Open Angle Glaucoma

6 Interesting Facts of Open Angle Glaucoma

  1. Primary open-angle glaucoma is a chronic, progressive optic neuropathy in adults characterized by optic nerve damage and retinal ganglion cell loss
    • Clinical features include an open anterior chamber angle and cupping of optic nerve head with corresponding loss of visual field
  2. Elevated intraocular pressure is a consistent risk factor, but it is no longer a defining characteristic
    • Primary open-angle glaucoma can occur when intraocular pressure is normal
  3. Patients are typically asymptomatic, even with more advanced disease
  4. Diagnosis of glaucoma is based on finding characteristic optic nerve changes associated with corresponding visual field defects, regardless of intraocular pressure
  5. Current treatments are aimed at reducing intraocular pressure by medical therapies, laser modalities, or surgical management
    • Reducing intraocular pressure slows the onset and progression of glaucoma
  6. Prognosis depends on disease severity at time of diagnosis and on patient adherence to treatment
    • Left untreated, disease results in gradual visual field loss, which may progress to an island of central vision and, ultimately, complete loss of vision


  • Normal intraocular pressure value does not rule out glaucoma
  • Omission of gonioscopy in evaluation of suspected glaucoma may lead to incorrect diagnosis
  • Refer patients who have high risk for glaucoma for complete eye examination by an eye specialist (eg, those with diabetes, those with family history of glaucoma, African American people aged 50 years or older, Hispanic American people aged 65 years or older)
    • Early detection and treatment are key to protecting vision

Glaucoma is a group of optic neuropathies characterized by optic disk damage and associated visual field loss; increased intraocular pressure is a major modifiable risk factor

Leading cause of global irreversible blindness 

2 major subtypes: angle closure and open angle, based on status of eye’s drainage system

Primary open-angle glaucoma is a chronic, slowly progressive optic neuropathy in adults that is characterized by optic nerve damage and retinal ganglion cell loss 

It includes:

Open anterior chamber angles (junction between iris and cornea)

Evidence of optic nerve damage from either or both:

Structural abnormalities of optic disk (cupping) or retinal nerve fiber layer

Visual field abnormality

No identifiable secondary cause (eg, uveitis, trauma, pigment dispersion)

Elevated intraocular pressure is a consistent risk factor for glaucoma, but it is no longer a defining characteristic 

Nearly 40% of patients with primary open-angle glaucoma may not have elevated intraocular pressures 

Generally bilateral; severity may be asymmetrical between eyes

Typically worsens over many months to years; left untreated, ultimately results in irreversible blindness


  • Primary 
    • Idiopathic
  • Secondary 
    • Develops owing to other ocular or systemic condition (eg, trauma, tumor, uveitis)

Clinical Presentation


  • Patients are typically asymptomatic, even with more advanced disease
    • Painless, slow, progressive loss of peripheral vision
    • Visual field loss is typically peripheral and asymmetrical, allowing compensation from overlapping images from other, less affected eye
    • About 50% of glaucoma cases are undiagnosed, even in developed countries 

Physical examination

  • Optic disk changes may be noted on direct ophthalmoscopic examination (glaucomatous optic neuropathy)
    • Increased cup to disk ratio; may be asymmetrical
    • Focal notching of optic disk rim
    • Optic disk splinter hemorrhages (ie, Drance hemorrhages; more common in low-tension glaucoma; usually a sign of worsening disease)
  • Elevated intraocular pressure by tonometry (approximately 60% of patients) 
  • Reduced visual acuity (on Snellen chart) in advanced disease
  • Visual field testing by confrontation typically finds normal results, except in very advanced disease (in which a central island of vision may develop)
  • Relative afferent pupillary defect (ie, Marcus Gunn pupil) if optic neuropathy is asymmetrical


  • Degenerative damage to optic nerve 
    • Acquired focal or general loss of neural rim tissue (described as cupping) is characteristic of glaucomatous optic neuropathy
    • Causation remains unclear; thought to be multifactorial (structural and vascular)
  • Intraocular pressure elevation
    • Important risk factor in development and progression of glaucomatous optic neuropathy, although not part of the definition of open-angle glaucoma
      • Intraocular pressure: a balance between aqueous humor production by ciliary body and drainage, primarily through trabecular meshwork located at anterior chamber angle (junction of iris and cornea)
        • Trabecular meshwork thought to be site of resistance to outflow in open-angle glaucoma, resulting in increased intraocular pressures transmitted to optic nerve
      • Individual susceptibility to levels of intraocular pressure that cause optic nerve damage is variable
        • Patients with relatively high pressures may never develop glaucomatous damage
        • Patients with pressures in the reference range may develop glaucomatous optic neuropathy

