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CPD 61: AN EYE ON GLAUCOMA Biography - Sinead Ryan graduated from the University of Brighton in 2008, and completed her pre-registration in Chelsea and Westminster Hospital NHS Foundation Trust, London. She worked in a number of clinical positions in London before returning to Ireland in 2011. She completed her higher diploma in community pharmacy from Trinity College Dublin in 2014. Sinead is currently working as a community pharmacist in Limerick.

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Glaucoma is the second most common cause of blindness both in Europe and worldwide, and the most common cause of irreversible blindness in the world. It is estimated that 2% of the Irish population over 40 years of age have Chronic Open Angle Glaucoma, rising to almost 10% in people older than 75 years. Approximately 10% of Irish sight impaired registrations are attributed to glaucoma and it accounts for between 20 and 40% of hospital outpatient eye service appointments each year. Glaucoma can be classified into two broad types: primary glaucoma, which includes chronic open angle glaucoma, which accounts for 80% of cases, and closed angle glaucoma. Secondary glaucoma has many causes including medicines (e.g. corticosteroids), inflammation and tumours. Chronic Open Angle Glaucoma (COAG) is the most common form of glaucoma but is unusual in patients under 40 years of age. Ocular hypertension (OHT) is a major risk factor for developing COAG, although COAG can occur with or without raised eye pressure.

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An eye on Glaucoma Glaucoma is an umbrella term given to a wide range of conditions which have different features and mechanisms, but which can all potentially lead to characteristic optic disc damage, loss of vision and eventual permanent sight loss. It is usually associated with raised intraocular pressure (IOP) and usually occurs when aqueous humour does not drain from the eye correctly. It can be asymptomatic until advanced and many people will be unaware there is a problem with their eyes until severe visual damage has occurred.

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Once diagnosed, people with COAG require lifelong monitoring so that any progression of visual damage can be detected. Once lost, sight cannot be restored, and controlling the condition, together with prevention, or at least minimisation of ongoing damage, is crucial to maintaining a sighted lifetime. Glaucoma progression depends on many factors, including age at time of diagnosis, visual function and the rate of progression. There are a number of treatment options for Chronic Open Angle Glaucoma. Reducing intra-ocular pressure (IOP) is the only treatment strategy with good evidence of clinical effectiveness in open angle glaucoma. There is no specific target for lowering IOP; the target and monitoring interval varies according to the severity of the disease and risk of progression. Prostaglandin analogues include latanoprost, tafluprost and travoprost. These, in addition to bimatoprost (a prostamide), are usually used as first-line treatment because they are the most-effective IOP-lowering agents, do not cause significant systemic side effects, are well tolerated and are used once a day. Closed angle glaucoma accounts for 50% of glaucoma related sight impairment cases worldwide and progresses rapidly. It is classified as a medical emergency that requires urgent medical treatment. It is caused by a closed drainage angle, and glaucomatous damage, which results in a dramatic rise in intraocular pressure (IOP) if not dealt with promptly. Symptoms include pain, redness, blurring of vision, the presence of halos around lights, nausea and vomiting.

60 Second Summary Glaucoma is the second most common cause of blindness both in Europe and worldwide, and the most common cause of irreversible blindness in the world. It is estimated that 2% of the Irish population over 40 years of age have Chronic Open Angle Glaucoma, rising to almost 10% in people older than 75 years. Glaucoma can be classified into two broad types: primary glaucoma, which includes chronic open angle glaucoma, which accounts for 80% of cases, and closed angle glaucoma. Secondary glaucoma has many causes including medicines (e.g. corticosteroids), inflammation and tumours. There are a number of treatment options for Chronic Open Angle Glaucoma. Reducing intra-ocular pressure (IOP) is the only treatment strategy with good evidence of clinical effectiveness in open angle glaucoma. There is no specific target for lowering IOP; the target and monitoring interval varies according to the severity of the disease and risk of progression. Chronic Open Angle Glaucoma is a progressive optic neuropathy caused by mechanical and vascular factors affecting the optic disc and optic nerve. It is most often caused by the rising of the internal pressure within the eye, which is called intra-ocular pressure (IOP). Prostaglandin analogues/beta blocker combinations are available for patients who do not achieve the target IOP with monotherapy. These include XalacomÂŽ (timolol and latanoprost), GanfortÂŽ (timolol and bimatoprost) and Duo-TravÂŽ (timolol and travoprost). Acute closed angle glaucoma is an ocular emergency that requires urgent treatment in accident and emergency. The goal of therapeutic management by the ophthalmologist is to reduce the IOP to a safe level as quickly as possible.


