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September 2019

The International Myopia Institute (IMI) Reports and Clinical Management Guidelines

Dr Kate Gifford

Clinical Optometrist, Gerry & Johnson Optometrists, Brisbane

Visiting Research Fellow, Queensland University of Technology

The IMI has a message for eye-care professionals: it’s no longer best practice to simply prescribe single vision spectacles for progressing myopes.

The International Myopia Institute (IMI) White Paper Reports were published in the high-ranking journal Investigative Ophthalmology and Visual Science in February 2019. In a similar spirit to the Tear Film and Ocular Surface Society Dry Eye Workshop (TFOS DEWS and DEWS II) reports, the IMI Reports present a comprehensive peer consensus from over 85 participant authors on a wide scope of topics relating to research of myopia mechanisms, product research and development, clinical and industry best practice and the public health message. The IMI Reports are open-access and freely available, creating a clear picture of the current landscape of myopia research and practice, with an eye to the future.

The IMI Reports have come at exactly the right time. Over the past few years there has been a dramatic increase in clinician awareness and product innovations by industry to match the research findings of a global increase in the prevalence of myopia, forecast to affect 50 per cent of the world’s population by 2050.¹ The well-informed optometrist would benefit from reading any and all of the IMI Reports, however, if pressed for time, the place to start is the Myopia Control Reports Overview and Introduction, which details the background of risk factors for myopia onset and progression, along with providing an overview of each report to direct further learning. From there, essential practitioner reading includes the following Reports:

Defining and Classifying Myopia – Get clear on the definitions of pre-myopia, myopia, high myopia, and myopia complication with key references.²

Interventions for Myopia Onset and Progression – Understand the research behind optical, pharmacological, environmental (behavioural) and surgical interventions for myopia.³

Clinical Management Guidelines  – Appreciate the scope of risk identification, parent and patient communication, informed consent, basic examination procedures, follow-up schedules, when to change and stop treatment, future treatments and additional resources for clinical practice.⁴

Industry Guidelines and Ethical Considerations for Myopia Control – Consider factors in the ethical development, registration, marketing, on- and off-label prescribing and patient use of myopia control treatments, including risk versus benefit and quality of life considerations.⁵

The Clinical Management Guidelines (CMG) Report⁴ provides a framework for putting research into practice. Best practice myopia management involves an understanding of the causes and risk factors for myopia; the long-term eye health risks; the efficacy and safety of the available optical, pharmacological and visual environment interventions; and the skills to translate this into lay language for both the patient and parent. The CMG Report commences with an outline of myopia development causes—identifying the pre-myope—through the risk factors of family history (one or two myopic parents), less time spent outdoors and specific binocular vision disorders (esophoria and accommodative lag). The key identifier of the pre-myope, though, is the child who is less hyperopic than age normal; specifically: a child who is +0.75 or less at age 6–7 years.

Evidence-based interventions for this child are currently limited to education on achieving around 90+ minutes of time outdoors per day. Managing binocular vision disorders associated with myopia onset may also be beneficial, although specific studies on delaying myopia with this sort of intervention have not been undertaken.


Once a child becomes myopic, a management strategy should be instigated which not just corrects myopia but also aims to slow its progression. Based on the available evidence, this can be implemented for children as young as six years of age and should continue until the mid-to-late teens, although rebound effects on treatment cessation and young adult myopia progression are both yet to be fully understood.

Figure 1. Clinical tests in myopia management, published from the IMI Clinical Management Guidelines


The CMG Report provides guidance firstly on discussing myopia and its treatments—options, efficacy, safety, additional corrections and informed consent—while emphasising the importance of establishing reasonable expectations and informed consent (Chapters two and three). The report then proceeds to the key elements of the baseline exam for myopia control (Chapter four; see Figure 1 of the CMG Report, and Figure 2). The standard procedure for examination includes appropriate history taking relative to the treatment, distance and near acuity, subjective and/or objective refraction, accommodative and binocular vision assessment and ocular health examination. Cycloplegic refraction is considered useful annually, or as indicated. Fundus examination through dilated pupils is also suggested as an annual exam component, especially for high myopes (> 5 D) and/or if axial length is 26 mm or greater.

Figure 2. Clinical review schedules based on treatment type, adapted from the IMI Clinical Management Guidelines.


While axial length measurement is considered a necessity for a research study, for clinical practice it is currently considered preferable, but not a necessity, every six months. This is a particular issue with orthokeratology (OK) treatment where refractive change is more difficult to measure; and with atropine therapy where a mismatch between axial length and refractive control has been repeatedly noted. These two treatments also carry their own specific recommendations for follow-up examination—OK monitoring requires corneal topography, and atropine monitoring requires assessment of pupil size and function and intraocular pressure.

The bulk of the CMG Report is then dedicated to selecting a treatment strategy and management guidelines. Considering a child’s baseline refractive error (for example, astigmatism limits certain contact lens treatments) and capacity is important alongside treatment consideration such as advice on add powers in multifocal soft contact lenses and detail on spectacle lens options (Chapter 5).

Guidelines for clinical care (Chapter 6) detail all aspects of treatment and advice from ideal wearing time (at least five to six days a week, dependent on the treatment), back up corrections, advice on visual environment, when to change or end treatment and special considerations such as late onset and high myopia. A summary of follow-up schedules by treatment is provided in Figure 2. The CMG Report concludes with information on clinical references – key research papers, websites, courses and communication tools – where much is provided as weblinks in the supplementary digital content.

Looking to the future

The report holds more promise for the influence that current research may have on future clinical practice. The myopia managing clinician of the future may be measuring parameters such as relative peripheral refraction, aberrometry, pupillometry, sub-foveal choroidal thickness and utilising light exposure and visual activity data from wearable devices (Chapter 4). Each of these is an arena for current research and as their role in predicting myopia progression or treatment response is understood, these may translate into clinical practice. The hot topics of OK and multifocal soft contact lens optimisation are detailed in Chapter 7, along with emerging treatments such as the 7-methylxanthine nutritional supplement in Denmark and scleral reinforcement in Russia.


The publication of the IMI White Paper Reports is a landmark moment for the eye-care profession and industry. By providing a full-scope, critically-evaluated and robustly synthesised expedition through the world of myopia research and practice, these reports clearly draw a line in the sand for future coordinated efforts for the ultimate benefit of our young myopic patients.

The clear message for eye-care professionals right across the world is that it’s no longer best practice to simply prescribe single vision spectacles for progressing myopes when better options to control myopia are available. Myopia management, at minimum, starts with a discussion on the consequences of myopia, risk factors and treatments—allowing parents and patients to make informed decisions which could influence lifelong eye health outcomes. While there is no way to predict the level of progression or perfect treatment for the individual myope—and there may never be—there are many tools and treatments available.

