Medical management of glaucoma.
COURSE CODE: C-13472 O/SP/AS
Although glaucoma is largely managed by ophthalmologists in a hospital setting, there are many optometrists who are intending, or already are, practising glaucoma management in a shared care setting, either in their own practice, in a hospital or at a polyclinic. This article is aimed to provide an overview of the management of glaucoma by optometrists, to equip them with the necessary skills to perform this service. Before discussing the actual medical management options, it has to be emphasised that correct diagnosis based on the patient's history and examination is an essential precursor to correct treatment.
Guidelines for the diagnosis and management of adult chronic open angle glaucoma and ocular hypertension from the National Institute for Health and Clinical Excellence (NICE) aims to standardise care for glaucoma sufferers and prevent people from going blind. This article should therefore be read in conjunction with this guidance, which provides greater detail regarding specific monitoring and treatment pathways. The guidance is available at www.nice.org.uk. (1)
Diagnosis--does the patient really have glaucoma and if so what kind?
Primary open angle glaucoma (POAG) is still the most common form of glaucoma in the UK population, and the majority of it is suited to medical management alone. However, the proportion of people with glaucoma in areas with a significant ethnic population is actually much more than the incidence traditionally found in the UK and American literature. (2,3,4) One example is the increased incidence of angle closure glaucoma (ACG) without hypermetropia in the Chinese population. There is a danger that diagnosis of POAG is assumed automatically because it is common and that the medical treatment of secondary and complex glaucoma may not control the condition. Another example is unilateral glaucoma from previous trauma, perhaps from a long time ago, which resulted in secondary glaucoma from angle recession or peripheral anterior synechia. These more unusual diagnoses may be more common than you think and it is important not to miss them.
The diagnosis of glaucoma is determined principally by the patient's and family history (taking account of increased risk factors such as diabetes and hypertension), the presenting intraocular pressure (IOP) measured by Goldmann applanation tonometry (adjusted for central corneal thickness), gonioscopy, visual field examination and optic nerve head assessment with dilated pupils and using stereoscopic indirect ophthalmoscopy (Figure 1). Optic nerve and nerve fibre layer imaging are also useful. The initial diagnosis should be considered provisional and recorded at the outset but may need reviewing; for example POAG that progresses despite "normal" IOP may need to be changed to normal tension glaucoma (NTG), or the drainage angle may be initially open but become narrower over time.
Deciding to treat: where to set target IOP
The problem here is trying to decide where along the continuum between ocular hypertension and NTG the individual case lies. The main question to ask is whether the optic nerves are already damaged and are not tolerating the presenting IOP (if so, the patient has glaucoma) or if the raised IOP is not causing damage, whether it is so high that you think the onset of glaucoma is a certainty, or that there is a risk of retinal vein occlusion (if so, the patient has ocular hypertension). If the patient has a "normal" IOP, no history of previous secondary temporary glaucoma (eg trauma, vitreoretinal surgery etc.) with definite glaucomatous damage, the diagnosis of NTG is straightforward and you need to set a low target IOP. If the case is not clear-cut, some factors in the history may help you to make a decision, such as family history suggesting NTG, vasospasm or migraine. Another clue is the pattern of visual field loss; the visual field loss of NTG is typically more central compared with IOP-dependant POAG. Often, however, it is a case of "suck it and see"--reviewing target IOPs as you go. For example, you may have two patients that present at the same time with identical moderately raised IOP and early glancomatous damage. Five years later, one patient may have done fine just with monotherapy achieving a target IOP of 18mmHg, with no progression at all. The second patient may have progressed and needs triple therapy with a target IOP adjusted to 10mmHg. Sadly, at present, there is no way of predicting with any certainty which path an individual patient will take. Hopefully, ongoing research into genotyping and phenotyping may help us to better tailor treatment to the individual at the point of presentation.