CPD 61: AN EYE ON GLAUCOMA

Characteristic changes in Glaucoma

Risk Factors for COAG

- Reduced peripheral vision

- Increasing Age: risk of glaucoma increases with every decade of life after the age of 40.

- Structural changes to optic nerve

- Increase in Intra-ocular pressure (IOP)

- Positive family history in a first degree relative with COAG

- Decrease in size or obstruction of drainage angle

- Ethnicity – higher incidence in African or Caribbean decent

Classification of Glaucoma

- Elevated eye pressure

 Primary Glaucoma - not associated with other ocular or systemic disease.

- High Myopia (Large Distance Vision Prescription)

- Chronic Open Angle Glaucoma (COAG)

- Co-morbidities – Diabetes and Hypertension

 Secondary Glaucoma – associated with other ocular or systemic disease

Usually asymptomatic until there is significant loss of peripheral and central vision. Early COAG can be challenging to diagnose, as it is often symptomless until a large amount of neural damage has occurred, resulting in vision loss. A reduction in vision in one eye may be missed due to compensation of the other eye and the patient does not notice their vision has changed. In the later stages of the condition the patient will notice that they have ‘tunnel vision’.

- Acute Closed Angle Glaucoma (CAG)

- Pseudoexfoliative Glaucoma - Steroid Induced Glaucoma

 Congenital Glaucoma – Glaucoma present at birth or early infancy caused by obstruction of the drainage angle or obstruction of aqueous outflow. Primary Glaucoma - Chronic Open Angle Glaucoma (COAG) Chronic Open Angle Glaucoma is a progressive optic neuropathy caused by mechanical and vascular factors affecting the optic disc and optic nerve. It is most often caused by the rising of the internal pressure within the eye, which is called intra-ocular pressure (IOP). This causes damage to the internal structures of the eye and can lead to sight loss. COAG has a characteristic appearance of the optic nerve head and retinal nerve fibre layer.

Symptoms of COAG

Treatment of COAG The European Glaucoma Society (EGS) states the aim of treatment in glaucoma is to “maintain the patient’s visual function and related quality of life, at a sustainable cost.” Currently, pharmacological treatment is used first-line unless the patient presents with sightthreatening COAG. Ocular hypotensives (e.g. prostaglandin analogues, beta-blockers, alpha-adrenergic agonists and carbonic anhydrase inhibitors) act either to reduce the production of intra-ocular

fluid, increase the outflow, or a combination of both. Two significant clinical trails the Collaborative Normal Tension Glaucoma Study (CNTGS) and the Early Manifest Glaucoma Trial (EMGT) have confirmed the role of IOP-lowering drugs in the treatment of COAG. The greatest reduction of IOP is achieved by the prostaglandin analogues, followed by non-selective beta-blockers, alpha-adrenergic agonists, selective beta-blockers and finally topical carbonic anhydrase inhibitors.NICE guidelines recommend monotherapy as first line treatment. If the first monotherapy tried does not bring the IOP to the required target, or the patient does not tolerate the treatment, then NICE guidelines recommend changing to another monotherapy. If the patient does not respond to one prostaglandin analogue they may be switched to another prostaglandin analogue, as there are reports that patients who do not respond to one prostaglandin analogue may respond to another. The NICE guidelines recommend if the patient shows signs of responding to the monotherapy treatment and is tolerating the drug but did not achieve target levels of IOP then a second drug is added. Combination drops are generally used to improve adherence and decrease the amount of preservatives to which the patient is exposed to. Prostaglandin Analogues (PGA) and Prostamides The prostaglandin analogues latanoprost (Xalatan®), tafluprost (Saflutan®), and travoprost (Travatan®), and the synthetic prostamide, bimatoprost (Lumigan®), increase uveoscleral outflow and subsequently reduce intra-ocular pressure. These are the first line treatment for COAG as they are the most effective IOPlowering agents; they do not cause systemic side effects, are generally well tolerated and are used once a day, which improves adherence.


