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GLAUCOMA


an osmotic diuresis, can reduce the outflow of aqueous humour. Topical pilocarpine 1-2 % can be used to constrict the pupil and open the drainage angle. Beta-blockers, sympathomimetics, and prostaglandin analogues can also be used, with corticosteroids used to reduce inflammation. Typically, the unaffected eye is also treated as a means of prophylaxis.3-5


Open-angle glaucoma is the most common type accounting for approximately 10% of blindness registrants in the Scotland and the UK. Open-angle glaucoma is often reported as symptomless in early stages, as each eye working in tandem can usually compensate for minor defects in the visual fields. This condition usually affects both eyes and occurs in approximately 2% of people aged over 40 years, rising to a peak of 10% in those over 75 years of age.6 There is a strong hereditary link with a person at a 10 times greater risk of developing open-angle glaucoma if a first-degree relative is already affected by the condition. The condition is much more common in patients who also suffer from diabetes.


OPEN-ANGLE GLAUCOMA Open-angle glaucoma is characterised by damage to retinal ganglion cells and the optic nerve, resulting in a steady loss of visual field. Often the slow onset of this disease means it is usually not detected by the patient and most often is picked up by routine screening by an optometrist.7


For treatments to be effective in the cases of open–angle glaucoma, early diagnosis is key. The ultimate aim of treatment is to reduce intraocular pressure by 20-40 % and to prevent further damage to the optic nerve and visual field. 7 Prostaglandin analogues such as latanaprost or prostamide 6,8 are the first line of treatment. Alternatively, if these agents are contraindicated or ineffective, a beta-blocker can also be used. Sympathomimetics and carbonic anhydrase inhibitors are second line therapies. Combination preparations can be used to help with patient compliance, particularly in older people, as they can reduce the frequency of administration and reduce the resulting “washout” effects. 9 Miotic agents can be effective, however often they are not used as first line. This is mainly due to the unpleasant ocular side effects, which can manifest, including


burning, itching, and blurred vision.


CONGENITAL GLAUCOMA (BUPHTHALMOS) Congentical glaucoma is present from birth, however is rarely recognised until infancy or early childhood. It results from incorrect development of the eye’s aqueous outflow system, and similarly leads to increased ocular pressure and a loss of visual field. Intraocular pressure rises can be experiences in utero, under the age of three, or up to 16 years old. The disease is realtively rare however the impact upon the person’s visual development can be significant. Early recognition and initiation of appropriate therapy can drastically improve vision, and ensure healthier visual development. 10 Signs of congenital glaucoma include enlargement of the eyes, watering eyes, and often these symptoms are in combination with photophobia and clouding of the cornea.


This form of glaucoma requires surgery in order to rectify the abnormal development. The patient will also require continuous monitoring of intraocular pressure post operatively.


SECONDARY GLAUCOMA Rises in intraocular pressure are frequent complications of other eye conditions, and can include:


Inflammation of the iris – Iritis can result in focal adhesions of the iris and lens, blocking the flow of aqueous humour between the two chambers of the eye. Chronic infiltration of pro- inflammatory cells can lead to physical


blockage of the trabecular meshwork. 11


Steroid-induced glaucoma – Prolonged use of steroids (including nasal, dermal, inhaled, or systemic) can result in this form of glaucoma. The rise in intraocular pressure is reversible, however the visual field defects are irreversible.12


Injury – Intraocular injury can directly affect the angel or can cause obstruction of the trabecular meshwork by blood cells. Cataract like changes following an injury can lead to lens swelling and partial obstruction of the forward chamber within the eye.


Neovascularisation of the iris – growth of new blood vessels on the iris can result in fibrosis and closure of the angle. New vessels can also block the meshwork directly if they grow into


the anterior angle. This usually occurs


as a side effect of diabetic retinopathy. 13


PHARMACOLOGICAL TREATMENTS FOR GLAUCOMA Parasympathomimetic drops (miotics) – such as pilocarpine (1-4%) eye drops. These constrict the pupil and exert a ‘pull’ on the trabecular meshwork thereby increasing outflow of aqueous humour from the anterior chamber. They may cause blurred vision (due to loss of accommodatory change) especially in younger patients. It should be noted that pilocarpine should not be used if inflammation is present in the eye.