Risk factors and/or associations

  • Prevalence increases with older age 
  • Men are slightly more likely to have primary open-angle glaucoma than women (odds ratio, 1.36) 
  • Family history of open-angle glaucoma in first-degree relative increases risk
    • Having a sibling with glaucoma is associated with an odds ratio of 3.7 for development of open-angle glaucoma 
  • Prevalence is highest in people of West African, Afro-Caribbean, or Hispanic/Latino origin 
    • Prevalence is 3 times higher in African American people and Hispanic people of Mexican ancestry compared with non-Hispanic white people
    • Leading cause of blindness in African American people
Other risk factors/associations
  • Ocular 
    • Intraocular pressure elevation
      • Important modifiable risk factor for development and progression of glaucomatous optic neuropathy (and, to date, the only known one)
    • Central corneal thickness
      • Thinner central cornea is an independent risk factor associated with primary open-angle glaucoma; association may be related to inability to measure intraocular pressure accurately in these patients with current technology
    • Low ocular perfusion pressure
      • Lower blood flow at optic nerve head may contribute to progressive damage
    • Myopia
      • Longer axial length of ocular globe may weaken scleral support at optic nerve
    • Larger cup to disk ratio
  • Systemic 
    • Type 2 diabetes mellitus
      • Possibly due to microvascular changes in optic nerve
    • Migraine and peripheral vasospasm
      • May decrease autoregulation of optic disk blood flow; more commonly found in patients with open-angle glaucoma and intraocular pressure in reference range
    • Steroid use
      • Increased risk of intraocular pressure elevation in some patients
    • Blood pressure alterations
      • Antihypertensive medication use for systemic hypertension may cause nonphysiologic hypotension with lower diastolic perfusion pressure, resulting in decreased perfusion of optic nerve
        • Exaggerated nocturnal blood pressure reduction may accelerate glaucomatous damage owing to drop in ocular perfusion pressure (ischemia-reperfusion insult)

How is Open angle glaucoma diagnosed?

  • Diagnosis is based on complete history (ie, medical, ocular, family) and comprehensive bilateral eye evaluation by ophthalmic practitioner, including the following key, specific elements:
    • Patient history, including: 
      • Family history of glaucoma
      • Systemic history (eg, diabetes, migraine headaches, vasospasm, asthma, chronic obstructive pulmonary disease)
      • Ocular history (eg, trauma, prior eye surgery)
      • Medications, with special attention to corticosteroid use
    • Best corrected visual acuity, distance and near
    • Observance of pupils for reactivity and relative afferent pupillary defect 
      • Asymmetry in disease severity can cause a relative afferent pupillary defect 
    • Anterior segment of eye examination (ie, cornea, iris, lens, anterior chamber) by slit lamp biomicroscopy for evidence of:
      • Narrow anterior chamber angles (eg, shallow peripheral anterior chamber depth or crowded anatomy at angle between iris and cornea), which raise concern for angle-closure glaucoma
      • Secondary causes of elevated intraocular pressure (eg, neovascularization, inflammation, pigment dispersion, hemorrhage, acquired or congenital abnormalities of cornea/angle/iris)
    • Intraocular pressure measurement bilaterally by tonometry 
      • Goldmann applanation tonometry is most accepted method
      • No specific intraocular pressure cutoff for diagnosis of open-angle glaucoma
        • Great individual variability exists in susceptibility to optic nerve damage from elevated intraocular pressures, and normal-tension glaucoma is possible
    • Anterior chamber angle measurement by gonioscopy
      • Diagnosis of primary open-angle glaucoma requires open angle on gonioscopy 
        • Exclude diagnosis of angle-closure glaucoma or other secondary causes (eg, peripheral anterior synechiae, angle recession, neovascularization, inflammatory precipitates)
        • Other modalities for evaluation include ultrasonographic biomicroscopy and spectral domain optical coherence tomography
    • Optic nerve head and retinal nerve fiber layer examination 
      • Can be viewed by direct ophthalmoscopy; however, ophthalmic providers typically use indirect ophthalmoscopy with slit lamp biomicroscopy and a handheld lens and view through dilated pupil, providing a stereoscopic view
      • Observe for features of glaucomatous optic nerve damage, including:
        • Cupping, due to progressive neuroretinal rim loss, is the structural hallmark of glaucoma 
          • Vertical elongation of cup with associated thinning of neuroretinal rim width
            • In healthy eyes, the neuroretinal rim has characteristic rim widths and follows the ISNT rule: 
              • Neuroretinal rim is broadest inferiorly (I), followed by superiorly (S) and nasally (N), and then thinnest temporally (T)
            • In glaucoma, the earliest loss usually occurs in inferotemporal and superotemporal areas
        • Excavation of central cup (loss of retinal ganglion cell axons and deformation of supporting connective tissues)
        • Notching or thinning of neural rim
        • Hemorrhages of optic nerve
        • Thinning of retinal nerve fiber layer
      • Document appearance of optic nerve structure to allow serial comparison 
        • 2 useful adjuncts can provide different, complementary information about optic nerve status
          • Stereoscopic photography: documents qualitative optic nerve head appearance
          • Computer-based imaging: provides quantitative information about optic nerve head and retinal nerve fiber layer
            • Supplements clinical examination of optic nerve
            • Can detect structural changes before functional changes occur
              • Measure thinning of retinal nerve fiber layer and distinguish glaucomatous changes compared with database of age-matched reference values
              • Interpret in concert with findings from clinical examination and other supplementary testing 
            • Computer-based imaging includes:
              • Confocal scanning laser ophthalmoscopy
              • Optical coherence tomography
              • Scanning laser polarimetry
        • Drawing or nonstereoscopic photograph of optic nerve head can be used for documentation, but it is less desirable
    • Fundus examination through dilated pupil (if feasible) to search for other abnormalities that may cause optic nerve damage and/or visual field defects (eg, macular degeneration, retinovascular occlusion, disk drusen, retinal detachment, other retinal disease) 
    • Central corneal thickness measurement by corneal pachymetry
      • Reference thickness is considered 540 to 560 µm; thin cornea has higher risk; thicker cornea has lower risk
    • Visual field testing
      • Automated static threshold perimetry with white-on-white stimuli remains the gold standard 
  • Diagnose glaucoma based on characteristic optic nerve changes associated with corresponding visual field defects, regardless of intraocular pressure 


