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GLAUCOMA


> increasing the social and economic burden of this disease1


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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 treatment4,5


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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


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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


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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 eye5,8


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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.


20 - PhARmAcY IN focUS


Around 20 per cent 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 factor6,9


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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 one in ten of those with untreated ocular hypertension will go on to develop


too many side effects and so eye drop formulations are used1,4


.


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-term1,4


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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 alone1,4


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combination eye drops are also available to reduce IoP when single


• Use your finger to gently pull down lower eyelid • hold bottle over eye and allow a single drop to fall into pocket you have created in the lower lid


• close your eye and keep it closed for at least two to three minutes • If using more than one type of eye drop, leave at least five minutes between instillations


Table 2: Eye drop instillation advice,5


glaucoma. As a result, some people with ocular hypertension will receive treatment based on their estimated risk of developing coAg1,9


.


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


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


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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 optician’s. 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


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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/1 205298-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]


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