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Ophthalmology›Condition·Updated Jun 27, 2026·v1

Glaucoma

Glaucoma is a progressive optic neuropathy and the leading cause of irreversible blindness, affecting 76 million people worldwide. It is characterized by retinal ganglion cell death, optic nerve cupping, and visual field loss, often but not always associated with elevated IOP. The only proven treatment is IOP lowering, achieved through prostaglandin analogs, SLT, or surgery. A definitive diagnosis requires concordant structural (OCT) and functional (perimetry) damage. Staging with the Hodapp-Parrish-Anderson system guides target IOP: mild (> -6 dB, target 18-21 mmHg), moderate (-6 to -12 dB, target 15-18 mmHg), severe (< -12 dB, target ≤14 mmHg). Acute angle-closure and neovascular glaucoma are emergencies requiring immediate intervention. Ethnicity, myopia, family history, and corticosteroid use are major risk factors. Lifelong monitoring is essential, as early disease is asymptomatic.

High Evidence547 references·12,472 words·50 min read·v1
glaucomaprimary open-angle glaucomaacute angle-closure glaucomaintraocular pressureoptic neuropathytrabeculectomyselective laser trabeculoplastyprostaglandin analogsvisual fieldoptical coherence tomography

Quick Reference

RxDrug of choiceLatanoprost 0.005% one drop QHS (prostaglandin analog), first-line for most open-angle glaucomas; mean IOP reduction 25-33%
AltAlternativesTravoprost 0.004%, bimatoprost 0.01%; timolol 0.5% BID; brimonidine 0.2% TID; dorzolamide 2% TID; netarsudil 0.02% QHS; fixed combinations (e.g., latanoprost/timolol)
⊘AvoidBeta-blockers (timolol) in asthma/COPD/bradycardia; brimonidine in children <6 years; pilocarpine in neovascular or uveitic glaucoma; oral glycerin in diabetics
DxTest of choiceCombination of spectral-domain OCT (circumpapillary RNFL and macular GCIPL thickness) and standard automated perimetry (Humphrey 24-2 SITA-Standard), concordance of structural and functional damage is diagnostic gold standard
ScKey scoreHodapp-Parrish-Anderson (HPA) classification: mild (MD > -6 dB), moderate (MD -6 to -12 dB), severe (MD < -12 dB) based on visual field mean deviation
→When to referAdvanced disease (MD < -12 dB), progression despite low IOP, normal-tension glaucoma, pediatric glaucoma, uveitic/neovascular glaucoma, need for incisional surgery, acute angle-closure crisis
Glaucoma is a treatable but incurable optic neuropathy; early detection and sustained IOP reduction are the only proven strategies to prevent blindness. Every 1 mmHg IOP reduction lowers progression risk by ~10%.
Glaucoma is a chronic, progressive optic neuropathy and the leading cause of irreversible blindness worldwide, affecting approximately 76 million people in 2020. It is characterized by degeneration of retinal ganglion cells, leading to characteristic optic nerve cupping and visual field defects. While elevated intraocular pressure (IOP) is the only proven modifiable risk factor, glaucoma can occur at any IOP. Management focuses on lowering IOP through medications, laser, or surgery, with the goal of preserving vision and quality of life. Early detection is critical as the disease is asymptomatic until moderate-to-severe stages.

Overview and Recommendations

Background

  • •Glaucoma is a chronic, progressive optic neuropathy defined by the degeneration of retinal ganglion cells and their axons, leading to characteristic optic nerve cupping and corresponding visual field defects. It is the leading cause of irreversible blindness globally, affecting 76 million people in 2020, projected to reach 112 million by 2040.
  • •The disease is not defined by intraocular pressure (IOP) alone; while elevated IOP is the only proven modifiable risk factor, approximately 30-50% of patients have IOP in the normal range at diagnosis (normal-tension glaucoma). The Ocular Hypertension Treatment Study (OHTS) showed that a 20% reduction in IOP reduces the 5-year risk of developing primary open-angle glaucoma (POAG) from 9.5% to 4.4%.
  • •Glaucoma is classified anatomically by the appearance of the anterior chamber angle (open-angle vs. angle-closure) and by etiology (primary, with no identifiable cause, vs. secondary, due to another ocular or systemic condition). Primary open-angle glaucoma (POAG) accounts for ~74% of cases globally, while primary angle-closure glaucoma (PACG) causes a disproportionate share of bilateral blindness, especially in Asia.
  • •The pathophysiology involves three integrated domains: increased resistance to aqueous humor outflow through the trabecular meshwork (the primary driver of IOP elevation in POAG), biomechanical strain on the lamina cribrosa leading to axonal transport failure, and a cascade of mitochondrial dysfunction, oxidative stress, and neuroinflammation that triggers retinal ganglion cell death. The Rho kinase (ROCK) pathway is central to trabecular meshwork dysfunction, and ROCK inhibitors like netarsudil are a novel therapeutic class.
  • •Major risk factors include age (prevalence rises steeply after 40, reaching >10% in those aged ≥80), family history (2- to 4-fold increased risk), African ancestry (3.5-fold higher POAG prevalence vs. White individuals), myopia (each diopter increases risk by ~20%), and corticosteroid use. Protective factors include statin use (12-20% risk reduction) and metformin use (28% risk reduction vs. other antidiabetic agents).
  • •The disease is asymptomatic until moderate-to-severe stages; by the time a patient notices a blind spot, approximately 40% of retinal ganglion cells have been lost. This highlights the critical importance of screening in at-risk populations and the need for lifelong monitoring and treatment.