  • Ultrasonographic corneal pachymetry 
    • Measures central corneal thickness by using high-frequency sound waves; requires direct corneal contact by ultrasonic probe
    • Aids in interpretation of intraocular pressure readings and stratifying risk for ocular damage
      • Measurement of intraocular pressures (especially by applanation tonometry) may be affected by central corneal thickness (ie, thicker central corneal thickness may result in artifactually high intraocular pressure and vice versa)
      • Thinner central cornea may be independent risk factor for development of primary open-angle glaucoma

Functional testing

  • Automated static perimetry
    • Test of visual field function that determines minimum threshold to detect presence of static, constant-sized, white light stimulus in various parts of visual field 
    • Glaucoma damage typically has loss of sensitivity to light at characteristic locations in visual field (eg, nasal step, arcuate scotoma)
      • At near end-stage disease, only central island of vision remains
    • Visual field loss may not be detected until after 30% of retinal ganglion cells have been lost 


General explanation
  • Measurement of intraocular pressure
  • Goldmann applanation tonometry is preferable method 
    • Estimates force required to flatten a fixed area of cornea
    • Consists of plastic biprism which gently contacts cornea and creates 2 semicircles when viewed through slit lamp (cobalt blue light and fluorescein are used for visualization) 
      • Tension dial on instrument is turned until ends of semicircles are aligned and touching; reading is then obtained from dial
  • Required for screening and management of patients with known or suspected glaucoma



