Open-angle glaucoma

Background

• This is a common cause of gradual visual loss, affecting around 2% of the adult population.
  • More common in Afro-Caribbean individuals
• The exact cause is not known (the iridocorneal junction is still open- the hypothesis is that there is some dysfunction of the trabecular meshwork).  There is still a rise in intraocular pressure and an optic neuropathy associated with it too.
  • May be due to cellular components, pigments or neovascularisation blocking the trabecular meshwork;
  • Occasionally can be caused by steroids (usually topical- increase the resistance to outflow by affecting the transport of aqueous humour)
  • Angle recession (occurs with age) may also contribute to the development of glaucoma
    • People who are myopic (short-sighted i.e. long eye)

Presentation

• There is a gradual and insidious loss of vision (the classic picture is loss of the peripheral fields first).
  • this is usally late on in the disease process when it is too late to save the patient’s vision.
  • Patient may also complain of gradually worsening pain.
• On examination, there may be redness and the patient may be photophobic.  The optic disc classically shows ‘cupping’ (raised border with shallow centre).

Management

• Pharmacological management
  • Prostanoids e.g. latanoprost (‘xalatan’) first line
  • Beta blockers e.g. timolol, betaxolol can be used if there is ocular hypertension without features of glaucoma i.e. optic atrophy
• If there is no response and glaucoma continues to progress on treatment, the following may be tried as well as a prostanoid.
  • Beta blockers
  • CA inhibitors e.g. dorzolamide (topical) or acetazolamide (IV)
  • α2- adrenergic agonists e.g. brimonidine (‘alphagan’)
• For severe disease, surgery (laser trabeculoplasty or traditional trabeculotomy +/- chemotherapy (5-FU/mitomycin) augmentation