Improving the access of our young myopic patients and their parents to the right information and treatments is built on a foundation of practitioner education and confidence in implementation. The IMI White Papers, and particularly the Clinical Management Guidelines, are designed to support practitioners through this imperative evolution of clinical practice.

Dr Gifford (PhD BAppSc (Optom) Hons GCOT  FBCLA  FIACLE  FCCLSA  FAAO) is a clinician-scientist in Brisbane private practice, a peer educator, and a Visiting Research Fellow at the Queensland University of Technology. She is the Chair of the Clinical Management Guidelines Committee of the International Myopia Institute and lead author on their report.


1. Holden BA, Fricke TR, Wilson DA et al. Global Prevalence of Myopia and High Myopia and Temporal Trends from 2000 through 2050. Ophthalmology 2016; 123: 1036-1042
2. Flitcroft DI, He M, Jonas JB et al. IMI – Defining and classifying myopia: a proposed set of standards for clinical and epidemiologic studies. Invest Ophthalmol Vis Sci. 2019; 60: M20-M30.
3. Wildsoet CF, Chia A, Cho P et al. IMI – Interventions for Controlling Myopia Onset and Progression Report. Invest Ophthalmol Vis Sci. 2019; 60: M106-M131.
4. Gifford KL, Richdale K, Kang P et al. IMI – Clinical Management Guidelines Report. Invest Ophthalmol Vis Sci. 2019; 60: M184-M203.
5. Jones L, Drobe B, González-Méijome JM et al. IMI – Industry Guidelines and Ethical Considerations for Myopia Control Report. Invest Ophthalmol Vis Sci. 2019; 60: M161–M183.

Key resources with links
BlogTo read more on axial length in clinical practice, the author has written a blog entitled ‘Axial length measurement – a clinical necessity?’
JournalThe International Myopia Institute White Paper Reports – special issue of Investigative Ophthalmology & Visual Science, Volume 60 Issue
WebsitesThe International Myopia Institute – a summary of prevalence, impact and solutions for the global myopia problem, with information on the Committees and links to the White Paper Reports. ( )
The website Myopia includes easy access to the CMG Supplementary Digital Content and a new podcast series with IMI Report lead authors, along with numerous educational blogs and resources for putting myopia management into practice (
The BHVI Global Myopia Centre, a portal to online courses, calculators and resources.
Online magazineIssue 47 of, entitled ‘Myopia Matters: Summarising the IMI Reports’. This free-to-access resource includes an editorial written by this author, a summary of each of the white papers by the researchers of the Centre for Ocular Research and Education (CORE – University of Waterloo, Canada) and a practitioner reference factsheet download on the Clinical Management Guidelines.
Facebook groupThe companion Facebook Group ‘Myopia Profile’, administered by the author – a closed, industry-only group which includes more than 5,000 eye care practitioners from over 50 countries discussing the latest research, industry developments and clinical
Electronic newsletterReview of Myopia Management, a new electronic newsletter and website with a variety of clinical and practice management blogs and resources.Subscribe here

School myopia: a new perspective

Professor Ian Morgan
Research School of Biology, Australian National University, Canberra, ACT

Amanda French
BAppSci (Orth) Hons

Dr Kathryn Rose
GradDipNeurosci PhD
Discipline of Orthoptics, Graduate School of Health, University of Technology Sydney, Ultimo, NSW

Our new understanding of school myopia offers the realistic promise of effective control of progression of myopia, and some prospect of overall reductions in prevalence.

We have all used the term ‘school myopia,’ but often, it has been no more than a description of a condition that appears during the school years, along with the prevailing, if somewhat contradictory, belief that myopia was predominantly, if not exclusively, a genetic condition.¹

With the emergence of an epidemic of school myopia in East and Southeast Asia, a deeper understanding of school myopia has emerged over the past few years. There, the prevalence of school myopia has increased roughly three-fold over the last 50 years, with around 80 per cent of those completing 12 years of school now myopic (Figure 1). In the same parts of the world, the prevalence of high myopia (more severe than -6.00 D) has increased even more spectacularly (10–20-fold), with 10–20 per cent of students in their final years of schooling now highly myopic.² High myopia is generally associated with an increased risk of pathological myopia, which, in general, cannot be prevented or corrected by standard optical correction.³

Figure 1. In East Asia, around 80 per cent of those completing 12 years of school are myopic


These rapid changes are not consistent with the idea that school myopia is overwhelmingly genetically determined, since population gene pools cannot change that fast. Environmental factors must be involved. In a recent review, we have discussed in some detail why the debate in this area has been so confused.⁴

The two epidemics of myopia and high myopia are closely connected. In the current epidemic of myopia there has been an increasingly early onset of myopia, with over 50 per cent of children myopic by the end of primary school.⁵ A large proportion of children develop myopia at an age when progression is still rapid, with more time for progression before myopia stabilises late in the young adult years. Thus, an epidemic of myopia inevitably leads to an epidemic of high myopia, with increased loss of vision due to pathological myopia.

Environmental factors

Two environmental factors appear to play a major role in the emergence of the current epidemic.² The first is increased exposure to education. In the past, in societies where children received little formal education, the prevalence of myopia was only one to two per cent, most of which was probably genetic myopia. But as societies have developed more intensive mass education systems, the prevalence of school myopia has increased, no more so than in East and Southeast Asia.

The association between myopia and education is remarkably consistent, with children achieving higher school grades more likely to be more myopic.⁶ Similarly, in adults, final refraction is on average higher in those who have completed more years of schooling or achieved higher qualifications.⁷ But these associations do not establish causality, although some of the social correlations result from what are close to intervention trials. For the purists, the direction of causation, from education to myopia, has recently been demonstrated in a Mendelian randomisation study.⁸*

In parallel, children who spend more time outdoors are less likely to develop myopia. This is not a simple substitution effect, in which more time outdoors means less study, since the most at risk are children who combine lots of near work with little time outdoors, whereas children who combine lots of near work with lots of time outdoors are protected.⁹ Causality has been demonstrated in randomised school-based interventions,¹⁰ and the proposed causal mechanism, increased release of dopamine from the retina in the brighter light outdoors during daylight hours, has been confirmed in studies on experimental myopia.¹¹ The ‘high prevalence of myopia’ societies report much lower amounts of time spent outdoors by children than in western societies, where the prevalence of myopia is lower. Thus, it is likely that the epidemic of myopia in East and Southeast Asia results from a combination of intense education and limited time outdoors. It is currently unclear if time outdoors slows progression as well as onset, but marked seasonal effects on progression suggest that it might.

