 2–3 doses, then q6h.
  • Hyperosmotic agent if needed: mannitol 0.5–1 g/kg IV over 45–60 minutes (use caution in heart/kidney disease).
  • Topical corticosteroid to reduce inflammation.
• Definitive: laser peripheral iridotomy (LPI) as soon as the cornea clears; treat fellow eye prophylactically unless contraindicated.

Procedural and surgical management

• Selective laser trabeculoplasty (SLT): Office-based laser to trabecular meshwork; reasonable as initial therapy or adjunct in POAG/ocular hypertension; repeatable [3,5].
• Laser peripheral iridotomy (LPI): Creates an alternative aqueous pathway to relieve pupillary block in angle-closure spectrum; often combined with lens-based strategies if persistent angle narrowing.
• Lens extraction in primary angle-closure: Cataract or clear lens extraction deepens the chamber and widens the angle; considered in selected cases with persistent angle closure or elevated IOP after LPI [6] (non-US trial evidence).
• Minimally invasive glaucoma surgery (MIGS): Trabecular microbypass (e.g., iStent), Schlemm’s canal scaffolds (e.g., Hydrus), goniotomy/viscodilation devices, usually combined with cataract surgery in mild–moderate POAG to reduce drop burden [7].
• Trabeculectomy with antimetabolite (e.g., mitomycin C) and glaucoma drainage devices (Ahmed, Baerveldt): For moderate–advanced or refractory disease; greatest IOP lowering but higher risk of complications.
• Cyclodestructive procedures (transscleral or endoscopic cyclophotocoagulation): For refractory glaucoma or poor surgical candidates.

Special populations

• Pediatric glaucoma: Definitive management is surgical (goniotomy, trabeculotomy, trabeculectomy/tubes); medications are adjunctive and many are off-label in children. Monitor axial length and corneal diameter.
• Pregnancy/lactation: Minimize exposure; consider punctal occlusion after drop instillation. Beta blockers may cause fetal/neonatal bradycardia; brimonidine is generally avoided near delivery and in nursing infants; prostaglandin analogs have limited human data. Coordinate care with obstetrics and pediatricians [3].
• Normal-tension glaucoma: Lower IOP (often ≥30% from baseline) while addressing systemic factors that may worsen perfusion (e.g., nocturnal hypotension) in coordination with primary care; evidence for non-IOP therapies is limited [3].
• Elderly and multimorbidity: Review systemic contraindications and polypharmacy; simplify regimens and support adherence.

Prognosis

With timely diagnosis and sustained IOP control, many patients maintain useful vision for life. Risk of progression depends on baseline optic nerve damage and fields, IOP level and fluctuation, central corneal thickness, disc hemorrhages, adherence, and age. Angle-closure without prompt treatment can cause rapid, permanent vision loss.

Prevention and Patient Counseling

• Routine comprehensive eye examinations with IOP, gonioscopy, optic nerve evaluation, and visual fields in at-risk groups (older age, family history, African American and Hispanic/Latino ancestry).
• Adherence: correct instillation technique, dosing schedule, and refill planning; consider SLT to reduce drop burden.
• Lifestyle: No proven supplement prevents glaucoma; manage vascular comorbidities (sleep apnea, blood pressure extremes) with primary care.
• Distinguish chronic symptoms: dry, gritty irritation suggests dry eye (see /blog/dry-eye-syndrome), not glaucoma; acute painful red eye with halos requires urgent evaluation.

When to Seek Immediate Care

• Severe eye pain with headache, nausea, halos around lights, or sudden blurred vision.
• A red, hard eye with decreased vision.
• Sudden vision loss, new large floaters with flashes, or a curtain over vision.
• Eye injury with pain or vision changes.
• After glaucoma surgery: increasing pain, vision drop, or purulent discharge. Call 911 or go to the emergency department if symptoms are severe or rapidly worsening.

References

1. National Eye Institute. Glaucoma Facts and Prevalence. Accessed 2026. https://www.nei.nih.gov/learn-about-eye-health/eye-conditions-and-diseases/glaucoma [Tier 1].
2. Centers for Disease Control and Prevention. Vision Health Initiative: Glaucoma. Accessed 2026. https://www.cdc.gov/visionhealth/basics/eye_disorders/glaucoma.htm [Tier 1].
3. American Academy of Ophthalmology Preferred Practice Pattern. Primary Open-Angle Glaucoma. San Francisco, CA: AAO; 2020. https://www.aao.org/preferred-practice-pattern/primary-open-angle-glaucoma-ppp-2020 [Tier 1].
4. Kass MA, Heuer DK, Higginbotham EJ, et al. The Ocular Hypertension Treatment Study: a randomized trial determines that topical ocular hypotensive medication delays or prevents the onset of primary open-angle glaucoma. Arch Ophthalmol. 2002;120(6):701-713. doi:10.1001/archopht.120.6.701.
5. Gazzard G, Konstantakopoulou E, Garway-Heath D, et al. Selective laser trabeculoplasty versus drops for newly diagnosed glaucoma and ocular hypertension (LiGHT). Lancet. 2019;393(10180):1505-1516. doi:10.1016/S0140-6736(18)32213-X. [Non-US trial]
6. Azuara-Blanco A, Burr J, Ramsay C, et al. EAGLE study: Clear-lens extraction for primary angle-closure glaucoma. Lancet. 2016;388(10052):1389-1397. doi:10.1016/S0140-6736(16)30956-4. [Non-US trial]
7. Singh K, Shrivastava A, et al. Minimally invasive glaucoma surgery: AAO Ophthalmic Technology Assessment. Ophthalmology. 2022;129(12):e195-e208. doi:10.1016/j.ophtha.2022.08.009.
8. Prum BE Jr, Rosenberg LF, Gedde SJ, et al. Primary Angle Closure Preferred Practice Pattern. Ophthalmology. 2016;123(1):P1-P40; update accessed 2026 via AAO PPP portal.
9. Weinreb RN, Aung T, Medeiros FA. The pathophysiology and treatment of glaucoma. JAMA. 2014;311(18):1901-1911. doi:10.1001/jama.2014.3192. [Foundational review]

This article is for informational purposes and is not a substitute for professional medical advice, diagnosis, or treatment. Always consult a qualified eye care professional about your specific condition. If you have sudden vision loss, severe eye pain, or an eye injury, seek emergency care immediately.