Glaucomas are optic neuropathies associated with raised intraocular pressure (IOP).


  • Incidence: 50.00 cases per 100,000 person-years
  • Peak incidence: 70+ years
  • Sex ratio: 1:1
<1 1-5 6+ 16+ 30+ 40+ 50+ 60+ 70+ 80+


Primary open-angle glaucoma (POAG, also referred to as chronic simple glaucoma) is present in around 2% of people older than 40 years. Other than age, risk factors include:
  • genetics: first degree relatives of an open-angle glaucoma patient have a 16% chance of developing the disease
  • black patients
  • myopia
  • hypertension
  • diabetes mellitus
  • corticosteroids


Glaucomas can be classified based on whether the peripheral iris is covering the trabecular meshwork, which is important in the drainage of aqueous humour from the anterior chamber of the eye. In open-angle glaucoma, the iris is clear of the meshwork. The trabecular network functionally offers an increased resistance to aqueous outflow, causing increased IOP. It is now recognised that a minority of patients with raised IOP do not have glaucoma and vice versa.

Clinical features

POAG may present insidiously and for this reason is often detected during routine optometry appointments. Features may include
  • peripheral visual field loss - nasal scotomas progressing to 'tunnel vision'
  • decreased visual acuity
  • optic disc cupping

Fundoscopy signs of primary open-angle glaucoma (POAG):
  • 1. Optic disc cupping - cup-to-disc ratio >0.7 (normal = 0.4-0.7), occurs as loss of disc substance makes optic cup widen and deepen
  • 2. Optic disc pallor - indicating optic atrophy
  • 3. Bayonetting of vessels - vessels have breaks as they disappear into the deep cup and re-appear at the base
  • 4. Additional features - Cup notching (usually inferior where vessels enter disc), Disc haemorrhages

  • Case finding and provisional diagnosis is done by an optometrist
  • Referral to the ophthalmologist is done via the GP
  • Final diagnosis is done by investigations as below


  • automated perimetry to assess visual field
  • slit lamp examination with pupil dilatation to assess optic neve and fundus for a baseline
  • applanation tonometry to measure IOP
  • central corneal thickness measurement
  • gonioscopy to assess peripheral anterior chamber configuration and depth
  • Assess risk of future visual impairment, using risk factors such as IOP, central corneal thickness (CCT), family history, life expectancy


The majority of patients with primary open-angle glaucoma are managed with eye drops. These aim to lower intra-ocular pressure which in turn has been shown to prevent progressive loss of visual field.

NICE guidelines:
  • first line: prostaglandin analogue (PGA) eyedrop
  • second line: beta-blocker, carbonic anhydrase inhibitor, or sympathomimetic eyedrop
  • if more advanced: surgery or laser treatment can be tried2

  • important to exclude progression and visual field loss
  • needs to be done more frequently if: IOP uncontrolled, the patient is high risk, or there is progression

MedicationMode of actionNotes
Prostaglandin analogues (e.g. latanoprost)Increases uveoscleral outflowOnce daily administration

Adverse effects include brown pigmentation of the iris, increased eyelash length
Beta-blockers (e.g. timolol, betaxolol)Reduces aqueous productionShould be avoided in asthmatics and patients with heart block
Sympathomimetics (e.g. brimonidine, an alpha2-adrenoceptor agonist)Reduces aqueous production and increases outflowAvoid if taking MAOI or tricyclic antidepressants

Adverse effects include hyperaemia
Carbonic anhydrase inhibitors (e.g. Dorzolamide)Reduces aqueous productionSystemic absorption may cause sulphonamide-like reactions
Miotics (e.g. pilocarpine, a muscarinic receptor agonist)Increases uveoscleral outflowAdverse effects included a constricted pupil, headache and blurred vision

Surgery in the form of a trabeculectomy may be considered in refractory cases.