Primary Open Angle Glaucoma

Adult onset optic neuropathy with open angles

1% of the population but up to 50% may be undiagnosed

Risk factors

• Age
• Ethnicity: Afro-caribbean
• Family history
• Steroid induced IOP elevation (“steroid responder”)
• Vascular disease (diabetes, HTN)
• Myopia: possibly due to scleral canal morphology
• Genetics: GLC1A (TIGR/MYOC) was the first POAG gene discovered on chromosome 1
  • Encodes myocilin, a protein that can be induced in the TM by topical steroid
  • Found in 3% of adults with POAG
  • Even more so associated with juvenile onset glaucoma

Clinical features

• Typically asymptomatic
• IOP >21 with higher than usual diurnal variability
• C:D asymmetry
• High C:D for disc size
• Vertical elongation of the cup
• NRR notch/thinning out-of-keeping with ISNT rule
• Disc haemorrhage
• Vessel bayoneting
• Nasally displaced vessels
• Peripapillary atrophy: “beta” zone PPA is directly adjacent to disc
• Visual field defects: focal defects respecting the horizontal meridian
  • Nasal step
  • Baring of blind spot
  • Paracentral scotomas
  • Arcuate defects
  • Altitudinal defects
  • Generalized depression of the field

Management

• Counselling including implications for driving and importance of drop compliance

• Define target IOP: typically at least a 20% reduction at first. Aim for <18 in moderate and <15 in advanced disease

• Review initial treatment at 6 weeks

• Topical therapy

  • Prostaglandin analogues
  • Beta blockers
  • Alpha2 agonists
  • Carbonic anhydrase inhibitors

• Laser trabeculoplasty: argon (ALT) or selective (SLT)

  • IOP control may fall with time (50% failure at 5 years)

• Trabeculectomy +/- augmentation

  • Occasionally a primary treatment in advanced disease with a need for low target IOP especially if intolerant of topical therapy
  • Mitomycin C is anti-scarring

• Shunt procedures: Baerveldt, Molteno or Ahmed tubes

• Ciliary body destruction: diode laser cycloablation

NICE guidelines for chronic open angle glaucoma (COAG)

• Do not offer treatment if IOP <24 and patient is not at risk of visual impairment in their lifetime

• Initial treatment: offer 360 degree selective laser trabeculoplasty (SLT) unless pigment dispersion syndrome

  • SLT can delay need for eye drops
  • SLT can be offered to patients with OHT if IOP is >24 and they are at risk for visual impairment within their lifetime

• Generic prostaglandin analogue if:

  • Patient does not wish SLT
  • SLT not suitable (eg. pigment dispersion syndrome)
  • Patient requires interim treatment prior to SLT
  • IOP not sufficiently lowered by SLT

• If ongoing progression: check adherence with drops and instillation technique

• If satisfactory adherence/technique:

  • Add further topical treatment with another drug class
  • Offer 360 degree SLT if not previously tried
  • Consider glaucoma surgery with augmentation

• Always consider SLT or surgery if unsatisfactory control with 2 or more topical agents

• If a topical therapy cannot be tolerated, consider an alternative drug agent or a preservative free preparation

• Patients who present with advanced COAG can be offered glaucoma surgery with augmentation directly, with topical therapy as an interim measure

• Follow-up times are based on the IOP control, perceived risk of conversion to COAG (for OHT patients) or risk of sight loss