Prevention protocols

This new picture provides a clear link to prevention: through reducing educational pressures and increasing time outdoors. Reducing educational pressures may be difficult, given the importance of education in modern societies. However, it may be possible to modify some of the features of East Asian education that contribute to the development of myopia, such as the very early onset of educational pressures, with homework starting in pre-school, long school days with little time outdoors, heavy homework loads and extensive use of coaching classes. These features seem be related to intense competition for selective pathways that culminate in the final university entrance examination.

While change in these areas may be difficult, introducing more time outdoors into school programs is likely to be more feasible, provided that it does not intrude too much on the core business of education. Using existing optical, pharmacological and behavioural interventions for slowing myopia progression,¹² it should now be possible to nearly eliminate all but the clearly genetic forms of high myopia. Increased time outdoors is already a core part of national myopia prevention in Singapore and Taiwan, and is likely to have a significant part in mainland China’s developing myopia prevention protocols.

What does all this mean for Australia? In clinical practice, control of myopia progression now has to go hand in hand with correction. A number of optical and pharmacological approaches to prevention appear to work, but not all are strongly backed by evidence. Clinicians therefore need to investigate thoroughly the underlying evidence on the approaches they offer to clients. It also makes sense for clinicians to encourage more outdoor time, since myopia prevention does not appear to involve UV exposures and vitamin D levels, and is thus fully compatible with Australian skin protection policies.

One issue for the future is whether Australia will face increasing levels of myopia, as some modelling suggests. While there has been some increase in the prevalence of myopia in Australian children, this largely appears to be due to the increasing proportion of Australians of East Asian ancestry, who bring with them their cultural attitudes to education, and thus more myopia. In children of European ancestry, the prevalence of myopia is still under 20 per cent at the end of the school years (Figure 2). In those of East Asian ancestry, the prevalence of myopia may actually decline over time, if these communities increase engagement in outdoor activities, including sport. This development could be encouraged within schools.

Figure 2. The prevalence of myopia is still under 20 per cent for children of European ancestry at the end of their school years.


Other developments could, in contrast, lead to increases. In the past, we have heard repeated calls to adopt East Asian educational practices. In addition, there is increasing interest in the provision of universal pre-school education, to better prepare children from disadvantaged backgrounds for schooling. We need to ensure that this is delivered in a way that avoids the early onset of myopia now so common in East Asia. There is also considerable interest in the development of vertical pre-schools and schools. These could be a matter of concern, if they are designed in a way that limits student access to time outdoors.

Overall, the new understandings of school myopia offer the realistic promise of effective control of progression of myopia, and some prospect of overall reductions in prevalence. But at the same time, there are likely to be future challenges, and we need to keep an eye out for proposed changes in education that could compromise these advances.

*Footnote: Mendelian randomisation uses genetic variation as a natural experiment to investigate the causal relations between potentially modifiable risk factors and health outcomes in observational studies. The assumptions and limitations of the approach have been clearly reviewed.¹²³ In the case of myopia, genes associated with a small but measurable increase in years of schooling were also associated with increased myopia, where genes associated with a small increase in myopia were not associated with an increase in years of schooling.⁸


1. Sorsby A, Sheridan, M, Leary GA. Refraction and its components in twins. Special Reports Series of the Medical Research Council 1962; 303.
2. Morgan IG, French AN, Ashby RS et al. The epidemics of myopia: Aetiology and prevention. Prog Retin Eye Res 2018; 62: 134-49.
3. Ohno-Matsui K, Lai TY, Lai CC et al. Updates of pathologic myopia. Prog Retin Eye Res 2016; 52: 156-87.
4. Morgan IG, Rose KA. Myopia: is the nature-nurture debate finally over? Clin Exp Optom 2019; 102: 3-17.
5. Lin LL, Shih YF, Hsiao CK et al. Prevalence of myopia in Taiwanese schoolchildren: 1983 to 2000. Ann Acad Med Singapore 2004; 33: 27-33.
6. Saw SM, Cheng A, Fonf A et al. School grades and myopia. Ophthal Physiol Optics 2007; 27: 126-9.
7. Mirshahi A, Ponto KA, Hoehn R et al. Myopia and level of education: results from the Gutenberg Health Study. Ophthalmology 2014; 121: 2047-52
8. Mountjoy E, Davies N, Plotnikov D et al. Education and myopia: a Mendelian randomisation study. BMJ 2018.
9. Rose KA, Morgan IG, Ip J et al. Outdoor activity reduces the prevalence of myopia in children. Ophthalmology 2008; 115: 1279-85.
10. He M, Xiang F, Zeng Y et al. Effect of Time Spent Outdoors at School on the Development of Myopia Among Children in China: A Randomized Clinical Trial. JAMA 2015; 314: 1142-8.
11. Ashby R, Ohlendorf A, Schaeffel F. The effect of ambient illuminance on the development of deprivation myopia in chicks. Invest Ophthalmol Vis Sci 2009; 50: 5348-54.
12. Huang J, Wen D, Wang Q et al. Efficacy Comparison of 16 Interventions for Myopia Control in Children: A Network Meta-analysis. Ophthalmology 2016; 123: 697-708.
13. Davies NM, Holmes MV, Davey Smith G. Reading Mendelian randomisation studies: a guide, glossary, and checklist for clinicians. BMJ 2018; 362: k601

Paediatric eye care reference guide

An outline of the components of a comprehensive vision and eye health examination for children, from birth to 14 years.

Reprinted from the 2019 Optometry Australia Clinical Practice Guide for paediatric optometry, this reference offers an overview of standard testing protocols by age, a guide to clinical normative values for accommodation and vergence parameters and average stereoacuity by age.

Download the Paediatric eye care reference guide


June 2019

Evidence-based advice for AMD

Dr Laura Downie
BOptom PhD(Melb) PGCertOcTher  FAAO FACO DipMus(Prac) AMusA
Senior Lecturer, Department of Optometry and Vision Sciences, Faculty of Medicine, Dentistry and Health Sciences
The University of Melbourne

Clinical classifications, modifiable lifestyle factors and the quality of eye care

While therapeutic interventions exist for late-stage neovascular age-related macular degeneration (AMD), currently there are no approved medical therapies for earlier stages of the disease or late-stage geographic atrophy (GA). Given its association with sight-threatening retinal pathology, reducing progression to late-stage AMD is vital for decreasing vision loss and the associated individual and community burden of AMD.

AMD clinical classification

AMD is characterised by retinal changes that occur in a two-disc diameter radius of the fovea in people aged 55 years or older. The early stages of AMD are indicated by the appearance of drusen, comprising accumulations of lipoproteineous substance between the retinal pigment epithelium (RPE) and Bruch’s membrane. Drusen can also be associated with disruptions to the RPE, evident clinically as areas of relative hyper- or hypo-pigmentation. AMD can then progress to late-stage GA of the RPE and/or choroidal neovascularisation (CNV).