So you have decided to treat and set a target IOP
This now gets more straightforward. Fortunately, in the last 25 years, there has been great progress in developing an arsenal of effective medications. To give some idea of the change, in the mid-1980s options were restricted to pilocarpine and an adrenaline pro-drug, Propine. Timolol had been introduced five years earlier but was deemed too expensive to prescribe. Since then, the pharmaceutical industry has introduced topical carbonic anhydrase inhibitors (Trnsopt), alpha-2 agonists (Iopidine) and, best of all, prostaglandin analogues (Xalatan), followed by combination drugs and other rival branded preparations in these three new categories. There has been a small retrograde step recently in the UK with the NICE recommendation that prostaglandin analogues are not recommended first line therapy in the under 65s, on the grounds of cost, but this may change as Xalatan will shortly go off patent and so these drugs will fall in price.
As with diagnosis, it is important to measure IOP with applanation tonometry and adjust for corneal thickness. As a very rough rule of thumb, the favoured first and second line treatments are beta-blockers or prostaglandin analogues, unless contraindicated. On their own, these should achieve up to 30% IOP reduction and up to 50% together. It then is a simple matter of arithmetic; a patient with a presenting IOP of 24mmHg is probably fine on monotherapy having set a target IOP of 16mmHg, whilst a lower target IOP dictates dual therapy. If you are looking for a reduction beyond 50%, then surgery may be the best first line option (it is not unusual for a few patients with POAG to present with IOPs of over 40mmHg).
Specific medications Topical beta-blockers
Topical beta-blockers are a common first line treatment for existing glaucoma patients. They are relatively cheap and have a good track record of efficacy, with few topical side effects. Beta-blockers work by reducing aqueous production and should produce an IOP reduction of 20% to 30%. Examples of commonly used beta-blockers include:
* Timolol (Timoptol and Timoptolol-LA)
* Levobunolol (Betagan)
* Betaxolol (Betoptic)
* Carteolol (Teoptic)
The principle side effects of beta-blockers are systemic and relate to pre-existing systemic conditions. Beta-blockers are contraindicated in patients with bradycardia and hypotension. They can worsen peripheral vascular disease, can cause impotence and some patients have reported nightmares. One rare but significant side effect is that they can mask hypoglycaemia in diabetics. In addition, a patient may be asymptomatic but have a latent tendency to, for example, reversible airways disease, which becomes manifest after you start topical treatment.
[FIGURE 1 OMITTED]
Topical beta-blockers are absolutely contraindicated in heart failure and some forms of heart block, and in asthma and chronic obstructive airways disease (COAD). They should be used with caution in patients with diabetes and patients on calcium channel blockers. If patients are on systemic beta-blockers, there is a small risk that they may end up with too much beta-blocker. Also, the efficacy may be reduced as the patient is already benefiting from a small IOP reduction from the systemic beta-blocker.
In some patients, particularly those with NTG, topical beta-blockers may be counterproductive at night. They may exacerbate nocturnal bradycardia, and cause blood pressure to dip and possibly impair optic nerve head perfusion. In these patients, beta-blockers are prescribed for morning use only.
These systemic interactions may sound alarming but provided you exclude the important contraindications, it is unlikely that a patient under 65 years of age will develop problems. In older patients, there is a higher risk that they will have one of these conditions (COAD has an incidence of 15% and cardiovascular disease has an incidence of 25% in the over 65s), and that the beta-blocker will uncover something they did not know they had. It is very important that their GP knows they have been prescribed a beta-blocker and that there is communication between you both.
[FIGURE 2 OMITTED]
Examples of commonly used prostaglandin analogues include:
* Latanoprost (Xalatan)
* Travoprost (Travatan)
* Bimatoprost (Lumigan)
Prostaglandin analogues work by increasing uveoscleral outflow in the eye. In theory, acting in a physiological way is an advantage as these agents do not reduce aqueous production, which provides essential nutrition to the cornea and lens. In normal Caucasian eyes, it was estimated that 10% of outflow is through the uveoscleral route but this can be up to 35% in some individuals. In glancomatous eyes, which by definition have impaired trabecular outflow, the uveoscleral channel assumes more of the flow. Prostaglandin analogues are highly effective and may reduce IOP by up to 35%.
