Open-angle glaucoma: Difference between revisions

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==Background==
==Background==
*An optic neuropathy characterized by an increase in intraocular pressure leading to damage to the optic nerve and irreversible vision loss.
[[File:Schematic diagram of the human eye en.png|thumb|Eye anatomy.]]
*Second leading cause of irreversible blindness worldwide
[[ File:Gray883.png|thumb|Eye angle anatomy.]]
[[File:PMC4614311 qmj-2015-01-0006-g002.png|thumb|Mechanism of open vs closed angle closure glaucoma.]]
*Elevated intraocular pressure and resulting optic nerve damage manifested initially as visual field loss and ultimately irreversible blindness if left untreated
*Unclear pathogenesis, however thought to be related to two mechanisms:
**Increased aqueous production
**Decreased outflow


===Risk Factors===
===Etiologies<ref>Optometric Clinical Practice Guideline Care of the Patient with Open Angle Glaucoma. Fingeret, M. American Optometric Association Original Consensus Panel on Care of the Patient with Open Angle Glaucoma.  American Optometric Association, 2011</ref>===
*Age (4% prevalence in age >80)
*Primary
*Race (3 times higher in Black patients)
*Secondary
*Family History (2-3 fold increase for individuals with affected sibling or parent)
**Another ocular disease
*[[Hypertension]]
**Systemic disease
*[[Diabetes]]
**Trauma
*Other: Myopia, pseudoexfoliation, low diastolic perfusion pressure, cardiovascular disease, [[hypothyroidism]]
**Drugs
 
===Pathophysiology===
Not entirely clear, but may be related to an increased intraocular pressure that leads to compression of the optic nerve at the site where it exits the eye. This causes a progressive decrease in the number of retinal ganglion cells.


==Clinical Features==
==Clinical Features==
''Most commonly presents with progressive peripheral vision loss, followed by central vision loss''
[[File:Glaukompapille2.jpg|thumb|Retinal findings in advanced glaucoma disease.]]
*Painless
*Rarely experience symptoms, in contrast to [[acute angle closure glaucoma]]
*Cupping of the optic disc
*Typical pattern characterized by progressive peripheral visual field loss followed by central field loss, usually but not always associated with elevated intraocular pressure
*Loss of peripheral visual field
*Preservation of central vision


==Differential Diagnosis==
==Differential Diagnosis==
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==Evaluation==
==Evaluation==
===Testing===
===Workup===
====[[Fundus examination]]====
*[[Eye exam]] with IOP check
*Cupping >50% of the vertical disc diameter
*Thinning or notching of disc rim
*Progressive change of size/shape of cup
[[File:glaucoma-cupping-1024x414.jpg|thumb|Glaucoma cupping]]
 
====[[Visual field testing]]====
 
====[[Intraocular pressure]]====
*Does not establish diagnosis of Open angle glaucoma. 1/2 of patients with OAG have normal intraocular pressure
*Normal Intraocular pressure ranges from 10 to 20 mmHg
*Pressure >21 mmhg considered ocular hypertension


===Diagnosis===
===Diagnosis===
At least one of the following:
*Characteristic nerve damage (eg, cupping) on fundus examination
*Evidence of optic nerve damage from structural abnormalities (thinning, cupping, notching of disc rim)
*Visual field abnormalities
*Adult Onset
*+/- elevated IOP (>21 mmHg)
*Open, normal appearing anterior chamber angles
*Absence of known secondary causes of open-angle glaucoma


==Management==
==Management==
*β-blockers: [[Timolol]] maleate 0.25%-0.5%, one drop BID
*Typically managed chronically with long-term eye drops or outpatient procedures and does not typically requir immediate emergency intervention
*α-adrenergic agonist: Brimonidine 0.2% one drop BID
*Carbonic Anhydrase inhibitors: Dorzolamide 2% one drop BID
*Prostaglandins: Latanoprost 0.005% one drop qD
*Persistent elevated intraocular pressures: [[Acetazolamide]] 125-250mg PO bid-QID


==Disposition==
==Disposition==
Indications for ophthalmologic referral:
*Outpatient
*IOP>40mmHg: emergency referral
*IOP 30-40 mmHg: referral within 24hr if no symptoms suggesting acute glaucoma
*IOP 25-29 mmHg: Evaluation within 1 week
*IOP 23-24 mmHg: repeat measurement and referral for comprehensive eye examination


==See Also==
==See Also==
*[[Acute vision loss (noninflamed)]]
*[[Acute angle-closure glaucoma]]
*[[Acute angle-closure glaucoma]]


==External Links==
==External Links==


==References==
==References==

Latest revision as of 23:16, 4 February 2026

Background

Eye anatomy.
Eye angle anatomy.
Mechanism of open vs closed angle closure glaucoma.
  • Elevated intraocular pressure and resulting optic nerve damage manifested initially as visual field loss and ultimately irreversible blindness if left untreated
  • Unclear pathogenesis, however thought to be related to two mechanisms:
    • Increased aqueous production
    • Decreased outflow

Etiologies[1]

  • Primary
  • Secondary
    • Another ocular disease
    • Systemic disease
    • Trauma
    • Drugs

Clinical Features

Retinal findings in advanced glaucoma disease.
  • Rarely experience symptoms, in contrast to acute angle closure glaucoma
  • Typical pattern characterized by progressive peripheral visual field loss followed by central field loss, usually but not always associated with elevated intraocular pressure

Differential Diagnosis

Acute Vision Loss (Noninflamed)

†Emergent Diagnosis

Evaluation

Workup

Diagnosis

  • Characteristic nerve damage (eg, cupping) on fundus examination
  • Visual field abnormalities
  • +/- elevated IOP (>21 mmHg)

Management

  • Typically managed chronically with long-term eye drops or outpatient procedures and does not typically requir immediate emergency intervention

Disposition

  • Outpatient

See Also

External Links

References

  1. ↑ Optometric Clinical Practice Guideline Care of the Patient with Open Angle Glaucoma. Fingeret, M. American Optometric Association Original Consensus Panel on Care of the Patient with Open Angle Glaucoma. American Optometric Association, 2011
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