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Primary Open-Angle Glaucoma

ROUTINE — Glaucoma

Symptoms

  • usually asymptomatic until advanced stages ("the silent thief of sight")
  • painless, progressive loss of peripheral vision
  • central vision typically remains 20/20 until end-stage disease
  • bilateral, though frequently asymmetric in severity
  • History: always ask about steroid use (nasal, skin, joints) to rule out secondary causes

Clinical Findings

Diagnostic triad

  • open, normal-appearing angle on gonioscopy (no closure/pigment/exfoliation)
  • characteristic optic nerve cupping (structural damage)
  • corresponding visual field defects (functional damage)

Structural signs (optic nerve)

  • vertical cup-to-disc ratio (c:d) >0.6 or asymmetry ≥0.2 between eyes
  • isnt rule violation: thinning of the inferior/superior rim first
  • drance hemorrhage: splinter hemorrhage at the disc margin; a sign of active progression
  • rnfl wedge defects: visible as dark "slits" on red-free exam or oct

Functional signs (visual fields)

  • nasal step, arcuate (bjerrum) scotoma, or paracentral defects
  • defects respect the horizontal midline (unlike neuro-defects which respect the vertical)

Pachymetry (CCT)

  • thin corneas (<555 μm) are a major independent risk factor for progression
  • thin corneas "under-read" iop, making the measured pressure seem safer than it is

Etiology

Pathophysiology

  • increased resistance to aqueous outflow through the trabecular meshwork
  • mechanical and vascular stress leads to retinal ganglion cell apoptosis

Risk factors

  • age >60, african or hispanic ancestry (higher prevalence and earlier onset)
  • elevated iop, family history (1st-degree relatives), and high myopia
  • systemic: diabetes, hypertension, and low ocular perfusion pressure

Red Flags

  • progression at "normal" iop: suggests normal-tension glaucoma or nocturnal dips
  • optic nerve pallor > cupping: suggests a non-glaucomatous (neurologic) cause
  • rapid field loss: warrants immediate reassessment of target iop and compliance
  • split fixation: field loss threatening the central 5 degrees; requires urgent surgery

Investigations

Baseline workup

  • applanation tonometry (gold standard) and gonioscopy (to confirm open angle)
  • ultrasonic pachymetry to measure central corneal thickness (cct)

Imaging & perimetry

  • oct of the rnfl and ganglion cell complex (gcc) for structural baseline
  • humphrey visual field (hvf) 24-2 (or 10-2 if advanced) for functional baseline
  • high-quality disc photography to track structural changes over years

Atypical workup

  • if field loss doesn't match the nerve, consider mri orbits/brain or labs (b12, syphilis)

Treatment

First-line

  • topical prostaglandins (latanoprost, bimatoprost) once daily at bedtime
  • selective laser trabeculoplasty (slt): proven as an effective first-line alternative to drops

Medical adjuncts

  • beta-blockers (timolol), alpha-agonists (brimonidine), or rho-kinase inhibitors
  • carbonic anhydrase inhibitors (dorzolamide/acetazolamide)

Surgical intervention

  • trabeculectomy or tube shunts for uncontrolled progression
  • migs (minimally invasive glaucoma surgery) often performed during cataract extraction

Clinical Pearl

normal tension glaucoma (ntg): glaucomatous damage with iop always <21 mm hg. requires same treatment principles — target iop reduction 30% from baseline. disc hemorrhage is an independent predictor of progression. rnfl thinning on oct often precedes visual field loss by years.

Differential Diagnosis

  • • secondary open-angle (pseudoexfoliation, pigmentary, steroid-induced)
  • • normal-tension glaucoma (ntg)
  • • physiologic cupping (large disc with large cup, but thick rim and normal hvf)
  • • neuro-ophthalmic mimics (ischemic optic neuropathy, compressive lesions)

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