The principle side effects are local and are i) a tendency to induce a red eye, particularly upon initial use, ii) increased iris and eyelash pigmentation, and in mildly pigmented patients may cause darkening of the skin around the eyes, iii) eyelash growth, and iv) may precipitate or worsen cystoid macular oedema in aphakic eyes.
Although initial theoretical concerns about a general effect on cell division have proved unfounded, it is still contraindicated in pregnancy, mainly because prostaglandins are actually used to induce labour.
Topical carbonic anhydrase inhibitors
Examples of commonly used topical carbonic anhydrase inhibitors (CAIs) include:
* Dorzolamide (Trusopt)
* Brinzolamide (Azopt)
Topical CAIs act by reducing aqueous production and are slightly less effective than prostaglandin analogues or beta-blockers. They are thought to reduce IOP by 18% to 20% but this amount can be less in some individuals. Generally, these agents are found to cause more irritation than the prostaglandin analogues and can leave a bitter metallic taste in the mouth. Occasionally, they can be associated with corneal oedema. In spite of these issues, topical CAIs are a very useful second or third line therapy.
Systemic CAIs are rarely used in a shared care setting outside the hospital. They are more effective than topical CAIs and are successful in reducing very high IOPs quickly, but are a powerful systemic medication with significant side effects. Nevertheless, they have a role in severe chronic glaucoma that is hard to control and are safe in selected patients, if blood electrolytes are monitored.
Examples of commonly used alpha-2 agonists include:
* Apraclonidine (Iopidine)
* Brimonidine (Alphagan)
Alpha-2 agonists are useful in the hospital service for reducing peak IOPs. Iopidine is licensed for short-term use only, whilst brimonidine is licensed for long-term use as well, although their chemical structure and mechanism of action are very similar. These agents are effective particularly in the short term with up to 30% reduction in IOP. Alpha-2 agonists tend to be used as a third or fourth choice treatment in chronic glaucoma because of the relatively high prevalence of allergic conjunctivitis, which often presents months or even years after starting (Figure 2). Alpha-2 agonists can cross the blood-brain barrier and should be used with caution in elderly people because of risk of lethargy and confusion. They can also cause hypotension and have been associated with respiratory arrest in infants.
Examples of commonly used cholinergic agonists include:
Cholinergic agonists are the original glaucoma medication of 1856. They are still used in acute angle closure glaucoma but they now have a limited role in chronic glaucoma. They are actually contraindicated in phacogenic glaucoma because they cause a forward rotation of the ciliary body. Cholinergic agonists work by increasing aqueous outflow by a mechanical effect on the trabecular meshwork. This causes dimming of vision through miosis, blurring through accommodation in phakic patients, and red eye. Systemically, these agents are associated with headache and sometimes nausea, confusion and even vomiting.
Remember that each of these topical medications can cause allergic reactions to the principle ingredient, or to the preservative. Preservative-free treatments currently available for glaucoma management are shown in Table 1. Beta-blockers and Trusopt are available without preservative and a preservative-free prostaglandin analogue, Saflutan, has been recently released in the UK.
Diagnosis made, treatment started, what next?
Although the patient will come to no harm for several months if they fail to respond to treatment, it makes sense to establish that the patient is achieving target IOP. Therefore, patients should be assessed after four weeks unless they are taking prostaglandin analogues--these take longer to act and so the response should be checked in six weeks.
Before the patient leaves the initial consultation, you need to spend time explaining the nature of the condition, especially the fact that glaucoma is silent and asymptomatic in the earlier stages, and the importance of treatment and to emphasise that it is almost certainly for life. Some patients will have a relation or will know of someone who has gone blind from glaucoma, and will be anxious by the diagnosis. It therefore helps a great deal to explain that early-diagnosed glaucoma is treatable. Patients vary greatly in the amount of information they want from you, some will be happy to take your advice and follow it but others can be reluctant to accept it. Some have no questions, some have many, and others will be searching the Internet as soon as they get home.
