Open-angle glaucoma


  • 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)


  • 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).


  • 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

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