Glaucoma: an overview
Stay abreast of glaucoma with an essential guide to its causes, diagnosis and management.
Glaucoma is an eye disorder characterised by raised intraocular pressure. The condition is usually asymptomatic; and age, race, family history and diabetes are risk factors. Reducing intraocular pressure is the aim of treatment of the condition.
- Glaucoma is a range of disorders usually characterised by raised intraocular pressure and leads to damage of the optic nerve.
- Damage to the optic nerve can occur with a normal intraocular pressure.
- Glaucoma can be classified as primary or secondary.
- Primary glaucoma includes primary open‐angle glaucoma (chronic simple glaucoma), the most common form of glaucoma, and primary angle‐closure glaucoma.
- Primary open‐angle glaucoma is caused by blockage in the trabecular meshwork, which drains the anterior chamber of the eye to the episcleral veins through the Schlemm’s canal.
- Primary angle‐closure glaucoma is generally acute in onset and may require treatment as a medical emergency.
- Primary angle‐closure glaucoma results from decreased outflow of aqueous humour, causing accumulation of fluid in the eye.
- Secondary glaucomas can result from a wide range of causes, such as inflammation, tumours or congenital abnormalities.
This guide will focus on the most common form of glaucoma: primary open-angle glaucoma.
Risk factors associated with primary open‐angle glaucoma are:
- age: glaucoma affects 2 in 100 over the age of 40 years, and 1 in 10 over the age of 70 years
- race: people of African origin have greater incidence, earlier onset and greater severity
- family: 10% likelihood of first‐degree relatives developing glaucoma
- short sight: people who are short-sighted are prone to glaucoma
- diabetes: this condition is believed to increase the risk of developing glaucoma.
In the UK, those aged over 40 years of age with an immediate family member diagnosed with glaucoma are entitled to free annual sight tests.
Signs and symptoms
- Glaucoma is usually asymptomatic, unless it is in the advanced stages.
- Symptoms include worsening of vision.
- Signs include raised intraocular pressure and increased variation in intraocular pressure.
- Most patients are diagnosed at routine eye appointments:
- intraocular pressure measured by tonometry
- appearance of the optic nerve observed with ophthalmoscopy
- peripheral vision assessment taken using perimetry (spot testing).
- It is important that all three tests are carried out to confirm diagnosis.
- The aim of treatment is to reduce intraocular pressure.
- Five main classes of drug are used for treatment of glaucoma; all work by reducing intraocular pressure by different mechanisms:
- beta‐blockers (e.g. timolol, levobunolol) reduce aqueous humour production
- prostaglandin analogues (e.g. latanoprost) increase uveoscleral outflow
- sympathomimetics (e.g. brimodine) improve drainage through the trabecular meshwork and decrease aqueous production by stimulation of α2‐adrenoceptors
- carbonic anhydrase inhibitors(e.g. dorzolamide) reduce aqueous humour production
- miotics (e.g. pilocarpine) are usually given for acute glaucoma to increase drainage through the trabecular meshwork.
- Topical beta‐blockers or prostaglandin analogues are first choice.
- Tonometry, ophthalmoscopy and perimetry should be monitored for effectiveness of treatment.
- Systemic absorption of beta‐blockers may occur; therefore, they are contraindicated in asthma, chronic obstructive pulmonary disease, and uncontrolled heart failure, bradycardia and heart block. Systemic side effects are described in the cardiovascular section.
- Local adverse effects of beta‐blockers include ocular stinging, burning, itching, pain, erythema, dry eyes and allergic reactions.
- Changes in eye coloration should be monitored with prostaglandin analogue therapy as brown pigmentation may occur
- Local side effects of prostaglandin analogues include thickening and lengthening of eye lashes, blepharitis, ocular irritation and pain, and congunctival hyperaemia.
- Sympathomimetics have local side effects including conjunctival hyperaemia, burning, stinging, pruritis and visual disturbances.
- Carbonic anhydrase inhibitors can cause local burning, itching, blurred vision, tearing, conjunctivitis, ocular discharge and eye lid pain.
- Miotics can cause blurred vision, allergic conjunctivitis, lens changes, myopia, pain and ciliary spasm. Headache commonly occurs, especially in the first 2–4 weeks of treatment.
Although rare, systemic side effects may occur in susceptible individuals with any of the five classes of drug.
- Patients should wash their hands before applying eye drops.
- Patients should not allow the tip of the container to touch their eyes or areas around the eye.
- Contamination with bacteria can cause eye infections, potentially causing loss of vision.
- When advising on the administration of eye drops, the following points should be covered:
- tilt head back and pull the lower eyelid down slightly to form a pocket between the eyelid and eye
- invert the container and press lightly with thumb and forefinger until a single drop is instilled into the eye
- replace the cap immediately after use.
If more than one preparation is being used, they should be administered at least 10 minutes apart.
Citation: The Pharmaceutical Journal URI: 20202911
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