Most patients will also need advice about instilling the drops. Some patients will find this difficult due to arthritis or tremor or they may have a psychological aversion. It is worth finding out if their partner, friend or a kind neighbour, could do this for them instead or whether as a last resort a community nurse needs to be engaged. The dropper aids that some companies provide can sometimes be of value (Figure 3).
Afterwards you need to communicate with the patient's GP, as regardless of the system used to prescribe in your particular service, the repeat prescription will be the responsibility of their GP and in theory, they will be responsible for any adverse reactions. Also, many patients find that initially they use up their bottle of drops before the month is out and need another from their GP before you see them again.
[FIGURE 3 OMITTED]
The first check four or six weeks after diagnosis is to ensure that patients are getting the drops in correctly, whether the drops are causing any problems, and to check whether the target IOP has been achieved. The patient may well have thought of queries since you last saw them and this is a good opportunity to make sure they have all the information they need.
If the target IOP is achieved, it is still not certain if the process of glaucoma has been arrested. The initial review should be at four months with visual fields assessment and/or optic disc imaging, then if all remains well further reviews should be conducted at six months, and then nine months from diagnosis. If patients are completely stable over the first year, then yearly visits are reasonable from then on. If at the first visit the target IOP is not achieved, compliance should be checked and then a second line treatment should be added. The follow up plan as outlined above should be instigated.
Despite your best efforts the patient progresses
The gold standard for checking progression is automated perimetry. The main advantage is that this actually measures visual function but the disadvantage is that it is a subjective test. The Humphrey visual field analyser is the commonly accepted standard for monitoring glaucoma in the UK. Patients with early glaucoma change, however, may not yet have demonstrable visual field loss and until now the measure of progression was traditionally monitoring optic disc appearance, which is necessarily subjective. The development of imaging techniques for the optic disc and retinal nerve fibre layer has meant that assessment of possible progression of glaucoma is now much more objective.
The other group of patients in whom it is hard to establish whether or not there is progression are those who find it hard to perform the visual fields test, either for mechanical reasons such as tremor, kyphosis (curvature of the upper spine) etc. or more commonly because they lack or are losing the cognitive function to manage the test properly. Conversely, it is well known that we get better at the visual field test with practice, so the slight deterioration of field exhibited by some patients may be masked by better performance over time. The best clue as to how useful the visual field test result is lies in the data on fixation, the rate of false positive and false negative errors, and the time the test took to complete. If you feel the visual field test is or has become "non-contributory", record the fact so that the patient doesn't have to be asked again to undergo visual field testing. This group of patients may, in future, be better monitored with objective imaging.
The most commonly used visual fields test for glaucoma is the SITA 24-2 algorithm. In advanced glaucoma, where macular function is most important, the 10-2 algorithm is a more relevant measure. In end stage glaucoma (Figure 4), even the 10-2 becomes less relevant and a simple visual acuity (VA) is the most useful measure.
One important factor in whether your treatment plan is really helping is patient compliance. Sometimes patients "remember" to take their drops only a day or two before their appointment and so although the IOP may appear to be on target, there may be clear evidence of progression. Usually, this problem will be highlighted because there will be no response to short-term increase in treatment. Some patients are reluctant to admit this and the best approach is to avoid seeming judgmental and to get the point across that if they can give an accurate account, it will help you to treat them and may avoid the need for an operation. In this situation, if you ask the patient to ensure compliance for just a month, you may then find the IOP is back on target and the patient has learnt that those drops really do make a difference. It helps to keep the drop regime as simple as possible, using combination preparations if it helps. Fixed dose combination treatments currently available for glaucoma management are detailed in Table 2. Some patients, despite full compliance, genuinely are poor responders to their first line therapy. In these cases, it would be more logical to try switching to an alternative before going to double therapy.
