Glaucoma

Glaucoma is one of the most common eye conditions encountered in primary care. It is a disease of the optic nerve including characteristic damage to the optic nerve head and typical defects in the visual field, with or without increased intraocular pressure (IOP)¹. This generally leads to a progressive loss of sight affecting one or both eyes, though it often progresses more quickly in one eye than in the other². Glaucoma is a leading cause of blindness with approximately 10% of UK blindness registrations attributed to the disease and on a global scale, it is the second leading cause of blindness after cataracts^1,3. Therefore it is critical that we as pharmacists should have a deep understanding of this condition, how it presents and the medication used to treat it.

Risk factors associated with glaucoma include:

• Positive family history – incidence increases two to four fold if have an affected sibling
• Age – glaucoma becomes more likely as get older, with most people aged over 75 at diagnosis
• People of African, Afro-Caribbean or Asian descent are at increased risk of developing certain types of glaucoma
• Raised IOP
• Myopia (short sightedness)
• Diabetes
• Female gender
• Conditions that significantly restrict blood flow to eye e.g. diabetic retinopathy
• Prolonged use of steroids
• Eye trauma
• Systemic hypertension²

There are several different types of glaucoma. Table one outlines the most common types.

Chronic open angle glaucoma (COAG):

This is the most common type of glaucoma accounting for over 70% of cases. As there is a chronic degenerative obstruction that does not allow the aqueous humour to properly drain away from the eye, IOP is increased². The condition usually develops slowly and painlessly over many years, so that damage to the optic nerve and loss of sight are gradual. A patient will often not realise they have COAG as the peripheral vision is affected first. Without treatment, vision towards the centre of the eye may also be lost and patients may present with significant loss of sight^4,5.

In the UK, around 1 in 50 people aged over 40 have COAG, rising to around 1 in 10 people aged over 75. It is unusual in those aged under 35. If left completely untreated, progression to severe sight impairment typically takes between 25 to 70 years from onset, with those of African descent more likely to become blind². With an aging population and longer life expectancy, the number of patients with COAG is predicted to rise, increasing the social and economic burden of this disease¹.

Acute angle-closure glaucoma (AACG):

As the drainage of aqueous humour is blocked by the bowing of this iris against the trabecular meshwork, pressure in the eye builds up. This type of glaucoma is a medical emergency that requires urgent reduction of IOP to prevent loss of vision. Symptoms can include intense eye pain and redness, headache, tenderness around the eyes, blurred vision and nausea. Patients presenting with these types of symptoms should be immediately referred for specialist assessment and treatment^4,5.

Secondary glaucoma:

This is an uncommon type of glaucoma caused by another eye problem. Symptoms vary considerably but may include a gradual loss of peripheral sight, blurred vision, eye pain, eye redness and seeing halos around lights⁵. Steroid-induced glaucoma is a form of secondary glaucoma that is usually associated with topical steroid use, though it may develop with inhaled, oral, intravenous, or intravitreal steroid administration. Steroid-induced glaucoma typically occurs within a few weeks of starting steroid therapy and spontaneously resolves in most cases within a few weeks or months after stopping the steroid. In rare cases, intra-ocular pressure remains raised⁷.

Childhood glaucoma:

Also referred to as congenital glaucoma, this is a type of glaucoma affecting babies and young children typically diagnosed within the first year of life. It is a rare condition that causes ocular fluid and pressure build up resulting from developmental eye defects. This in turn damages the optic nerve. Symptoms can be difficult to identify, but can include unusually large eyes, excessive tearing, light sensitivity and red or cloudy eyes. Surgery is often needed to correct structural defects within the eye^5,8.

Normal-tension glaucoma:

Patients with a normal IOP who develop optic nerve damage and visual field defects are defined as having normal-tension glaucoma, also referred to as low-tension glaucoma. Around 20% of patients with glaucoma have normal IOP (typically defined as being between 12 – 22mmHg). The causes are still unknown and research continues to uncover why some optic nerves are damaged by relatively low eye pressures. Interestingly, people with a history of systemic heart disease such as an irregular rhythm have been found to be of greater risk. This suggests vascular dysregulation could be a contributing factor^6,9.

Ocular hypertension:

Some patients have increased IOP with no damage to the optic nerve or loss of vision. Raised eye pressure without signs of glaucoma is called ocular hypertension. This condition increases a person’s risk of developing glaucoma. Around 1 in 10 of those with untreated ocular hypertension will go on to develop glaucoma. As a result, some people with ocular hypertension will receive treatment based on their estimated risk of developing COAG^1,9.