Sympathomimetic drops – such as brimonidine tartrate drops (selective alpha-2-adrenoceptor agonist) can be used as a monotherapy alternative to beta-blockers in patients who are at risk of pulmonary complications. They may be effective in reducing intraocular pressure alone or as adjunctive therapy with beta-blockers.


Beta-blocker topical drops – such as betaxolol, carteolol, levobunolol, or timolol. Topical application of these drugs reduces secretion of aqueous humour. Contra-indications to their use include a history of pulmonary or heart disease (since topical drops may cause a systemic beta-blockade). The use of punctal occlusion or simply shutting eyes for several minutes after application of drops can reduce drug entry into the lacrimal ducts and subsequently to the systemic circulation.


Prostaglandin analogues and prostamides – such as latanoprost, travoprost, tafluprost, or bimatoprost (synthetic prostamide). These medicines increase uveoscleral flow and subsequently reduce intraocular pressure. They are indicated and recommended as a first line for open-angle glaucoma and ocular hypertension. Each of these medicines has the advantage of once daily administration however patients should be warned that they might increase the brown pigment in the iris.


Carbonic anhydrase inhibitors - There are two topical carbonic anhydrase inhibitors, dorzolamide and brinzolamide. Brinzolamide is generally accepted as more comfortable for patients to use, owing mainly to neutral pH. Acetazolamide tablets (250mg - 1g/day) and SR capsules (250- 500mg/day) are now rarely prescribed; these serve to reduce


secretion of aqueous humour and can quickly reduce intraocular pressure. They can induce several side effects including nausea, lethargy, and development of renal stones; hence the need to be used with caution.


Glaucoma continues to be a commonly encountered disease of the eye, with pharmacological intervention a core treatment option for many patients. As Pharmacists within the community setting, it is important to be familiar with the pharmaceutical therapeutics available, and also be aware of the signs and symptoms for medical emergencies associated with the eye; and also, the chronic conditions which affect so many of the general population. This will help ensure the highest quality of pharmaceutical care continues to be available for each patient. •


REFERENCES:


1. Epidemiology of common eye disease. The Scottish Government. Available: http://www.gov.scot/Publica- tions/2006/12/13102441/18. Accessed 7th July 2015.


2. Bell JA. Glaucoma, primary open angle. eMedicine ophthalmology from WebMD 2013. Available: http://emedi- cine.medscape.com/article/1206147- overview. Accessed 7th July 2015. 3. Rhee DJ. Angle-closure glaucoma, Treatment. The Merck Manuals online Medical library. Available: http://www. merckmanuals.com/professional/eye_dis- orders/glaucoma/angle- closure_glau- coma.html. Accessed 7th July 2015. 4. Harvey R. In the management of acute angle closure glaucoma is intrave- nous acetazolamide now an outdated treatment? Eye News 2009; 15: 44-50. 5. European Glaucoma Society Guide- lines. Terminology and guidelines for glaucoma, 3rd edition. 2010. Available: http://www.eugs.org/eng/egs_guide- lines_reg.asp. Accessed 7th July 2015. 6. National Institute for Health and Clinical Excellence. Glaucoma Quick Reference Guide CG85, NICE 2009. Avail- able: http://www.nice.org.uk/nicemedia/ live/12145/43791/43791.pdf. Accessed 8th July 2015.


7. Rhee DJ. Primary Open angle glaucoma. The Merck Manuals online Medical library 2012. Available: http:// www.merckmanuals.com/professional/ eye_disorders/glaucoma/primary_ open- angle_glaucoma.html. Accessed 8th July 2015.


9. Konstas AGP. 24 hour control with a latanoprost-timolol fixed combination versus timolol alone. Arch Opthalmol 2006; 124: 1553-57.


10. Cibis GW et al. Glaucoma, primary congenital. eMedicine Ophthalomol- ogy from WebMD 2011. Available: http://emedicine.medscape.com/ article/1206081-overview. Accessed 8th July 2015.


11. Farooqui SZ et al. Uveitis, classifica- tion. eMedicine from WebMD, 2012. Available: http://emedicine.medscape. com/article/1208936-overview. Accessed 8th July 2015.


12. Mohan R and Muralidharan AR. Steroid induced glaucoma and cataract. Ind J Ophthalmol 1998; 37(1): 13-16. 13. Freudenthal J et al. Neovascular Glaucoma. eMedicine from WebMD, 2011. Available: http://emedicine. medscape.com/article/1205736-overview. Accessed 9th July 2015.


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