  • Penetrating globe injuries


  • Corneal defects
  • Infection (unless using sterile cover)
  • Uncooperative patient (may induce injury)
  • Corneal abrasions
Interpretation of results 
  • Normal intraocular pressure has been defined as 10 to 21 mm Hg, but this definition has shortcomings 
    • Intraocular pressure in the population does not follow a Gaussian (normal) distribution
    • Glaucomatous and nonglaucomatous intraocular pressure curves display significant overlap
    • Intraocular pressure shows diurnal fluctuation, and elevation can occur only intermittently
      • Several pressure measurements (over several months at different times of day) are recommended before clinical intervention
  • Great individual variation exists in susceptibility of optic nerve to effects of intraocular pressure 
    • Intraocular pressure greater than 21 mm Hg has poor predictive value as a cutoff for screening or diagnosis of primary open-angle glaucoma
  • In general, prevalence of primary open-angle glaucoma increases as level of intraocular pressure increases; reduction of intraocular pressure decreases risk of visual field progression in open-angle glaucoma 
General explanation 
  • Ophthalmologic technique to visualize structures in anterior chamber angle (iridocorneal angle) of eye and determine whether angle is open or closed
  • A handheld, mirrored instrument (goniolens) is placed on cornea to examine angle of eye in conjunction with slit lamp
  • Required in all patients for diagnosis of glaucoma
    • Exclude diagnosis of angle-closure glaucoma
    • Determine presence of secondary causes for elevated intraocular pressure (eg, angle recession, pigment dispersion, peripheral anterior synechiae, neovascularization, inflammation)
  • Immediate postoperative period
  • Suspicion for open globe injury
  • Corneal abrasions
  • External ocular infection
  • Hyphema
Interpretation of results 
  • Diagnosis of primary open-angle glaucoma requires open anterior chamber angles and absence of secondary causes

Differential Diagnosis

  • Differential diagnosis for clinical presentations of visual field loss 
    • Optic nerve causes
      • Ischemic optic neuropathy
        • Due to low perfusion; may involve anterior or posterior portion of optic nerve
        • Arteritic ischemic optic neuropathy
          • Ischemic optic neuropathy resulting from vasculitis of short posterior ciliary artery and resultant optic nerve head infarction; occurs in patients older than 50 years
            • Can occur as ocular manifestation of giant cell (temporal) arteritis, an ocular emergency requiring rapid treatment with high-dose systemic steroids
              • Systemic symptoms include headache, scalp tenderness, jaw claudication, fever, weight loss, myalgias, and fatigue
          • Presents with acute, painless, unilateral decreased visual acuity and/or visual field loss
          • Diagnose clinically by afferent pupillary defect and optic disk edema (pale or hyperemic); flame hemorrhages may surround disk
            • Laboratory findings include elevated erythrocyte sedimentation rate (often 70-100 mm/minute), elevated platelet count, and elevated C-reactive protein level; confirm by temporal artery biopsy
      • Compressive optic neuropathy
        • Mechanical compression of optic nerve due to aneurysms or orbital/chiasmal masses (eg, pituitary adenomas, meningiomas)
        • Can lead to gradual, progressive visual field loss and optic nerve damage
        • Differences from glaucoma include that the following are more common in compressive optic neuropathy: normal intraocular pressure, decreased visual acuity, and unilateral involvement; proptosis (exophthalmos) can be present
        • Optic disk appearance and visual field loss depend on location of lesion; usually more pallor and less cupping of optic disk, degree of cupping disproportionate to visual field defect, and visual field loss patterns not consistent with glaucomatous field loss
        • Diagnose by indirect ophthalmoscopy and neuroimaging (eg, MRI) of orbit and chiasm
    • Retinal causes
      • Retinal detachment
        • May present as defect in visual field; typically starts at periphery and may progress slowly
        • Unlike in glaucoma, flashes and floaters are frequently noted and optic disk and intraocular pressures are usually normal
        • Diagnostic tools include indirect ophthalmoscopy and ocular ultrasonography
      • Retinal vascular occlusions
        • Cause unilateral, painless vision loss
          • Visual field losses may be partial, similar to those of glaucoma, but are typically acute in onset
        • Arterial (Related: Retinal artery occlusion)
          • Due to decreased retinal perfusion
            • Branch retinal artery occlusions can result in visual field defects corresponding to damaged retinal tissue
          • Differences from glaucoma can include the following: optic nerve may show more pallor than cupping in the affected neural rim area; in acute phase, whitened areas may be noted on retina along arterial distribution; and cherry-red spot may be noted in acute central retinal artery occlusion
          • Diagnostic tools include indirect ophthalmoscopy and fluorescein angiogram
        • Venous (Related: Retinal vein occlusion)
          • Due to venous stasis resulting in retinal edema, hemorrhage, and potential ischemia
          • Differentiated by retinal hemorrhages, tortuous retinal vessels, macular edema, and no optic nerve cupping
          • Diagnosed by indirect ophthalmoscopy; confirmed by fluorescein angiography
    • Central nervous system causes
      • Multiple sclerosis
        • Can cause unilateral vision loss secondary to optic neuropathy
        • Visual field defects are often bilaterally congruous on testing if due to brain lesions
        • Optic disk is usually normal without pallor or cupping (inflammation typically retrobulbar)
        • Diagnosis is confirmed by MRI and cerebrospinal fluid analysis
      • Stroke (Related: Ischemic stroke)
        • Usually visual deficits are bilateral with congruous visual field defects
        • Optic nerve is without pallor or cupping
        • Diagnosis is based on MRI/CT imaging of brain
  • Differential diagnosis for cupped/abnormal optic disks
    • Optic disk coloboma: congenital abnormality of optic disk
    • Congenital optic pit: congenital excavation of optic disk
    • Morning glory disk: congenital malformation of optic nerve
    • Myopic disks: optic disks can be significantly larger with high myopia; may be associated with visual field defects that are not usually progressive
    • Physiologic cupping: normal large optic disk with large cup to disk ratio; should be symmetrical