In 2013, the Beckman Initiative for Macular Research Classification Committee, a panel of international experts in the field, published a key paper defining an AMD clinical classification for implementation in clinical research and practice.¹ This classification system (summarised on pages 14 and 15 of the June issue of Pharma) defines five categories, based on retinal features, and is of value for predicting an individual’s risk of developing late-stage AMD.¹

There are several key points worth noting about this AMD classification scheme,² as follows:

  • AMD severity is described in three stages: ‘early,’ ‘intermediate’ and ‘late’
  • the terms ‘wet AMD’ and ‘dry AMD’ are not used in this classification. These descriptors were judged to be potentially confusing, as ‘dry AMD’ has historically been used to describe a spectrum of AMD-related changes, ranging from isolated drusen to GA
  • drusen are defined by their size (at their smallest diameter); subjective descriptors such as ‘soft’ and ‘hard,’ are not used
  • the presence of only drupelets (a small druse of less than 63 µm in diameter) within two-disc diameters of the fovea defines a pre-AMD category of ‘normal ageing changes,’ which is distinct from ‘early AMD.’

Risk factors for AMD

There are several risk factors for AMD. In terms of non-modifiable risk, advancing age is the strongest factor. The risk of developing AMD is three times higher in individuals older than 75 years, compared to those between 65 and 74 years of age.³ A family history of AMD, particularly having a first-degree family member affected by the condition, also confers a significantly-elevated risk of developing the disease.⁴ Of major clinical importance is identifying—and if possible modifying—lifestyle risk factors that can also influence the development and/or progression of AMD.

Tobacco smoking

Cigarette smoking is the single most important modifiable AMD risk factor;⁵ smoking at least doubles a person’s risk of developing the condition.⁶ Furthermore, a direct association has been identified between the number of cigarettes smoked over time and the risk of developing late-stage AMD.⁷ Despite these known links between tobacco smoking and sight-threatening ocular disease, studies suggest that primary eye care providers may not be routinely asking their patients about smoking or providing advice about the benefits of smoking cessation. Research undertaken in several developed countries,⁸-¹¹ including Australia,¹² involving surveys of eye care clinicians, identifies scope for optometrists to be more proactive in discussing tobacco smoking as a modifiable risk factor for eye disease with their patients. Eye care clinicians have identified a range of potential barriers to undertaking smoking counselling with their patients; these include a perceived lack of sufficient consulting time to perform this task, a perception that there should be sufficient public awareness about the health risks of smoking and/or considering discussing smoking habits with their patients to be too intrusive.¹²

With the intent of overcoming these barriers, and to assist eye care clinicians with capturing key information about a patient’s smoking behaviours and how these relate to AMD risk, my colleague Associate Professor Peter Keller and I developed a ‘Quantitative Clinical Smoking Behaviour Tool.’§ This tool, the first of its kind for eye-care clinicians, comprises 10 questions that capture information about a person’s smoking behaviours, across three main areas:

  • Current and former smoking status (using a validated classification system), and how this informs a person’s risk of developing AMD or having progressive disease.
  • Degree of smoking dependence, which relates to a current smoker’s level of nicotine dependence.
  • Level of motivation to cease smoking, to ascertain a current smoker’s readiness to consider smoking cessation, quantified on a validated behavioural scale.

For each of these three key areas, the tool provides an evidence-based summary (including a comprehensive list of relevant citations) that eye care clinicians can use to provide evidence-based advice to patients about the benefits of smoking cessation for their eye health.


Diet is another key area for potential AMD risk modification. Multiple epidemiological studies have reported the potential benefits of a healthy diet, rich in the macular carotenoids (zeaxanthin and lutein) and omega-3 fatty acids, for lowering the risk of developing AMD. A meta-analysis that included several observational studies reported that the consumption of two or more servings of oily fish per week was beneficial in the primary prevention of AMD.¹³

High glycaemic index diets and alcohol consumption (in excess of two drinks per day) may also increase the risk of AMD, although further studies are required to confirm these associations.¹⁴

A recent systematic review concluded that high consumption of vegetables rich in carotenoids and oily fish containing omega-3 fatty acids was beneficial for people at risk of AMD.¹⁴ However, emphasising the need to differentiate between nutritional components derived from whole foods and supplementation, consuming anti-oxidant supplements does not prevent the development of AMD.¹⁵

In terms of modifying AMD progression, a Mediterranean diet (rich in foods such as fruits, vegetables, legumes, and fish) has been linked to a reduced risk of AMD progression.¹⁶ Epidemiology studies suggest that a high dietary intake of omega-3 fatty acids is associated with a significant reduction in the risk of both intermediate¹⁷,¹⁸ and late-stage AMD.¹⁹,²⁰ It has also been recommended that vegetable oils and animal fats (which contain high levels of omega-6 fatty acids) and red/processed meat should be consumed minimally to reduce the risk of AMD progression.¹⁴


With respect to supplementation, the Age Related Eye Disease Study (AREDS) showed that daily, long-term, high-dose supplementation with vitamin C (500 mg), vitamin E (400 IU), beta-carotene (15 mg), zinc (80 mg, as zinc oxide), and copper (2 mg, as cupric oxide) in people with at least intermediate-stage AMD reduced the relative risk of progression to late AMD from 28 per cent to 20 per cent at five years.²¹ As such, it may be relevant to consider the potential benefit of a high-dose anti-oxidant vitamin and mineral supplement in individuals with intermediate-stage AMD. The decision to recommend such formulations to patients requires consideration of the patient’s systemic health, as well as the relative benefits versus risks of supplementation. For example, there is evidence that the risk of lung cancer is significantly increased with high-dose beta-carotene supplementation in current and former smokers.²²,²³

A quantitative clinical diet and nutritional supplement tool§ is also now available for optometrists to use in their practice. This simple survey, developed as a companion to the smoking behaviour tool, supports the capture of key clinical information relating to an individual’s diet that are relevant to the risk of AMD, as follows:

  • omega-3 fatty acid intake
  • lutein and zeaxanthin intake
  • nutritional supplement consumption.

Clinical audit

The MaD-CCAT tool

Through a collaborative project with Professor Robyn Guymer, Associate Professor Peter Keller, Dr Lauren Ayton, Professor Algis Vingrys and Ms Ji-hyun (Anna) Lee, funded by the Macular Disease Foundation Australia, my research team has developed an optometric clinical audit tool for assessing the quality of eye care provided to people with AMD.