Treatment

Eye drops are the main stay of treatment for glaucoma⁴. NICE recommends treatment with a prostaglandin analogue for those patients with early or moderate COAG (the most common type of glaucoma seen in community practice)¹. The most common prostaglandin analogues include Latanoprost, Tafluprost and Travoprost. These drugs reduce IOP by increasing the eyes outflow of aqueous humour⁴.

If IOP has not been reduced sufficiently to prevent the risk of progression of vision loss, alternative treatment can be offered. More than one agent may be used concurrently to achieve optimal IOP¹.

Beta-blockers reduce the rate of production of aqueous humour. Examples include Betazolol and Timolol. Oral administration results in too many side effects and so eye drop formulations are used^1,4.

Carbonic anhydrase inhibitors such as Brinzolamide and Dorzolamide eye drops decrease IOP by reducing aqueous humour production, but are generally used in patients resistant to beta-blockers or in those for whom beta-blockers are contra-indicated. Acetazolamide is a systemic carbonic anhydrase inhibitor given orally or via injection. It is used as an adjunct and should not be given long-term^1,4.

Sympathomimetics, such as the selective alpha₂-adrenoceptor agonist Brimonidine, are also an option in COAG treatment when other agents are either inappropriate or have failed to control IOP alone^1,4.

Combination eye drops are also available to reduce IOP when single agents alone are not adequate⁴. These products combine the beta-blocker Timolol with either a prostaglandin analogue or a carbonic anhydrase inhibitor. Examples include Latanoprost + Timolol and Brinazolamide + Timolol. Patient adherence can be improved as these products reduce the amount of drops a patient must instil.

It is vital to check patient adherence and eye drop instillation technique before alternative therapy is commenced as many patients do not use these eye drops correctly and so receive sub-optimal therapy. Table two outlines the key advice to give to patients instilling eye drops.

If eye drops alone do not lower IOP sufficiently, laser treatment may be offered. Also called laser trabeculoplasty, small holes will be created in the trabecular meshwork to improve aqueous humour drainage. Eye drops may still be needed after this treatment. Surgery is also an option. A trabeculectomy creates a channel for the aqueous humour to bypass the trabecular meshwork¹.

The outlook for glaucoma varies depending on which type a patient is diagnosed with, but generally it will result in some degree of permanent vision loss. It may affect the ability to carry out certain tasks, but most retain useful vision for life. Only a small proportion of people glaucoma cases result in blindness⁵. It is useful to remember that patients who drive and have glaucoma causing loss of vision in both eyes must, by law, inform the Driver and Vehicle Licensing Agency (DVLA)⁹.

The long-term outcome of glaucoma is better with earlier diagnosis and treatment. Glaucoma can usually be detected during a routine eye test at an opticians. This eye check can detect the early signs of glaucoma before significant vision loss has occurred. As pharmacists, we should encourage patients to have routine tests at least every two years, especially those aged over 50. These eye tests will include measurements of the intra-ocular pressure and tests of peripheral vision and are especially important for those with associated risk factors as listed at the start of this article⁵.

References

1. NICE Clinical Guideline 85 Glaucoma: diagnosis and management https://www.nice.org.uk/guidance/cg85 [Online]
2. Patient: Glaucoma and ocular hypertension http://patient.info/doctor/glaucoma-and-ocular-hypertension [Online]
3. Quigley, Br J Ophthalmol. The number of people with glaucoma worldwide in 2010 and 2020 http://bjo.bmj.com/content/90/3/262.short [Online]
4. British National Formulary Issue 72
5. NHS Choices Glaucoma http://www.nhs.uk/conditions/Glaucoma [Online]
6. Glaucoma Research Foundation. Normal-tension glaucoma http://www.glaucoma.org/glaucoma/normal-tension-glaucoma.php [Online]
7. Medscape. Drug-induced glaucoma http://www.emedicine.medscape.com/article/1205298-overview [Online]
8. Glaucoma Research Foundation. Childhood glaucoma http://www.glaucoma.org/glaucoma/childhood-glaucoma-1.php [Online]
9. Patient: Chronic open-angle glaucoma http://patient.info/health/chronic-open-angle-glaucoma glaucoma [Online]