CPD 61: AN EYE ON GLAUCOMA

Prostaglandin analogues act by increasing uveoscleral outflow, reducing IOP by 2530%. IOP increases during the night and is at its highest in the morning therefore the drops should be instilled at night to produce a maximum effect the following morning. Reduction in IOP starts two to four hours after first administration, with a maximum effect achieved three to five weeks after starting treatment. The main side effects of prostaglandin analogues are eye redness which usually reduces with continued treatment, prolific eyelash growth (hypertrichosis), darkening of the iris and changes to peri-orbital tissue fat atrophy. Beta-blockers Topical application of a beta-blocker to the eye reduces intra-ocular pressure effectively in primary open-angle glaucoma, by reducing the rate of production of aqueous humour. Beta-blockers used as eye drops include betaxolol (Betoptic®), carteolol (Teoptic®), levobunolol (Betagan®) and timolol (Timoptol®). Beta-blockers, generally used twice a day, reduce the production of aqueous humour and tend to be more effective during the day than at night. They decrease IOP by approximately 25%, but there have been reports of patients developing tolerance. The main disadvantage of beta-blockers is that they can cause systemic side effects, including wheezing, dysponea, bronchospasm, bradycardia and hypotension. They are contraindicated in patients with bronchial asthma, severe chronic obstructive pulmonary disease, bradycardia, severe heart block or overt cardiac failure. There is a risk of inducing bronchospasm with beta blocker eye drops in patients with asthma, therefore an alternative treatment should be used where possible. Contact dermatitis can arise from overflow of the drops on to the skin. Sympathomimetics (Alpha – adrenergic agonists) Brimonidine (Alphagan®) is a selective alpha2-adrenergic agonist. It has a dual action, reducing aqueous production and increasing outflow of aqueous humour. It is licensed as monotherapy for patients in whom betablockers are contraindicated, or as an add-on therapy for patients whose IOP target has not been met. It is less effective at lowering IOP than latanoprost but comparable to timolol. In clinical trials approximately 13% of patients experienced an allergic reaction to Brimonidine which included blepharitis and conjunctivitis this reaction occurred three to nine months after the start of treatment. Apraclonidine (Iopidine®) is also licensed as add-on therapy but has a higher incidence of allergic reactions than brimonidine.

ocular pressure by reducing aqueous humour production. They reduce IOP by less than 20%. Dorzolamide and brinzolamide are topical CAIs and Acetazolamide is a systemic CAI. The topical CAIs are less effective than systemic CAIs (e.g. acetazolamide) but cause fewer side effects. Dorazolamide causes more ocular irritation than brinzolamide, probably because its formulation has a lower pH. Each can cause a bitter taste in the mouth. They are licensed for use in patients resistant to beta-blockers or those in whom beta-blockers are contra-indicated. They can be used alone or in conjunction with topical betablockers. All Carbonic Anhydrase Inhibitors are sulphonamides, they are contraindicated for patients allergic to sulphonamide antibiotics.

the target IOP is not achieved another PGA is added or a PGA/beta-blocker combination is prescribed. If the target IOP is still not met, a PGA and a beta-blocker/CAI combination would be used. Then an alpha-agonist (e.g. brimonidine) can be added or can replace the CAI. At this point surgery is considered an option or earlier in the case of advanced COAG.

Combination Therapies

 Do not respond to therapy;

Prostaglandin analogues/beta blocker combinations are available for patients who do not achieve the target IOP with monotherapy. These include Xalacom® (timolol and latanoprost), Ganfort® (timolol and bimatoprost) and Duo-Trav® (timolol and travoprost). Since benzalkonium chloride can cause toxic conjunctivitis, combination products offer reduced exposure to this preservative (one drop per day, compared to three drops if the eye drops are administered separately).

 Are non-compliant with pharmacological treatment, or have a significant chance of not complying with treatment.

Carbonic Anhydrase Inhibitors/beta blocker combinations are available for patients who do not achieve the target IOP with monotherapy. Cosopt® (dorzolamide and timolol) and Azarga® (brinzolamide/timolol) are available.

Carbonic anhydrase inhibitors (CAIs) and systemic drugs

Treatment Strategies

The carbonic anhydrase inhibitors, acetazolamide (Diamox®), brinzolamide(Azopt®), and dorzolamide(Trusopt®), reduce intra-

NICE suggests that for early or moderate COAG, the treatment of choice is a prostaglandin Analogue (PGA). In practice, if

Surgery NICE recommends that surgery is indicated in individuals with COAG who  Are at risk of progressing to sight loss despite treatment;

Trabeculectomy or filtration surgery is the most commonly performed surgical procedure to lower IOP. This surgery creates an alternative pathway for the escape of aqueous humour. This ensures the IOP is lowered to target levels. Adherence and eye drop instillation technique It is important to check the person’s adherence to their treatment regimen. In addition, in some cases treatment failure can be attributed to incorrect eye drop instillation techniques. Patients sometimes have difficulty understanding the need for treatment in COAG as they perceive COAG as asymptomatic and need to be reminded of the long term consequences of non adherence to eye drops.