The MaD-CCAT tool enables optometrists to evaluate their practices with respect to the clinical care provided to their AMD patients, relative to current evidence-based standards. This process enables the identification of potential areas for practice improvement, to enhance the quality and outcomes of optometric patient care to people with AMD.

The MaD-CCAT supports streamlined auditing of multiple aspects of AMD clinical care, including: the identification of modifiable risk factors, diagnostic accuracy (including AMD severity classification), rate/timeliness and appropriateness of referrals for ophthalmologic evaluation, and the quality of clinical record keeping.

Data are captured using a check-box system, for ease of entry. A summary statistics worksheet then automatically populates information comparing an optometrist’s practices with current best-practice guidelines for diagnosing and managing AMD.

A representative snapshot of the data analytics ‘Overview’ page is provided in Figure 1. As audit data are progressively added, the summary statistics highlight areas of relative strength and potential areas for practice improvement. Clinicians can then self-identify practice areas for continuous improvement.

It is of vital importance that primary eye-care providers identify and provide evidence-based advice to their patients in relation to modifiable risk factors for AMD. The availability of new clinical tools to enable clinicians to undertake these assessments, and self-evaluate their own clinical practices, provides a basis for ongoing practice improvement to optimise the delivery of primary eye care to people with AMD.

Figure 1. Snapshot of the MaD-CCAT analytics page, which provides clinicians with summarised information about their clinical audit contributions.



1. Ferris FI, Wilkinson CP, Bird A et al. Clinical Classification of Age-related Macular Degeneration. Ophthalmology 2013; 120: 844-851.
2. Downie LE, Keller PR. Nutrition and age-related macular degeneration:  research evidence in practice. Optom Vis Sci 2014; 91: 821-831.
3. Klein R KB, Knudtson MD, Meuer SM et al. Fifteen-year cumulative incidence of age-related macular degeneration: the Beaver Dam Eye Study. Ophthalmology 2007; 114: 253-262.
4. Klein ML, Francis PJ, Ferris FL, 3rd et al. Risk assessment model for development of advanced age-related macular degeneration. Arch Ophthalmol 2011; 129: 1543-1550.
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6. Evans JA, Fletcher AE, Wormald RP. 28,000 Cases of age related macular degeneration causing visual loss in people aged 75 years and above in the United Kingdom may be attributable to smoking. Br J Ophthalmol 2005; 89: 550-553.
7. Khan JC, Thurlby DA et al. Smoking and age related macular degeneration: the number of pack years of cigarette smoking is a major determinant of risk for both geographic atrophy and choroidal neovascularisation. Br J Ophthalmol 2006; 90: 75-80.
8. Lawrenson JG, Evans JR. Advice about diet and smoking for people with or at risk of age-related macular degeneration: a cross-sectional survey of eye care professionals in the UK. BMC Public Health 2013; 13: 564.
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12. Downie LE, Keller PR. The self-reported clinical practice behaviors of Australian optometrists as related to smoking, diet and nutritional supplementation. PLOS One 2015.
13. Chong EW, Wong TY, Kreis AJ et al. Dietary antioxidants and primary prevention of age related macular degeneration: systematic review and meta-analysis. BMJ 2007; 335: 755.
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18. Seddon JM, George S, Rosner B. Cigarette smoking, fish consumption, omega-3 fatty acid intake, and associations with age-related macular degeneration: the US Twin Study of Age-Related Macular Degeneration. Arch Ophthalmol 2006; 124: 995-1001.
19. Chong EW, Kreis AJ, Wong TY et al. Dietary omega-3 fatty acid and fish intake in the primary prevention of age-related macular degeneration: a systematic review and meta-analysis. Arch Ophthalmol 2008; 126: 826-833.
20. Sangiovanni JP, Agron E, Meleth AD et al. {omega}-3 Long-chain polyunsaturated fatty acid intake and 12-y incidence of neovascular age-related macular degeneration and central geographic atrophy: AREDS report 30, a prospective cohort study from the Age-Related Eye Disease Study. Am J Clin Nutr 2009; 90: 1601-1607.
21. Age-related eye disease study research group. A randomized, placebo-controlled, clinical trial of high-dose supplementation with vitamins C and E, beta carotene, and zinc for age-related macular degeneration and vision loss: AREDS report no. 8. Arch Ophthalmol 2001; 119: 1417-1436.
22. The Alpha-Tocopherol, Beta Carotene Cancer Prevention Study Group. The effect of vitamin E and beta carotene on the incidence of lung cancer and other cancers in male smokers. N Engl J Med 1994; 330: 1029-1035.
23. Omenn GS, Goodman GE, Thornquist MD et al. Effects of a combination of beta carotene and vitamin A on lung cancer and cardiovascular disease. N Engl J Med 1996; 334: 1150-1155.

§ Optometrists interested in accessing the MaD-CCAT tool, the diet and nutritional supplement tool and the quantitative clinical smoking behaviour tool can email the author directly at

Anti-VEGF injections and the prevention of irreversible visual loss

Dr Simon Chen
MBBS (London), BSc (Hons)
Retinal & Cataract Surgeon
Conjoint Senior Lecturer, University of NSW

Kerryn Hart
BOptom GCertOcTher MPH
Clinical Skills Teacher In Optometry, Deakin University
Optometry Australia Policy and Standards Advisor
Clinical Editor of Pharma

The role of the optometrist in improving patient adherence to therapy

Anti-vascular endothelial growth factor (anti-VEGF) drugs have revolutionised the treatment of age-related macular degeneration (AMD) and have preserved the vision of patients throughout the world. Still, many millions remain at risk of severe AMD-related vision loss, and perhaps most disconcertingly, it is because they have chosen to discontinue their treatment.

Pharma’s Clinical Editor Kerryn Hart recently conducted an interview with retinal surgeon Simon Chen to discuss the burdens and benefits of intravitreal injections and the role of the optometrist in improving patient adherence to anti-VEGF therapy. An edited version of the interview appears below.

KH: Dr Chen, anti-VEGF therapy has been an established treatment for neovascular AMD (nAMD) since 2006. Has anything changed since its initial appearance?

SC: The treatment itself has not fundamentally changed, the anti-VEGF agent is administered into the eye via an intravitreal injection on a regular basis. Beyond that, there have been three fundamental changes: 1) there has been a movement toward customised treat-and-extend protocols; 2) a growing understanding of the importance of aggressive and long-term treatment of nAMD; and 3) since 2006, a wider range of anti-VEGF agents have become available.

Undeniably, we now have a much greater understanding of important aspects of anti-VEGF therapy such as the pros and cons of different treatment regimens, the importance of life-long treatment for most patients, the risks and benefits of treatment and the long term visual outcomes of therapy.