[FIGURE 4 OMITTED]
The patient really is progressing
If the patient is progressing then you need to revise the target IOP downwards. It is worth re-checking the corneal thickness at this point, and also to think again if there are any new findings such as a narrowing angle or signs of pigment dispersion, which may not have been obvious at presentation; these factors might suggest labile IOPs. At this point, in a well-supervised shared care arrangement, it would be useful to involve the ophthalmologist although, as is the case with younger patients with pigmentary glaucoma, you may want to arrange phasing, in which the IOP is measured at intervals over the course of the day. Although shared care programmes tend not to allow a fee schedule for this, it need not be too time consuming and can provide interesting information. For example, exercise in pigmentary glaucoma is known to produce an IOP spike and if your patient is a regular at the gym or runs/ goes jogging, it is worth asking them to exercise immediately prior to evaluation.
If you suspect that the patient is progressing and probably spiking, then surgery is probably the best option particularly if the patient is young. If you feel there is a real chance of arresting progression with further topical treatment, it would be quite reasonable to up the treatment as far as quadruple therapy, particularly if it is tolerated in the more elderly patients or those who are reluctant to have surgery. The important thing is not to spend time altering therapy in minor ways if the patient really needs a substantial IOP reduction. A frequent error is to make repeated minor adjustments to treatment with too long a period between visits, with the result that a whole year could pass yet the control was barely improved and the visual fields have progressed significantly. Clearly, surgery would have been a better option.
Another situation where it is important not to delay such treatment is if the glaucoma is beginning to encroach on the central 5[degrees] of the visual field. If you then allow progression to begin to threaten fixation, there is a serious risk that in this case, there may be decompensation of the few remaining nerve fibres at the time of surgery, causing a noticeable drop in VA and a very unhappy patient.
A final factor to consider is the age of the patient. The aim of glaucoma treatment is to maintain good functional vision until the end of the patient's lifespan. A young patient with progression would need a lower threshold for proceeding to surgery than an elderly patient whose functional vision looks like it might last long enough despite some progression.
IOP is under 12mmHg but is still progressing
The patient will have NTG in this scenario. You and the patient will have to accept that further progression may be inevitable, as the condition is principally a vascular neuropathy rather than primarily IOP-related. Nevertheless, there is good evidence that keeping the IOP as low as possible will slow progression significantly. Despite research at the time of writing, the only certain therapeutic lever we have is the lowering of IOP. Medications that directly help neuro-protection or directly improve optic nerve head perfusion are still some way off.
Post-glaucoma surgery medical treatment
You may find that a patient has had glaucoma surgery with a good result and is returned to your care but the IOP has begun to creep up again. Some patients maintain excellent control after surgery for years but it is more common for the IOP to rise again after a few years, so that you have to reintroduce drops. In this case, the best first line of treatment is a prostaglandin analogue as it is helps drainage rather than reducing aqueous production.
This article has attempted to cover most of the basic information that might be helpful to those of you interested or already working in a shared care glaucoma setting. Whilst this article is based on the training and current practice employed by the author and two optometry colleagues at the Waltham Forest Community Glaucoma Service, which has now been running for nearly five years, it should be read in coniunction with the NICE guidelines. The sheer volume of glaucoma patients and its projected increase in the UK means that the need to involve the optometry profession in glaucoma management will increase further.
MSc in Clinical Optometry CITY UNIVERSITY and OT have joined forces allowing readers to achieve CET points through to a full Masters in Clinical Optometry. The content of this article is part of the forthcoming Glaucoma module running July 18-20 2010. Please note that the OT/City exam will run on May 27 2010 and is based on the City CET articles published in 2009--'Diabetes' and 'Vision in the Aged' For further information please contact Dr Michelle L Hennelly by emailing (m.hennelly@ city.ac.uk) or call 0207 040 8352.