CPD 61: AN EYE ON GLAUCOMA This usually occurs in patients over 60 years of age and has a strong genetic component. There is often significant damage by the time the disease is diagnosed and it progresses rapidly, even in patients treated with IOP-lowering medicines. Secondary Glaucoma – Steroid- induced Glaucoma This is caused by structural changes to the drainage canal caused by corticosteroid use, which leads to decreased outflow facilities in certain predisposed patients. The risk of increased IOP depends on the strength of the corticosteroid, dose frequency, duration of therapy and route of administration. Risk factors for developing raised IOP with corticosteroids include a family history of glaucoma, diabetes, myopia, and old age. Elevated IOP usually develops two to six weeks after initiating corticosteroid therapy. Congenital Glaucoma

Primary Glaucoma - Acute closed angle glaucoma Acute closed angle glaucoma has a very distinct clinical presentation and its symptomatic nature means, such patients may be seen in primary care prior to attending the hospital eye services. It is the most visually destructive form of glaucoma. It is caused by an occluded drainage angle, which obstructs the outflow of aqueous humor, and glaucomatous damage will occur if the resulting rise in IOP is not dealt with promptly. The very high IOP can cause ischaemic damage to the iris, necrosis of the lens leading to opacities and damage to the optic nerve. Risk Factors for Acute closed angle glaucoma - Age over 40 years

- Ethnicity - higher prevalence in Asian populations - Females - 75% of cases

Symptoms and Signs of Acute closed angle glaucoma  Nausea and Vomiting  Blurred Vision  Halos around lights  Painful eye  Red swollen eye with mid-dilated pupil Treatment of Acute closed angle glaucoma Acute closed angle glaucoma is an ocular emergency that requires urgent treatment in accident and emergency. The

goal of therapeutic management by the ophthalmologist is to reduce the IOP to a safe level as quickly as possible. Once a safe IOP is established and inflammation has reduced a surgical procedure called laser iridotomy or surgical iridotomy is possible. This surgery creates a “hole in the iris” which allows the aqueous humour to be released. Systemic osmotic diuretics (e.g. oral glycerol or intravenous mannitol) are used to dramatically reduce IOP. Care needs to be taken inpatients with kidney or heart disease, as osmotic diuretics will initially increase blood volume. Topical Corticosteroids (Prednisolone 0.5%) eye drops are used to reduce inflammation. A combination of systemic carbonic anhydrase inhibitors, such as acetozolomide and topical IOP-lowering drugs such as prostaglandin analogues, beta-blockers and alpha-agonists. These are used to reduce aqueous humour production in the eye and thus lower IOP. Pilocarpine 2% eye drops are used to constrict the pupil and open the anterior chamber angle. However, it is ineffective until a decrease in pressure has been achieved with other medicines. Once the surgical/laser iridotomy has been performed on one eye, it is recommended that a prophylactic iridotomy be performed on the other unaffected eye due to the high risk of recurrence. Secondary Glaucoma – Exfoliative (Pseudoexfoliative) Glaucoma This is caused by a buildup of protein and pigment granules from the iris in the drainage canal, which inhibits the drainage of the aqueous humour resulting in an increase in IOP.

The treatment of choice in congenital glaucoma is surgery, as long-term pharmacological treatment is not practical. Ocular antihypertensive drugs are not generally used in children. Prostaglandin analogues are less effective in children (latanoprost and travoprost have paediatric licenses), and alpha-adrenergic agonists are contraindicated in young children. Carbonic anhydrase inhibitors or beta-blockers as treatment options, subject to license restrictions. Pharmacists Role  To educate and discuss patients’ diagnosis, prognosis and treatment and prevention of sight loss.  That COAG in the early stages has no symptoms.  To offer advice on compliance and adherence to their treatment regimen.  To emphasis the importance of the patients’s role in their own treatment – for example the ongoing regular application of eye drops to preserve sight.  How to apply eye drops including technique (punctual occlusion) and hygiene (storage recommendations).  Advise patients with dexterity issues on aids to help patients administer eye drops e.g. Opticare®, AutoSqueeze®  Support Groups  To advise that glaucoma can run in families and that family members over 40 years old may wish to be screened for the disease.

Cpd 61  
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