Treat and extend protocols

Retinal specialists are shifting away from pro re data (PRN) treatment protocols (where injections are only administered when signs of disease activity recur) and regular fixed interval treatment protocols (where all patients are injected every four weeks) and towards customised ‘treat and extend’ protocols whereby the frequency of injections is tailored to the individual patient according to their own response to treatment.

Treat and extend protocols have been shown to provide better visual results than PRN protocols while reducing the number of injections needed compared to regular fixed interval treatment protocols.¹

Importance of aggressive and long-term treatment

It’s now well-established that patients need to be treated early in the disease process (that is, as soon as signs of nAMD become apparent). Treatment also needs to be administered frequently, especially in the early stages, when the disease is most active. We now know that for the majority of patients with nAMD, long term, potentially life long, anti-VEGF treatment is required because high rates of disease reactivation and permanent visual loss have been reported in patients that cease therapy.

KH: I’ve read that patients are often lost to follow-up with their anti-VEGF regime. Does your experience show this?

SC: Recent studies in the United States have indicated that up to 25 per cent of patients that start anti-VEGF treatment are eventually lost to follow-up.² This figure, of course, varies significantly between ophthalmic practices due to differences in patient demographics (older patients may find it more difficult logistically to attend for treatment and may be limited by other co-morbidities), patient socio-economic status and geographic location of the clinic.

KH: What are the key factors for patient drop out?

SC: For new patients, fear about possible pain or complications associated with the injection procedure are a common and natural reaction, especially in patients with a tendency towards anxiety.

Logistic barriers are a common cause for patients to drop out of treatment. (Difficulties travelling to and from a clinic due to factors such as inability to drive, difficulties accessing public transport, limited wheel chair access, poor memory causing patients to forget appointments, the need to arrange carers who may need to take time off work for injection visits). Patients may experience guilt about the ongoing burden on carers which in turn may makes them less likely to attend for treatment.

In older patients, co-morbidities may limit their access to care. For example: a patient suffering a hip fracture may be hospitalised and require long-periods of post-op rehabilitation causing them to miss out on scheduled anti-VEGF injections.

For patients with financial difficulties, concerns about out-of-pocket-costs associated with treatment may impact their treatment decision. Over time, ‘injection fatigue’ can set in among patients as they become frustrated with the ongoing need for treatment causing their commitment to treatment to wane.

For some patients there may be a lack of perceived benefit especially if treatment has not led to an improvement in their vision or their vision has continued to deteriorate despite treatment.

KH: What role does the optometrist play in improving compliance with anti-VEGF injections?

SC: Optometrists have a vital role to play in optimising patients’ compliance with anti-VEGF therapy and therefore maximising their visual function and quality of life.

They can do this at an early stage by educating their patients with early-to-intermediate AMD about the long term risk of developing the neovascular form of AMD and making them aware of the potential vision-saving benefits of anti-VEGF injections before they have even developed nAMD. By exposing patients to the notion that anti-VEGF injections are an important treatment at an early stage, they may be better primed to accept the need for treatment when the time comes.

When optometrists refer patients with neovascular AMD to an ophthalmologist for anti-VEGF treatment, they can facilitate patient compliance by stressing the importance of attending the appointment without unnecessary delay. This should involve explicitly telling the patient that they are at risk of permanent visual loss if their condition is not assessed and managed in an appropriately urgent time frame. Without this information being provided to them, patients may not always appreciate the urgency of initiating treatment and so may delay seeing an ophthalmologist, potentially leading to irreversible visual loss due to progression of the neovascular process.

Optometrists also have an important continuing role in supporting patient compliance throughout the course of ongoing anti-VEGF therapy by providing ongoing educational and sometimes even emotional support. Patients should be reminded about the importance of ongoing treatment at every eye examination.

Many patients and their carers do not realise that nAMD is a chronic disease which is likely to require life-long treatment and unless patients are treated aggressively, they will generally lose vision. Real-world evidence has shown that anti-VEGF injection frequency is an important factor in achieving optimal gains in vision. In Australia, the Fight Retinal Blindness Study Group reported that visual acuity was maintained throughout five years of anti-VEGF treatment.³ On average patients receive about five injections per year. Despite this, relative under-treatment is common.

Consistent messaging from different health care providers, including ophthalmologists, optometrists and general practitioners, helps to maintain patient compliance with treatment.

Patients should be encouraged to continue having regular optometric reviews even when they are having regular anti-VEGF injections as it is important that patients have the best optical correction possible in order to maximise their limited vision. Optometrists are well positioned to detect interval ocular pathology such as cataracts and assess the potential need for low vision services in patients with reduced vision.

Some patients are reluctant to voice concerns with their ophthalmologist and feel more comfortable discussing them with their optometrist. Concerns about injection-related discomfort, clinic waiting times and out-of-pocket costs are examples of issues that patients may find easier discussing with their optometrist. By encouraging the patient to talk to their ophthalmologist or liaising with the ophthalmologist on behalf of the patient, these issues can be addressed and optometrists may potentially prevent patients being lost to follow-up.

KH: Can you give any examples of where the optometrist has played an important role in improving/maintaining compliance with anti-VEGF injections?

SC: One example I am often reminded of is that of an 85 year-old woman that I am still seeing for regular anti-VEGF injections. She is an avid reader and passionate about painting. She is fiercely independent. Approximately five years ago, she developed loss of central vision in her only seeing eye. The fellow eye had become blind following complications of cataract surgery. Her vision had deteriorated rapidly to 6/60 over the course of a week due to nAMD. She had lost the ability to read, paint and drive. She was distressed about the possibility of losing her independence as she lived alone. She was referred to me for assessment by her optometrist whom she had been seeing for approximately 20 years.

At the initial consultation, I confirmed a diagnosis of nAMD and urged her to have treatment with anti-VEGF injections the same day. Despite my best efforts, she refused treatment because of a fear of complications that might lead to her losing more vision, as had happened when she had previously had cataract surgery. She promised to return the next day for treatment after she had time to collect her thoughts. The next day she failed to attend our arranged appointment and treatment. I spoke with her on the phone and she stated that she had determined that she did not want treatment and would just take her chances, letting nature take its course.

I called to explain the situation to her optometrist who took quick action in calling her and managed to convince her to attend for treatment the same day. It was the long-term rapport that she had built up with her optometrist over the years that provided the confidence to trust his advice. He explained that we had shared numerous patients with nAMD together and that the results had been very positive. He reiterated the potential consequences on her quality of life of not having treatment. She responded extremely well to treatment, eventually regaining a visual acuity of 6/9 which has been maintained to this day. She remains fully independent and her passion for reading and painting is unchanged.

Figure 1. The intravitreal injection procedure. Images courtesy of Novartis.