Evaluation

  • •Suspect glaucoma in any patient aged >40 with risk factors: family history of glaucoma, African or Asian ancestry, high myopia (> -3 D), corticosteroid use, or a history of ocular trauma. Also suspect in patients with unexplained visual field loss, difficulty with night vision, or a sensation of missing steps.
  • •Ask about the onset and duration of symptoms: most patients with POAG are asymptomatic; acute angle-closure glaucoma (AACG) presents with sudden, severe unilateral eye pain, headache, nausea/vomiting, blurred vision, and colored halos around lights. Ask about a history of corticosteroid use (topical, periocular, systemic, inhaled).
  • •Examine visual acuity: central acuity is preserved until advanced disease. Assess pupillary function: a relative afferent pupillary defect (RAPD) suggests asymmetric or unilateral disease, quantifiable with neutral density filters.
  • •Measure intraocular pressure (IOP) by Goldmann applanation tonometry: normal range is 10-21 mmHg, but glaucoma can occur at any IOP. A single normal reading does not rule out glaucoma; consider a diurnal curve with multiple measurements if suspicion is high.
  • •Perform gonioscopy to classify the anterior chamber angle as open, narrow, or closed. Use a four-mirror lens; grade the angle using the Shaffer or Spaeth systems. Gonioscopy is mandatory to differentiate open-angle from angle-closure glaucoma and to identify secondary causes like neovascularization or pigment dispersion.
  • •Evaluate the optic nerve head (ONH) stereoscopically: look for vertical cup-to-disc ratio (CDR) >0.5, asymmetry of CDR >0.2 between eyes, focal or generalized neuroretinal rim thinning (notching), optic disc hemorrhages (small splinter hemorrhages at the rim), and beta-zone peripapillary atrophy.
  • •Assess the retinal nerve fiber layer (RNFL) with red-free light or spectral-domain optical coherence tomography (SD-OCT): look for dark wedge-shaped RNFL defects emanating from the disc margin. SD-OCT provides quantitative RNFL and ganglion cell-inner plexiform layer (GCIPL) thickness; abnormal if below the 1st percentile of age-matched normative data.
  • •Order standard automated perimetry (SAP), typically Humphrey 24-2 SITA-Standard, to assess functional loss. Abnormal if the Glaucoma Hemifield Test (GHT) is outside normal limits and pattern standard deviation (PSD) has p <0.05, or if there is a cluster of ≥3 points at p <0.05 on the pattern deviation plot (Hodapp-Parrish-Anderson criteria). Repeat testing within 1-3 months to confirm persistence; single unreliable tests (false positives >15%, fixation losses >20%) should be repeated.
  • •Integrate structural and functional data for definitive diagnosis: definite glaucoma requires concordant structural damage (RNFL or GCIPL below 1st percentile) and functional loss (SAP abnormality) in corresponding regions. Preperimetric glaucoma: structural defect with normal SAP. Glaucoma suspect: elevated IOP, suspicious disc, or family history without confirmatory OCT or SAP defect.
  • •Consider secondary causes if glaucoma is unilateral, asymmetric, presents at an unusual age (juvenile or very elderly), or if anterior segment findings are suggestive (pigment dispersion, pseudoexfoliation, neovascularization). Order targeted history, gonioscopy, and serology (syphilis, herpes, HLA-B27) as indicated.
  • •In suspected acute angle-closure glaucoma (AACG), recognize the emergency: fixed, mid-dilated pupil, corneal edema, IOP > 40 mmHg, and severe pain. Immediate management (see below) takes precedence over further diagnostic testing. Do not dilate the pupil in a patient with a shallow anterior chamber.
  • •In children, suspect congenital glaucoma if there is epiphora, photophobia, blepharospasm, corneal enlargement (buphthalmos, >12 mm in first year), or Haab striae. Examination under anesthesia is often required; measure IOP with a handheld tonometer and assess the optic nerve.