Treatment Goals

  • Reduce intraocular pressure to reduce risk of development and progression of visual field defects
  • Minimize adverse effects of treatment and impact on vision, health, and quality of life

Recommendations for specialist referral 

  • Refer patients at high risk for glaucoma to eye care specialist for evaluation (eg, older age, African American ancestry, family history of glaucoma, steroid use) 
  • Refer all patients with known or suspected glaucoma to ophthalmologist for evaluation, treatment, and management 
  • Refer patients who present with significant vision loss or blindness to vision rehabilitation 

Treatment Options

Reduce intraocular pressure to lower risk of development and slow progression of primary open-angle glaucoma, including normal-tension open-angle glaucoma 

  • Estimate target intraocular pressure 
    • A value or range at which disease progression is believed to be sufficiently slowed to reduce visual field loss
      • Established by multiple factors, including patient age, life expectancy, pretreatment pressure, and extent of optic nerve damage
    • Initially, reduce intraocular pressure to 20% to 30% below baseline 
      • Adjust up or down as indicated by disease course and severity

Methods for lowering intraocular pressure include topical and oral medications, laser therapy, and surgery; consider effects of treatment and quality of life in treatment decisions 

  • Medical treatment
    • Most common initial intervention
    • Choice of medication is based on cost, adverse effects, dosing schedules, and degree of pressure lowering needed; options include: 
      • Prostaglandin analogues: most frequently prescribed initial medication and most efficacious
      • β-blockers
      • α₂-adrenergic agonists
      • Carbonic anhydrase inhibitors, topical and oral
      • Cholinergics
      • Rho kinase inhibitors
    • Treat initially with prostaglandin analogue unless other conditions preclude use 
      • If monotherapy is insufficient to control intraocular pressure, replace with or add a medication with different mechanism of action
    • Use of combination drugs can increase patient adherence when needing more than 1 medication; also decreases exposure to preservatives (eg, dorzolamide-timolol, brimonidine-brinzolamide, brimonidine-timolol)
    • Inform patient about lacrimal duct occlusion or eyelid closure for 2 minutes after drug installation to limit systemic absorption when using eye drops
  • Laser trabeculoplasty
    • May be used as initial treatment, adjunct to medical therapy, or for patients who cannot tolerate or adhere to medication 
    • Reduction of intraocular pressure not typically immediate; evolves over several days to weeks
  • Incisional glaucoma surgery
    • Typically used when patient is refractory to medication and/or laser therapies 
    • Techniques that bypass aqueous humor externally to collect in subconjunctival space
      • Trabeculectomy
      • Aqueous shunts; role of such shunts has been expanding in recent years
    • A multicenter randomized clinical trial found that both techniques result in similar intraocular pressure reduction, requirements for supplemental medical therapy, serious complications, and vision loss at 5 years 
  • Other procedures to lower intraocular pressure
    • Microinvasive glaucoma surgery (minimally invasive glaucoma surgery) 
      • Newer group of surgical procedures that result in less trauma to ocular tissues; good safety profile
        • Intended to fill gap between medical therapy and more invasive incisional glaucoma surgery
        • Use ab interno approach (ie, from inside the eye); usually performed in conjunction with cataract surgery
        • Examples include:
          • iStent procedure: titanium microstent is implanted into Schlemm canal using preloaded inserter; bypasses the trabecular meshwork and directs aqueous to suprachoroidal space without bleb formation
          • Trabectome procedure: uses microelectrocautery to remove strip of trabecular meshwork
      • Long-term data are limited; procedures appear less effective at lowering intraocular pressure than trabeculectomy and aqueous shunt surgery, but they have better safety profiles in the short term 
    • Combined surgeries
      • Patients with glaucoma who have visually significant cataracts have various surgical treatment options
        • Cataract surgery with intraocular lens implantation alone can result in average of 2 mm Hg reduction in intraocular pressure 
        • Decision on whether to perform glaucoma or cataract surgery first, or whether to combine them, is made by ophthalmologist and patient after consideration of individual risks and benefits 
      • Combining cataract and glaucoma surgery has potential benefits, including: 
        • Protection against intraocular pressure rise that can complicate cataract surgery alone
        • Long-term glaucoma control with a single operation
        • Eliminate possible subconjunctival bleb failure if glaucoma surgery is performed before cataract surgery
    • Nonpenetrating glaucoma surgery (eg, deep sclerectomy, viscocanalostomy) 
      • Alternatives to trabeculectomy and aqueous shunt devices (full-thickness filtering procedures) with fewer complications; precise role undetermined 
      • Enhance natural aqueous outflow channels by creating filtration membrane (trabeculo-Descemet membrane) allowing passage into intrascleral space
      • High degree of surgical difficulty
    • Cyclodestructive surgery 
      • Ablation (ie, coagulation) of ciliary processes to decrease intraocular pressure by decreasing production of aqueous humor; classically used for refractory glaucomas
      • Procedures include:
        • Transscleral diode-laser cyclophotocoagulation: performed externally through sclera to ciliary body; option for eyes with limited visual potential or poor candidates for incisional ocular surgery 
        • Endoscopic diode-laser cyclophotocoagulation: performed internally with direct visualization of ciliary body process; previously for refractory cases, now being done in combination with cataract surgery in some patients with less advanced glaucoma 