KH: What happens to our (optometrists’) patients when they come for anti-VEGF injections? That is: what is the procedure they can expect to go through?

SC: Following referral of a patient with nAMD by an optometrist for anti-VEGF injections, patients can expect to consult with an ophthalmologist. A typical initial consultation will involve history taking, dilated clinical examination and retinal imaging with fundus photography and optical coherence tomography (OCT) scanning. Additional retinal imaging tests such as OCT-angiography, fluorescein angiography, indocyanine green angiography or fungus autofluorescence may also be performed to confirm a diagnosis of nAMD.

Once a diagnosis of nAMD has been confirmed a decision will be made regarding whether that patient may benefit from anti-VEGF therapy. A minority of patients may not benefit if their condition is too far advanced and they have evidence of severe permanent macular scarring. Assuming that anti-VEGF therapy is indicated, then the pros and cons of treatment will be discussed with the patient and they will be informed about the potential and likely need for long-term therapy. The initial anti-VEGF injection should be performed as soon after diagnosis as practical to avoid the potential for on-going visual loss to occur. Many ophthalmologists will initiate treatment at the first visit or within a few days of the initial visit. Treatment may be performed in the ophthalmologist’s clinic room, a dedicated treatment room in the clinic or in a day surgery setting.

The technical aspects of the injection can vary widely between ophthalmologists (the type of anaesthesia used, the type of antiseptic agent, whether or not a lid speculum is used, the use of post-injections drops) which can cause the patient experience to vary significantly between different ophthalmologists. However, the fundamental steps of the injection will always include the application of some form of ocular anaesthetic (drops, gel or subconjunctival injection) and topical antisepsis (with povidone iodine or chlorhexidine) followed by the intravitreal injection of anti-VEGF agent via a needle passed through the pars plana. Depending on the treating ophthalmologist’s preference, patients may be advised to use drops (lubricants, steroids or antibiotics) following the injection. Some ophthalmologists tend to treat both eyes of patients with bilateral nAMD on the same day, while others may prefer to treat each eye on different days.

Following the initial injection, patients may be reviewed anytime from within a few days after the injection to four weeks later. Patients are typically scheduled to have the second anti-VEGF injection four weeks after the first.

When the patient presents for the second injection, they will be clinically assessed to check their visual acuity and intraocular pressure. The ophthalmologist may perform a clinical exam and/or OCT scan to assess disease activity.

KH: What happens after the procedure?

SC: Depending on the routine of the treating ophthalmologist preference, some patients may have their treated eye covered by an eye pad or shield. They may be advised to use drops after the injection including lubricants, steroids or antibiotics. The trend is increasingly for no post-injection antibiotics to be prescribed due to evidence showing that they do not reduce endophthalmitis rates and concerns that their routine use may promote antibiotic resistance.

Generally, patients should not drive immediately after an injection.

It is common to experience minor dry eye symptoms secondary to the use of topical anaesthetic and antiseptic used during the procedure. These symptoms will usually resolve completely by the next morning but may occasionally persist for up to 72 hours.

KH: Many patients are worried that anti-VEGF treatment will be painful. What can we tell them?

SC: Patients should be reassured that it is a very natural response to worry that anti-VEGF injections may be painful. Although patients may experience minor discomfort during the injection process, the large majority of patients do not experience significant pain at any stage and most patients experience no pain at all at any stage.

Ophthalmologists experienced in administering anti-VEGF injections have typically performed many hundreds if not thousands of injections enabling them to hone their techniques to minimise pain and discomfort.

Having said that, a minority of patients may experience pain associated with an injection. There are many technical nuances to performing intravitral anti-VEGF injections that can have a large impact on patient comfort during or after an injection. It is important for patients to know that if they do have a painful experience, they should inform their ophthalmologist so that they can make amendments to the injection technique for the next injection. Different patients may respond quite differently to the same technique. For example: some patients find the use of povidone iodine causes severe pain whereas other patients may not, so in such a patient, switching the antiseptic used to chlorhexidine may enable a pain-free experience.

Patients should be informed that if they do experience pain during treatment, the pain is usually very brief and can be managed appropriately. Reminding the patient that the bigger picture is that the injections are important to optimise the patient’s vision and ultimately their quality of life and independence.

KH: What is the risk of serious complications?

SC: Fortunately, the risk of serious vision-threatening complications with anti-VEGF injections is low. Possible sight-threatening complications can occur and include:

  • endophthalmitis reported to occur at a rate between 0.019% and 0.09%. Many cases of endophthalmitis can be successfully treated with recovery of good levels of visual acuity but some cases may not respond as well ultimately leading to permanent loss of vision.
  • retinal detachment (under 0.05%)
  • cataract due to the needle used to inject the anti-VEGF agent inadvertently touching the crystalline lens

KH: What are the potential side effects?

SC: A number of non-sight threatening side effects may commonly occur, including:

  • subconjunctival haemorrhage which is common but harmless although it may be a cosmetic concern for some patients. It will typically resolve within 14 days.
  • dry irritable eye, transient floaters and transient blurring of vision immediately after the injection which usually resolve by the next day.


1. Mantel I. Optimizing the Anti-VEGF Treatment Strategy for Neovascular Age-Related Macular Degeneration: From Clinical Trials to Real-Life Requirements. Transl Vis Sci Technol. 2015; 4: 6.
2. Weiss M, Sim D, Herold T et al. Compliance and adherence of patients with diabetic macular edema to intravitreal anti-vascular endothelial growth factor therapy in daily practice. Retina 2018; 38: 2293–300.
3. Gillies MC, Campain A, Barthelmes D et al. Long-Term Outcomes of Treatment of Neovascular Age-Related Macular Degeneration: Data from an Observational Study. Ophthalmology. 2015; 122: 1837-1845

Clinical classification for Aged-Related Macular Degeneration (AMD)

Clinical classification for AMD

Reprinted from the 2019 Optometry Australia Clinical Practice Guide for the diagnosis, treatment and management of AMD, the Beckman classification offers a guide to identify normal, early, intermediate and late AMD.

Download the Clinical Classification for Age-Related Macular Degeneration (AMD)

March 2019

Confessions of a clinician

Dr Angelica Ly
PhD GradCertOcTher BOptom (Hons) FAAO
Integrated Care Co-ordinator and Lead Clinician (macula)
Centre for Eye Health


Age-related macular degeneration (AMD) is the leading cause of vision loss and blindness in Australia.