Management

  • •Set a target intraocular pressure (IOP) individualized to disease severity and rate of progression. For mild disease (visual field MD > -6 dB), target IOP 18-21 mmHg. For moderate disease (MD -6 to -12 dB), target 15-18 mmHg. For severe disease (MD < -12 dB or advanced structural damage), target ≤ 14 mmHg. For normal-tension glaucoma, a 30% reduction from baseline IOP is a common initial goal.
  • •Initiate first-line medical therapy with a prostaglandin analog (latanoprost 0.005%, travoprost 0.004%, or bimatoprost 0.01%): one drop in the affected eye(s) once daily at bedtime. These provide the greatest IOP reduction of any monotherapy class (mean 25-33% from baseline). Bimatoprost may have slightly greater efficacy but causes more conjunctival hyperemia.
  • •Alternatively, offer primary selective laser trabeculoplasty (SLT) as a first-line treatment for mild-to-moderate open-angle glaucoma or ocular hypertension. The LiGHT trial demonstrated SLT is noninferior to drops for IOP control and quality of life at 6 years, with 71% of SLT-treated eyes remaining drop-free. SLT is also cost-effective.
  • •If monotherapy (prostaglandin or SLT) fails to achieve target IOP, add a second agent. Fixed combinations (e.g., latanoprost/timolol, dorzolamide/timolol, brimonidine/brinzolamide) improve adherence. Beta-blockers (timolol 0.5% one drop BID) or alpha-2 agonists (brimonidine 0.2% one drop TID) are common second-line agents. Rho-kinase inhibitors (netarsudil 0.02% one drop QHS) can be added for an additional 3-5 mmHg reduction.
  • •For acute angle-closure glaucoma, administer immediate medical therapy to break the attack: one drop of topical beta-blocker (timolol 0.5%), alpha-2 agonist (brimonidine or apraclonidine), and carbonic anhydrase inhibitor (dorzolamide 2%) immediately. Give systemic acetazolamide 500 mg IV or 500-1000 mg PO as a single dose. If IOP remains >40 mmHg, add osmotic agents: mannitol 20% 1-2 g/kg IV over 30-60 minutes or glycerin 50% PO 1-1.5 g/kg (avoid in diabetics). Do not use pilocarpine until IOP is <40 mmHg.
  • •Perform laser peripheral iridotomy (LPI) as soon as the cornea clears, using argon and/or Nd:YAG laser. LPI creates a full-thickness hole in the peripheral iris to relieve pupillary block. Prophylactic LPI in primary angle-closure suspects reduces the risk of acute attack by 50% over 14 years (NNT=18). If LPI fails, proceed to laser peripheral iridoplasty (LPIp) or surgical intervention (phacoemulsification with goniosynechialysis, or trabeculectomy).
  • •For neovascular glaucoma (NVG), give urgent intravitreal anti-VEGF injection (bevacizumab 1.25 mg or ranibizumab 0.5 mg) to induce regression of iris vessels within 24-72 hours. Perform panretinal photocoagulation (PRP) as soon as media clears to reduce VEGF drive. Add topical IOP-lowering agents (beta-blocker, alpha-agonist, dorzolamide); avoid pilocarpine. If IOP remains >30 mmHg, consider glaucoma drainage device (e.g., Ahmed valve) or cyclophotocoagulation.
  • •Indications for incisional surgery: failure of medical and laser therapy, advanced disease at presentation, intolerance to medications, or pediatric glaucoma. Trabeculectomy with mitomycin C (MMC 0.2-0.4 mg/mL for 2-4 minutes) is the gold-standard procedure. The TAGS trial showed primary trabeculectomy achieves lower mean IOP (12.3 vs 14.8 mmHg) and better visual field preservation than medical therapy at 5 years.
  • •Tube shunts (Baerveldt or Ahmed) are preferred when trabeculectomy is high-risk (e.g., failed prior surgery, uveitic glaucoma, neovascular glaucoma). The PTVT study found similar 5-year failure rates for tube shunt (38%) and trabeculectomy (46%) in virgin eyes. For uveitic glaucoma, glaucoma drainage devices have better long-term success than trabeculectomy.
  • •Minimally invasive glaucoma surgery (MIGS) is reserved for mild-to-moderate disease, often combined with cataract surgery. The HORIZON trial showed cataract surgery with Hydrus microstent reduced IOP (14.6 vs 15.4 mmHg) and slowed visual field progression compared to cataract surgery alone at 5 years. Phacogoniotomy (phaco + goniosynechialysis + goniotomy) is noninferior to phacotrabeculectomy for angle-closure glaucoma with cataract.
  • •Monitor patients lifelong: IOP at 3-6 month intervals, visual field testing annually (or semiannually for advanced disease), and OCT of RNFL and GCIPL every 6-12 months. Assess adherence at every visit; nonadherence is a leading cause of progression. Escalate therapy if IOP exceeds target, visual field progression is confirmed (≥2 dB MD loss over 2 years), or structural loss accelerates.
  • •What NOT to do: Do not use beta-blockers (timolol) in patients with asthma, COPD, bradycardia, or heart block. Do not use brimonidine in children <6 years (risk of CNS depression and apnea). Do not perform laser iridotomy alone for plateau iris without iridoplasty. Do not use oral acetazolamide long-term without monitoring for metabolic acidosis, hypokalemia, and rare aplastic anemia. Do not perform filtering surgery alone for NVG without anti-VEGF and PRP (failure rate >80% at 6 months).
  • •Refer to a glaucoma specialist for: advanced disease at presentation (MD < -12 dB), normal-tension glaucoma with progression despite low IOP, pediatric glaucoma, uveitic glaucoma, neovascular glaucoma, or need for incisional surgery. Refer urgently (same day) for acute angle-closure or neovascular glaucoma.
  • •For pediatric glaucoma: First-line therapy is surgery (goniotomy or trabeculotomy for primary congenital glaucoma). Medical therapy is adjunctive: use timolol 0.25% (not 0.5%) or latanoprost 0.005%. Brimonidine is contraindicated in children <6 years. Perform examination under anesthesia for diagnosis. Glaucoma drainage devices have a 78% 1-year success rate but often require revisions.
  • •For pregnancy: IOP typically decreases in the second and third trimesters. Latanoprost is FDA Category C (avoid in third trimester due to theoretical risk of uterine contraction). Timolol 0.25% with punctal occlusion is preferred. Brimonidine is Category B and may be used. Avoid systemic acetazolamide in the first trimester. All glaucoma medications should be continued through labor; consider instrumental-assisted delivery to avoid IOP spikes.

