The basics - Glaucoma

Blindness from glaucoma can be prevented by early treatment, says Ms Samantha Levin.

Glaucoma is a disorder that causes progressive optic neuropathy. It is characterised by damage to the optic disc and visual field deficits.

Approximately 2 per cent of people aged over 40 have glaucoma. Between 5 and 10 per cent of these patients lose their sight and the disease is responsible for 10-15 per cent of those registered blind.

The most common form of glaucoma seen in the UK is primary open angle glaucoma (POAG), which is a chronic condition resulting in gradual loss of sight. Narrow angle and angle closure glaucoma are less common but can be acute and result in permanent sight damage unless treated quickly. In addition, glaucoma can occur secondary to other ocular conditions that increase pressure in the eye.

Risk factors
Glaucoma is commonly the result of an obstruction to the drainage of aqueous fluid from the eye. This produces raised intraocular pressure (IOP), causing damage to the optical nerve.

However, glaucoma can also occur in patients with ocular pressure in the normal range, as a result of poor blood supply or a weakness in the optic nerve. Up to a third of open angle glaucoma patients have a normal IOP.

Patients with a raised IOP but no optic nerve damage or visual field defect have ocular hypertension and might develop glaucoma in the future.

Treating ocular hypertension halves the five-year risk of developing glaucoma, but 15 people need to be treated to prevent one case of POAG.

IOP is the only modifiable risk factor for glaucoma. Other important risk factors are age, family history and race, with a higher prevalence of the condition in African-Caribbean patients.

Diagnosis
Glaucoma is detected through assessment of the optic nerve and visual field. In healthy patients, the optic disc is slightly elongated vertically and looks like a doughnut of pink tissue. The central cup varies in size according to the size of the disc, but it has a healthy rim of retinal ganglion cells.

In patients with glaucoma, the tissue of the optic disc rim is damaged because ganglion cells are lost. As this rim becomes thinner, the cup of the optic disc increases in size, a phenomenon known as 'cupping'.

Obvious cupping is easy to spot, but early changes to the optic nerve caused by glaucoma can be quite subtle.

Additional indicators of glaucoma include asymmetry between right and left discs, focal rim loss (notching), retinal nerve fibre layer loss and retinal atrophy around the disc.

Optic disc imaging is useful for monitoring the progression of POAG. Disc photography is the gold standard but requires subjective assessment.

Optic neuropathy due to glaucoma produces characteristic visual field defects. These usually follow changes in the optic disc.

Treatment
Treatments for glaucoma aim to prevent loss of vision by lowering IOP. Recent trials have confirmed that IOP lowering is effective in preventing the progression of glaucomatous damage. Lower IOP targets than previously used have been recommended.

The target ocular pressure is the estimated maximum IOP at which no further damage to the optic nerve will occur. This target varies according to the IOP of the patient presenting with glaucoma and the degree of existing damage.

If further damage occurs once the target IOP has been reached, the target pressure should be lowered. Medication, laser treatment and surgery are all options for lowering IOP, but eye drops are considered the safest primary therapy for POAG, with surgery reserved for patients who do not respond to topical treatment.

Topical treatments work by reducing the production of aqueous fluid, improving outflow or both (see table). First-line treatment is usually with prostaglandin analogues because these are effective with few systemic side-effects. Newer glaucoma drops have even fewer systemic side-effects, but symptoms of red eye and ocular irritation preclude their use in up to 10 per cent of patients.

If monotherapy fails to reduce IOP to the target level, dual therapy can be tried. The availability of combined preparations has made this more convenient for patients, aiding compliance and has also eliminated the problem of 'wash-out'.

Systemic absorption of eye drops should be minimised by compressing the tear drainage punctum immediately after administration, and/or closing the eyes for a few seconds. When good IOP control is achieved with drops, the patient must be advised that treatment is for life.

Systemic therapy with carbonic anhydrase inhibitors such acetazolamide is seldom used for long-term treatment because of unacceptable side effects, including paraesthesia.

Surgery
Drainage surgery is effective at reducing ocular pressure by up to 30 per cent from baseline IOP.

Trabeculectomy allows subconjunctival drainage of aqueous fluid via a scleral flap. However, it increases the five year cataract risk by 30 per cent.

Devices that drain aqueous fluid via a tube to a subconjunctival implant are used in higher risk cases but these are associated with complications. There are several types of laser treatment for glaucoma which are performed as an outpatient clinic procedure on a slit lamp-mounted laser.

Surgical techniques are being developed and the outcomes of traditional surgery have been improved by technique refinement. Recent animal and cell culture studies have identified increased neurone apoptosis at the optic disc in glaucoma.

Ms Levin is consultant ophthalmic surgeon at the Central Middlesex Hospital, London

Topical glaucoma treatments
Drug classMode of action Frequency Adverse effects
Prostaglandin analoguesIncrease fluid outflow DailyExacerbation of asthma, increased iris pigmentation
Beta-blockers Reduce fluid production Once or twice dailyBronchospasm, bradycardia dyspnoea, dizziness
Alpha-2 agonistsReduce production and enhance outflow of fluid2-3 times dailyFatigue, dry mouth, allergic reactions of the eye
Carbonic anhydrase inhibitorsReduce fluid production2-3 times dailyParaesthesia, blood dyscrasias, rash, headache
angioedema, polyuria, metabolic acidosis, Stevens Johnson Syndrome
SympathomimeticsIncrease fluid outflow1-4 times dailyPupil constriction, blurred vision, headache, retinal
detachment

References

  1. Kass M, Heuer D, Higginbotham E et al. The Ocular Hypertension Treatment Study: a randomized trial determines that topical ocular hypotensive medication delays or prevents the onset of primary open-angle glaucoma. Arch Ophthalmol 2002; 120: 701-3.
  2. AGIS investigators. The Advanced Glaucoma Intervention Study: The relationship between control of intraocular pressure and visual field deterioration. Am J Ophthalmol 2000; 130: 429-40.
  3. Leske M, Heijl A, Hussein M et al. Factors for glaucoma progression and the effect of treatment: the early manifest glaucoma trial. Arch Ophthalmol 2003; 121: 48-56
  4. Garcia-Valenzuela E et al. Programmed cell death of retinal ganglion cells during experimental glaucoma. Exp EyeRes 1995; 61: 33-44.

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