Drug therapy 

  • Prostaglandin analogues
    • Increase outflow through uveoscleral pathway
    • Adverse effects include lengthening of eyelashes, periocular hyperpigmentation, conjunctival injection, keratitis, periorbitopathy (ie, deepening of superior lid sulcus, ptosis, periorbital fat atrophy)
    • Most frequently prescribed initial medication; most efficacious, well tolerated, and offers once daily dosing 
      • Latanoprost
        • Latanoprost Ophthalmic drops, solution; Adults: 1 drop (1.5 mcg) applied to each affected eye every evening.
      • Bimatoprost
        • Bimatoprost Ophthalmic drops, solution; Adults: Instill 1 drop to the affected eye(s) once daily in the evening.
      • Travoprost
        • Travoprost Ophthalmic drops, solution; Adults and Adolescents >= 16 years: Apply 1 drop to each affected eye qPM.
  • β-blockers
    • Decrease aqueous humor production
    • Adverse effects include keratitis, bronchospasm (with nonselective β-blockers), bradycardia, and hypotension
    • Caution in patients with asthma, chronic obstructive pulmonary disease, or cardiac conditions
      • Betaxolol
        • Betaxolol Hydrochloride Ophthalmic drops, solution; Adults: Instill 1 to 2 drops in the affected eyes twice daily.
      • Timolol
        • Twice daily formulation (Timoptic)
          • Timolol Maleate Ophthalmic drops, solution; Children and Adolescents 2 years and older: Instill 1 drop of a 0.25% solution in affected eye(s) twice daily. Dosage may be increased to 1 drop of a 0.5% solution twice daily.Timolol Maleate Ophthalmic drops, solution; Children and Adolescents 2 years and older: Instill 1 drop of a 0.25% solution in affected eye(s) twice daily. Dosage may be increased to 1 drop of a 0.5% solution twice daily.
        • Once daily formulation (Istalol, Timoptic-XE)
          • Timolol Maleate Ophthalmic drops, solution; Adults: Instill 1 drop of a 0.5% solution in affected eye(s) every morning. If the IOP is not controlled, other agent(s) can be instituted.
          • Timolol Maleate Ophthalmic gel forming solution; Adults: Instill 1 drop of a 0.25% solution in affected eye(s) once daily. Dosage may be increased to 1 drop of a 0.5% solution once daily.
  • α₂-adrenergic agonists
    • Decrease aqueous humor production
    • Adverse effects include ocular allergy, dry mouth, hypotension, and conjunctival hyperemia
      • Apraclonidine
        • Apraclonidine Hydrochloride Ophthalmic drops, solution;  Adults: 1—2 drops into the affected eye(s) 3 times daily. Wait 5 minutes before or after using apraclonidine to instill other glaucoma agents.
      • Brimonidine
        • Brimonidine Tartrate Ophthalmic drops, solution; Adults, Adolescents, and Children 2 years and older: 1 drop to affected eye(s) 3-times a day (about every 8 hours).
  • Carbonic anhydrase inhibitors
    • Decrease aqueous humor production
    • Topical
      • Adverse effects include ocular irritation and metallic taste
        • Brinzolamide
          • Brinzolamide Ophthalmic drops, suspension; Adults: Instill 1 drop in the affected eye(s) 3 times daily; may be used concomitantly with other topical agents.
        • Dorzolamide
          • Dorzolamide Hydrochloride Ophthalmic drops, solution; Adults, Adolescents, Children, Infants, and Neonates >= 1 week: Instill 1 drop of a 2% solution into the affected eye(s) 3 times daily. Safety and efficacy of treatment greater than 3 months not established in pediatric patients.
    • Oral
      • Adverse effects include Stevens-Johnson syndrome, electrolyte imbalance, depression, malaise, renal calculi, diarrhea, paresthesias, blood dyscrasias, and metallic taste
      • Acetazolamide
        • Acetazolamide Oral capsule, extended-release; Adults: 500 mg PO twice daily. Max: 1 g/day.Acetazolamide Oral capsule, extended-release; Adults: 500 mg PO twice daily. Max: 1 g/day.
  • Cholinergics
    • Increase aqueous outflow through trabecular meshwork
    • Adverse effects include blurred vision, poor night vision, eye pain, and headache
    • Rarely used anymore; other medications offer better efficacy with fewer adverse effects
      • Pilocarpine
        • Pilocarpine Hydrochloride Ophthalmic drops, solution; Adults, Adolescents, and Children >= 2 years: Instill 1 drop into eye(s) up to 4 times per day.
  • Rho kinase inhibitor
    • Netarsudil
      • Netarsudil Ophthalmic drops, solution; Adults: Instill 1 drop into affected eye(s) once daily in the evening. If a dose is missed, continue with the next dose in the evening; twice daily dosing is not well tolerated and is not recommended. If more than 1 topical ophthalmic drug is being used, the drugs should be administered at least 5 minutes apart.
  • Combination topical medications
    • Brimonidine-timolol
      • Brimonidine Tartrate, Timolol Maleate Ophthalmic drops, solution; Adults, Geriatric, Adolescents, and Children >= 2 years: 1 drop to affected eye(s) twice daily (q12h).
    • Dorzolamide-timolol
      • Dorzolamide Hydrochloride, Timolol Maleate Ophthalmic drops, solution; Adults, Adolescents, and Children >= 2 years: 1 drop in affected eye(s) twice daily.
    • Brinzolamide-brimonidine
      • Brinzolamide, Brimonidine Tartrate Ophthalmic drops, suspension; Adults, Adolescents, and Children >=2 years: 1 drop to affected eye(s) 3 times daily. Separate administration of other ophthalmic drugs by at least 5 minutes.