Board Review — High Yield

  • •Primary Open-Angle Glaucoma (POAG), Most common form (~74% of cases globally); open angle on gonioscopy, elevated IOP (>21 mmHg) in most, but normal-tension glaucoma is a subtype with IOP ≤21 mmHg
  • •Hodapp-Parrish-Anderson Staging, Classifies visual field loss into mild (MD > -6 dB), moderate (-6 to -12 dB), and severe (< -12 dB); used to set target IOP (18-21, 15-18, ≤14 mmHg respectively)
  • •LiGHT Trial, Primary selective laser trabeculoplasty (SLT) is noninferior to drops for IOP control and quality of life at 6 years, with 71% of SLT patients remaining drop-free; SLT is cost-effective and guideline-endorsed first-line
  • •TAGS Trial, In advanced glaucoma (MD < -12 dB), primary trabeculectomy achieves lower mean IOP (12.3 vs 14.8 mmHg) than medical therapy at 5 years with similar quality of life; no difference in visual field progression
  • •Acute Angle-Closure Glaucoma, Emergency with IOP >40 mmHg, corneal edema, fixed mid-dilated pupil, pain; treat with topical beta-blocker + alpha-agonist + dorzolamide + IV acetazolamide; definitive laser is peripheral iridotomy; do not use pilocarpine until IOP <40 mmHg
  • •Normal-Tension Glaucoma, POAG subtype with IOP ≤21 mmHg; associated with disc hemorrhages, myopia, migraine, sleep apnea; target IOP is 30% reduction from baseline; genetic mutations in OPTN and TBK1 impair mitophagy
  • •Pseudoxfoliation Glaucoma, Fibrillar material obstructs trabecular meshwork; faster progression than POAG (mean MD loss -0.8 vs -0.3 dB/year); LOXL1 gene risk variant; zonular weakness increases surgical risk, use capsular tension rings during phaco
  • •Neovascular Glaucoma, Caused by retinal ischemia (CRVO, PDR); urgent intravitreal anti-VEGF (bevacizumab 1.25 mg) within 24 hours, then PRP; do not filter alone (failure >80%); Ahmed valve if IOP remains >30 mmHg
  • •Pediatric Glaucoma, Presents with triad of epiphora, photophobia, blepharospasm; buphthalmos (corneal diameter >12 mm in year 1); first-line is goniotomy/trabeculotomy; brimonidine contraindicated <6 years; prognosis depends on age at diagnosis (<1 month best)
  • •Neuroprotection and Ferroptosis, Retinal ganglion cells die by ferroptosis (iron-dependent lipid peroxidation) in some models; inhibitors like liproxstatin-1 rescue RGCs in experimental glaucoma, but no neuroprotective agent is FDA-approved for clinical use

Deep Dive — Evidence Details

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