Primary open-angle glaucoma
Introduction
Epidemiology
- 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+ |
Aetiology
- 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
Pathophysiology
Clinical features
- 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
Diagnosis:
- 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
Investigations
- 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
Management
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
Reassessment
- 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
Medication | Mode of action | Notes |
---|---|---|
Prostaglandin analogues (e.g. latanoprost) | Increases uveoscleral outflow | Once daily administration Adverse effects include brown pigmentation of the iris, increased eyelash length |
Beta-blockers (e.g. timolol, betaxolol) | Reduces aqueous production | Should be avoided in asthmatics and patients with heart block |
Sympathomimetics (e.g. brimonidine, an alpha2-adrenoceptor agonist) | Reduces aqueous production and increases outflow | Avoid if taking MAOI or tricyclic antidepressants Adverse effects include hyperaemia |
Carbonic anhydrase inhibitors (e.g. Dorzolamide) | Reduces aqueous production | Systemic absorption may cause sulphonamide-like reactions |
Miotics (e.g. pilocarpine, a muscarinic receptor agonist) | Increases uveoscleral outflow | Adverse effects included a constricted pupil, headache and blurred vision |
Surgery in the form of a trabeculectomy may be considered in refractory cases.