Open-angle glaucoma

Background

• An optic neuropathy characterized by an increase in intraocular pressure leading to damage to the optic nerve and irreversible vision loss.
• Second leading cause of irreversible blindness worldwide

Risk Factors

• 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

• Painless
• Cupping of the optic disc
• Loss of peripheral visual field
• Preservation of central vision

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

Testing

Fundus examination

• Cupping >50% of the vertical disc diameter
• Thinning or notching of disc rim
• Progressive change of size/shape of cup

Glaucoma cupping

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

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

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