Course code-C-13472 O/SP/AS
1. Which one of the following regarding topical beta-blockers is TRUE?
a. They are most effective when given at night
b. They are very expensive
c. They are contraindicated in aphakic eyes
d. They act by reducing aqueous production
2. Which one of the following statements is FALSE? Prostaglandin analogues:
a. Work by increasing uveoscleral outflow
b. Work by reducing aqueous production
c. May produce a red eye
d. Are contraindicated in pregnancy
3. Which one of the following statements regarding pilocarpine is TRUE?
a. It is not available without preservative
b. It significantly alters accommodation in pseudophakic patients
c. It acts by increasing outflow through the trabecular meshwork
d. It causes shortness of breath
4. Combigan is a combination of which two drugs?
a. Dorzolamicie and Timolol
b. Travoprost and Timolol
c. Brimonidine and Timolol
d. Bimatoprost and Brinzolmide
5. A patient has very advanced glaucoma in his left eye and the visual acuity (VA) has deteriorated from 6/6 to 6/12. There is no other cause for the drop in VA. What is the most relevant measure for monitoring future progression?
a. OCT nerve fibre layer
b. Humphrey visual field testing
c. Visual acuity
d. Recording cup:disc ratio
6. Which one of the following is FALSE regarding alpha-2 agonists?
a. Lopidine is licensed for long term use only
b. Brimonidine is licensed for long term use
c. A 30% reduction in IOP can be expected
d. There is a high prevalence of allergic conjunctivitis
7. Which medical condition is not a risk factor for glaucoma?
8. Azarga is a combination of which two drugs?
a. Travoprost and Timolol
b. Brinzolamide and Timolol
c. Bimatoprost and Betaxolol
d. Dorzolamide and Timolol
9. A patient is referred in accordance with NICE guidelines with NCT IOP readings of 23mmHg in both eyes. Corneal thickness is 595[micro]m and 560[micro]m. Visual fields and optic disc assessments are normal in both eyes. What is your provisional diagnosis?
a. Primary open angle glaucoma (POAG)
b. Glaucoma suspect
d. Normal tension glaucoma
10. A patient in your optometry practice has an IOP of 19mmHg both eyes, Corneal thickness is 490[micro]m and 500[micro]m. Visual fields are normal but the left optic disc is suspicious with a thinning of the inferior neuro-retinal rim. What is the most appropriate course of action?
a. Review in a year as the IOP is within NICE guidelines
b. Refer as a glaucoma suspect
c. Check visual fields in six months and refer if visual field loss develops
d. Repeat the visual field test
11. A patient of 40 years of age with pigment dispersion glaucoma appears to progress despite apparent good control of IOP on double therapy. Phasing shows spikes. What is the most appropriate course of action?
a. Increase the dose of the current medication
b. Continue to monitor on the same treatment
c. Refer on recommending surgery
d. Advise the patient against prolonged physical exertion
12. What time frame is usual for the first follow-up appointment if a patient has been prescribed a prostaglandin analogue?
a. One week
b. Two weeks
c. Four weeks
d. Six weeks
Stephen Bryan MA FRCS FRCOphth
Mr Bryan is consultant ophthalmologist at Whipps Cross Hospital, London, and the Clinical Lead at Waltham Forest Optometry-run community glaucoma clinic.
Table 1 Preservative-free treatments currently available for glaucoma management Trade Name Active Ingredients Pilocarpine Pilocarpine 2% or 4% Timolol Timolol 0.25% or 0.5% uBetoptic Betaxalol Modified Release 0.25% Betagan Levobunolol 0.5% Trusopt Dorzolamide 2% Cosopt Timolol 0.5% & Dorzolamide 2% lopidine Apraclonidine 1% Saflutan Tafluprost Table 2 Fixed-dose combination treatments currently available for glaucoma management Trade Name Generic Name Cosopt Timolol 0.5% & Dorzolamide 2% Xalacom Timolol 0.5% & Latanoprost 0.0005% Combigan Timolol 0.5% & Brimonidine 0.2% Ganfort Timolol 0.5% & Bimatoprost 0.03% Duotrav Timolol 0.5% &Travoprost 0.004% Azarga Timolol 0.5% & Brinzolamide 0.001%
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|Title Annotation:||CONTINUING EDUCATION & TRAINING|
|Date:||Mar 12, 2010|
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