Nondrug and supportive care

Educate patient and family members/caregivers on management of the disease 

  • Discuss nature of disease process, severity, prognosis, management options, and goals
  • Inform patient about lacrimal duct occlusion or eyelid closure to limit systemic absorption when using eye drops

Complementary and alternative medicine approaches

  • Herbal medicines or nutritional supplements lack scientific evidence for benefit in treating glaucoma 
  • No support for increased benefit and/or decreased risk has been found for use of cannabis to treat glaucoma compared with conventional medicines 
Laser trabeculoplasty

General explanation

  • Lowers intraocular pressure by using laser energy directed at trabecular meshwork to increase outflow of aqueous humor
  • Typically performed with argon, diode, or a frequency-doubled Nd:YAG laser (neodymium:yttrium-aluminum-garnet) 
  • Reduction of intraocular pressure, not typically immediate; evolves over several days to weeks 


  • Initial therapy for open-angle glaucoma
  • Open-angle glaucoma uncontrolled by medication
  • Alternative for patients at high risk for nonadherence to medical therapy


  • Angle-closure glaucoma
  • Hazy media reducing visualization of trabecular meshwork
  • Urgent need to control intraocular pressure
  • Serious complication from laser trabeculoplasty in other eye (elevated intraocular pressure)


  • Intraocular pressure elevation
  • Decreased visual acuity
  • Bleeding
  • Peripheral anterior synechiae
  • Iritis

General explanation 

  • Surgical procedure to lower intraocular pressure by providing alternative drainage system for aqueous humor
  • Fistula is created between anterior chamber and subconjunctival space beneath partial-thickness scleral flap, allowing aqueous fluid to filter into subconjunctival bleb
    • Chemotherapeutic antimetabolite agents (eg, fluorouracil, mitomycin) are typically applied to limit fibrosis in the area so that it remains patent


