Primary Open-angle Glaucoma

Background

• Primary open-angle glaucoma (POAG) is a chronic, progressive optic neuropathy in adults with characteristic acquired atrophy of optic nerve and loss of retinal ganglion cells and their axons and associated with open anterior chamber angle by gonioscopy.
• POAG suspect is characterized by clinical findings and/or a constellation of risk factors that indicate an increased likelihood of developing POAG.
• POAG and POAG suspect may be caused by increased intraocular pressure, abnormally low cerebrospinal fluid pressure in optic nerve subarachnoid space, impaired microcirculation, altered immunity, and other factors, or a combination of these factors.
• Complications include various forms of visual impairment, loss of peripheral vision, decreased contrast sensitivity, loss of ability to read or drive, and ultimately may lead to permanent irreversible blindness.

Evaluation

• Primary open-angle glaucoma (POAG) and POAG suspect are usually asymptomatic early in the disease course, and patients typically are identified through screening or based on abnormal findings on an eye examination.
• Patients who have progressed to definite glaucoma may have sufficient visual field loss to report impaired night driving, near vision, reading speed, or outdoor mobility.
• To assess for suspected POAG and POAG suspect:
  • Perform an ophthalmic evaluation focusing on specific elements of comprehensive adult medical eye evaluation including:
    • visual acuity measurement, pupil examination, and confrontation visual fields
    • slit-lamp biomicroscopy
    • intraocular pressure (IOP) measurement
    • gonioscopy
    • optic nerve head and retinal nerve fiber layer (RNFL) examination
    • fundus examination
  • Perform diagnostic testing including:
    • imaging of optic nerve head, retinal nerve fiber layer, and macular imaging
    • visual field evaluation
    • central corneal thickness measurement
• Consider a diagnosis of primary open-angle glaucoma suspect with any of following clinical findings in 1 or both eyes:
  • Elevated IOP is associated with a normal optic disc appearance, retinal nerve fiber layer, and visual field.
  • Appearance of the optic nerve head or retinal nerve fiber suspicious for glaucomatous damage.
  • A visual field suspicious for glaucomatous damage in the absence of clinical signs of another optic neuropathy or retinopathy.
• Diagnose primary open-angle glaucoma with the following characteristic clinical findings in 1 or both eyes:
  • Evidence of optic nerve damage characterized by either (or both):
    • optic disc or RNFL structural abnormalities
    • reliable and reproducible visual field abnormalities
  • Adult-onset, progressive disease (usually bilateral, but can be asymmetric).
  • Open anterior chamber angle on gonioscopy.
  • The absence of other known explanations for progressive glaucomatous optic nerve change (such as pigment dispersion syndrome, pseudoexfoliation syndrome, uveitis, trauma, and corticosteroid use).
• The severity of glaucoma damage may be classified based on the degree of visual field abnormalities as measured by standard automated perimetry (in the presence of definite optic disc or RNFL abnormalities consistent with glaucoma):
  • Mild: normal visual field
  • Moderate: visual field abnormalities in 1 hemifield that are not within 5 degrees of fixation
  • Severe: visual field abnormalities in both hemifields and/or loss within 5 degrees of fixation in ≥ 1 hemifield
  • Indeterminate: inability of patient to perform visual field testing, unreliable/uninterpretable visual field test results, or visual fields not yet performed
• Exclude other causes of optic disc abnormalities, retinal abnormalities, central nervous system abnormalities, and elevated IOP.

Management

• Management of primary open-angle glaucoma
  • Discuss with the patient the risks and benefits of medical treatment, laser trabeculoplasty, and incisional glaucoma surgery (including trabeculectomy), alone or in combination.
  • Management goals are to stabilize visual fields, optic nerve, and retinal nerve fiber layer by maintaining target intraocular pressure (IOP) at a range that reduces risk of visual field loss; 20%-30% below baseline is a reasonable initial target.
  • Medical therapy is the most common initial intervention to lower IOP
    • Prostaglandin analogs are the first-line therapy unless precluded by contraindications, cost, adverse events or intolerance, or patient refusal.
    • Second-line medications include:
      • beta-adrenergic antagonists (beta blockers)
      • alpha-adrenergic agonists
      • parasympathomimetic agents
      • topical or oral carbonic anhydrase inhibitors
      • rho kinase inhibitors
  • Surgical procedures
    • Consider laser trabeculoplasty as initial or adjunctive therapy in patients with primary open-angle glaucoma.
    • Consider standard trabeculectomy for lowering IOP if medications and laser therapy do not control the disease.
    • Other surgical procedures to consider include aqueous shunts, deep sclerectomy, minimal invasive glaucoma surgery, and cyclodestructive surgery.
  • Provide support and encouragement to the patient (including referral to peer-support groups or counseling) in regards to effects glaucoma may have on vision- and health-related quality of life.
  • Follow-up typically every 6-12 months if target IOP is achieved for > 6 months and there is no progression of optic nerve damage or visual field defect. Follow up more frequently if neither condition is met.