Open-angle glaucoma: Difference between revisions

Latest revision as of 03:22, 7 December 2022

Background

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

Clinical Features

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)

Painful
- Arteritic anterior ischemic optic neuropathy
- Optic neuritis
- Temporal arteritis^†
Painless
- Amaurosis fugax
- Central retinal artery occlusion (CRAO)^†
- Central retinal vein occlusion (CRVO)^†
- High altitude retinopathy
- Open-angle glaucoma
- Posterior reversible encephalopathy syndrome (PRES)
- Retinal detachment^†
- Stroke^†
- Vitreous hemorrhage
- Traumatic optic neuropathy (although may have pain from the trauma)

^†Emergent Diagnosis

Evaluation

Workup

Diagnosis

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

Management

Disposition

External Links

References

Authors:

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 ==Background==
-*An optic neuropathy characterized by an increase in intraocular pressure leading to damage to the optic nerve and irreversible vision loss.
+*Elevated intraocular pressure and resulting optic nerve damage manifested initially as visual field loss and ultimately irreversible blindness if left untreated
-*Second leading cause of irreversible blindness worldwide
+*Unclear pathogenesis, however thought to be related to two mechanisms:
+**Increased aqueous production
-=== Risk Factors ===
+**Decreased outflow
-* Age (4% prevalence in age >80)
-* Race (3x higher in African Americans)
-* Family History (2-3 fold increase for individuals with affected sibling or parent)
-* [[Hypertension]]
-* [[Diabetes]]
-* Other: Myopia, pseudoexfoliation, low diastolic perfusion pressure, cardiovascular disease, [[hypothyroidism]]
-=== 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==
-''Most commonly presents with progressive peripheral vision loss, followed by central vision loss''
+*Rarely experience symptoms, in contrast to [[acute angle closure glaucoma]]
-* Painless
+*Typical pattern characterized by progressive peripheral visual field loss followed by central field loss, usually but not always associated with elevated intraocular pressure
-* Cupping of the optic disc
-* Loss of peripheral visual field
-* Preservation of central vision
 ==Differential Diagnosis==
+{{Acute vision loss noninflamed DDX}}
 ==Evaluation==
+===Workup===
+===Diagnosis===
+*Characteristic nerve damage (eg, cupping) on fundus examination
+*Visual field abnormalities
+*+/- elevated IOP
 ==Management==
 ==Disposition==
 ==See Also==
+*[[Acute angle-closure glaucoma]]
 ==External Links==
 ==References==
 <references/>
+[[Category:Ophthalmology]]
-=== Diagnosis with at least one of the following:===
-* Evidence of optic nerve damage from structural abnormalities (thinning, cupping, notching of disc rim)
-* Adult Onset
-* Open, normal appearing anterior chamber angles
-* Absence of known secondary causes of open-angle glaucoma
-=== Diagnostic tests ===
-==== Fundus examination ====
-* 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
-=== Treatment and management ===
-* β-blockers: Timolol maleate 0.25%-0.5%, one drop BID
-* α-adrenergic agonistBrimonidine 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 ===
-Indications for opthalmologic referral:
-* 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
-=== References ===
-* Tsai LM, Pitha I, Kamenetzky SA. The Eye & Ocular Adnexa. In: Doherty GM. eds. CURRENT Diagnosis & Treatment: Surgery, 14e. New York, NY: McGraw-Hill; 2015.
-* Weinreb RN, Khaw PT. Primary open-angle glaucoma. Lancet 2004; 363:1711
-* UpToDate
-* American Academy of Ophthalmology, Glaucoma Panel. Primary open-angle glaucoma. Preferred practice pattern. San Francisco: American Academy of Ophthalmology, 2000:1–36