  • Generally indicated when medications and appropriate laser are insufficient to control disease
  • Considered as initial therapy in selected cases (eg, advanced disease at presentation or inability to adhere to medical regimen)


  • Intraocular hemorrhage
  • Shallow anterior chamber
  • Infection; can occur years after surgery if bleb is thin walled
  • Cataract
  • Hypotony
Aqueous shunts

General explanation

  • Synthetic, surgically implanted devices to aid in controlling intraocular pressure
    • Also referred to as tube shunts, glaucoma drainage devices, and setons
  • Consist of a tube that diverts aqueous humor to an end plate placed under conjunctiva in equatorial region of eye
    • A fibrous capsule develops around the end plate and provides the primary resistance to flow
    • Shunts may be nonvalved or valved, allowing mechanism to limit flow through shunt


  • Traditionally, used in medically uncontrolled cases in which trabeculectomy had failed or was deemed unlikely to succeed (eg, conjunctival scarring from previous surgery, neovascular glaucoma, uveitic glaucoma) 
  • Role has been expanding in recent years 
    • Concern about bleb-related complications has contributed to expanded use as alternative to trabeculectomy 


  • Corneal injury (eg, endothelial erosion, corneal edema)
  • Erosion of tube through conjunctiva 
  • Hypotony
  • Intraocular hemorrhage
  • Infection
  • Cataract


  • Monitor optic nerve structure and function for further damage and decrease target intraocular pressure if deterioration occurs 
    • Rate of progression over time is fundamental in treatment decisions
  • Follow-up guidelines for primary open-angle glaucoma management (American Academy of Ophthalmology) 
    • Clinical examination, as well as optic nerve head and visual field assessment as indicated
    • Target intraocular pressure achieved
      • No damage progression
        • Duration of control
          • 6 months or less: provide follow-up in approximately 6 months
          • More than 6 months: provide follow-up in approximately 12 months
      • Damage progression: provide follow-up in approximately 1 to 2 months
      • Many experts provide follow-up more frequently, because ongoing damage may not be realized for months to years after what was thought to be controlled intraocular pressure
    • Target intraocular pressure not achieved
      • No damage progression: provide follow-up in approximately 3 to 6 months
      • Damage progression: provide follow-up in approximately 1 to 2 months


  • Optic nerve damage
  • Visual field defects
  • Blindness


  • Prognosis depends on when disease is diagnosed and degree of patient adherence to treatment
    • Advanced disease at time of diagnosis and nonadherence to treatment increase risk of disease progression 
    • Approximately 14% of patients who receive full treatment will nonetheless have progression to blindness in 1 eye within 2 decades 
    • Approximately 5% to 10% of patients will become bilaterally blind over time 
  • Left untreated, typical disease course is gradual visual field loss that may progress to a central island of vision and, ultimately, loss of vision 


At-risk populations

  • US Preventive Services Task Force states that current evidence is insufficient to assess the balance of benefits and harms of routine screening for primary open-angle glaucoma in asymptomatic adults in the primary care setting, and that it does not support regular screening by primary care clinicians 
  • However, American Academy of Ophthalmology recommends eye examination by an eye professional as follows for general eye health, which includes glaucoma screening: 
    • General population
      • Aged 40 years: 1 examination if no signs, symptoms, or risk factors for ocular disease
      • Aged 41 to 54 years: every 2 to 4 years
      • Aged 55 to 64 years: every 1 to 3 years
      • Aged 65 years or older: every 1 to 2 years, even in absence of symptoms
    • High-risk populations (eg, African American people, Hispanic people, those with family history of glaucoma)
      • Younger than 40 years: every 2 to 4 years
      • Aged 40 to 54 years: every 1 to 3 years
      • Aged 55 to 64 years: every 1 to 2 years
      • Aged 65 years or older: every 6 to 12 months
  • Medicare covers annual testing for glaucoma for patients at high risk (eg, those with diabetes, those with family history of glaucoma, African American people aged 50 years or older, Hispanic American people aged 65 years or older) 

Screening tests

  • Tonometry and ophthalmoscopy with stereopsis (ie, binocularity) are screening tests recommended by the Glaucoma Research Foundation 


  • Early identification of high-risk patients and emphasis on treatment adherence can aid in lowering morbidity from glaucoma


Tham YC et al: Global prevalence of glaucoma and projections of glaucoma burden through 2040: a systematic review and meta-analysis. Ophthalmology. 121(11):2081-90, 2014 Reference 


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