One in four cases of AMD are classified as normal by eye care professionals.1 Poor visual acuity at presentation translates to poor outcomes and up to 87 per cent of patients with neovascular AMD have a visual acuity worse than 6/12 at the time of diagnosis.²,³ Additionally, one in five patients that need treatment may be lost to follow-up.⁴

These statistics paint a sobering picture on the state of AMD care in Australia and worldwide. In this article, I describe a series of clinical strategies to supercharge the way you diagnose, understand and manage AMD.

Confession 1: The rules keep changing

Solution: Clinical practice guidelines

There is a plethora of resources now available to practising clinicians aimed at improving clinical practice patterns and ultimately, patient outcomes. Broadly, these resources include convenient and easily-accessible forms of information, such as case studies, peer-reviewed publications, chair-side references and clinical guidelines (Table 1).⁵

Guideline title and web linkProduced byYear
Clinical practice guide for the diagnosis, treatment and management of age-related macular degenerationOptometry Australia2018
Age-related macular degeneration NICE guidelineNational Institute for Health and Care Excellence2018
BMJ Best Practice Age-related macular degeneration British Medical Journal2018
Referral pathway for AMD screening and management by optometristsThe Royal Australian and New Zealand College of Ophthalmologists2018
NZ National guidelines – management of neovascular AMDNew Zealand Association of Optometrists2018
Practical guidelines for the treatment of AMDReview of Optometry2017
Age-related macular degeneration preferred practice patternAmerican Academy of Ophthalmology2015
Guidelines for the collaborative management of persons with age-related macular degeneration by health- and eye-care professionalsCanadian Journal of Optometry2015
Age-related macular degeneration: Guidelines for managementRoyal College of Ophthalmologists2013
Treatment of age-related macular degenerationAustralian Prescriber2012
AMD – advice to optometristsOptical Confederation2010
Age-related macular degeneration (management recommendations)International Council of Ophthalmology2007
Care of the patent with age-related macular degenerationAmerican Optometric Association2004

Optometry Australia has recently developed a clinical practice guide, providing evidence-based information about current best practice in the diagnosis, treatment and management of age-related macular degeneration.  This is an open-access resource available on the Optometry Australia website.

Because the collective wisdom is constantly evolving, these tools can be helpful for distinguishing fact from fiction and often provide all of the relevant information succinctly, filtered through the lens of an expert committee. Although the evidence for efficacy of these materials is limited and the best approach for optimising their efficacy still requires clarification, they are indeed one of the few methods we have of translating research findings into clinical practice. They help to define and promote the use of evidence-based procedures of proven benefit and discourage ineffective alternatives.

In these materials, you can find ready support on a myriad of topics ranging from general management advice, diagnosis, procedures, referrals, test ordering, patient education, clinical prevention and professional-patient communication. They may be accessible through one or multiple means (either personally, online, through mass mailing and most commonly, via publication in a peer-reviewed journal) and result in a statistically significant improvement in professional practice.⁵

Confession 2: I am not confident about what I’m seeing

Solution: Clinical decision support platforms

Today’s ‘routine’ eye examination is incredibly complex. In AMD alone, we may be accustomed to performing a targeted history, a routine battery of entrance tests, followed by fundoscopy and retinal photography. It helps to know which instrument to use and when. Optical coherence tomography (OCT) is quickly becoming the norm⁶ and OCT angiography, fundus autofluorescence and other imaging techniques, including near infrared imaging or ultra-widefield imaging, are also effective.⁷,⁸ The combination of multiple modalities improves the diagnosis of ocular disease but may not always be accessible and is often time consuming and subject to interpretation.

Take for instance, a routine 512 x 128 macular OCT volume scan acquired using the Cirrus HD-OCT (Carl Zeiss Meditec). This means that in addition to the rest of the examination, the optometrist has an added duty of care to review each of the 128 serial line scans taken per eye, meaning a total of 256 B-scans per patient. Add to this the myriad of prognostic biomarkers, which are relevant to stratifying risk of AMD progression⁹ and the complexity is mind-boggling.

Support for accurately interpreting imaging results is on its way. With the aid of computational approaches and machine learning, we can expect to see a growing suite of clinical decision-making support tools. Risk calculators represent an example many will be more familiar with, which is commonly applied to case history data.

Figures 1 and 2 showcase two computational methods of analysing AMD-related ocular imaging data in development at the Centre for Eye Health.¹⁰,¹¹ Current commercially-available software on the Cirrus HD-OCT, described as ‘advanced retinal pigment epithelium (RPE) analysis,’ presents a similar tool with the capacity to automatically quantify drusen load.

Figure 1. A clinical decision support tool currently in development at Centre for Eye Health. This method uses unsupervised cluster analysis to semi-automatically classify drusen (red) and pigmentary abnormalities (blue). Each distinct colour in the profile map corresponds to a statistically separable, specific anatomic structure.

Figure 2. Case images taken 16 months apart from an eye with intermediate AMD. The change or difference map pictured on the right alerts the clinician to areas of drusen regression (red).


Confession 3: My patients refuse to quit smoking

Solution: Motivational interviewing and printed patient educational materials

Having fulfilled the onerous task of keeping up-to-date with the latest evidence, acquiring and correctly interpreting the sum of results from the eye examination, it can be tempting to presume that our job is done; however, all that work may be in vain if not disseminated to the patient. Several risk factors carry a well-described association with the onset and progression of AMD, such as age, family history and smoking. Hypertension, cardiovascular disease, raised BMI, poor diet and lack of exercise are less often considered but represent additional and more importantly, modifiable risk factors for disease. Therefore, your AMD management strategy should regularly include advice on improving dietary habits as well as the benefits of nutritional supplements and quitting or reducing smoking.

As optometrists, our unique position in the health care system empowers us to educate and reinforce key management strategies that can make a difference and ultimately, save sight. Behaviour change in chronic disease can be difficult, particularly in asymptomatic cases where the fear of change, ambivalence, lack of skills or a history of prior failures abound; however, it can also be one of the most rewarding aspects of routine optometric practice and a real relationship-builder between you and your patients.

I encourage you to have those ‘difficult’ conversations. But be advised that authoritarian, confrontational or guilt-inducing communications are often counter-productive. If you’re finding it hard to know where to start, motivational interviewing describes an evidence-based, directive counselling approach to behaviour change. I urge all practitioners to learn more about its application in chronic diseases.¹² Personalising the message to the individual is important and relevant material or contact from patient support groups, such as the Macular Disease Foundation Australia, or low vision services, including Guide Dogs Australia or Vision Australia, can also be invaluable.

Optometry has entered a period with an ever-increasing range of tools and information to supercharge the way we manage AMD and other diseases. With this comes both challenges and opportunities to apply strategies for the benefit of our patients. How will you improve the way you manage AMD tomorrow?

Conflicts of interest: The author is a named inventor on a provisional patent relating to the use of pattern recognition on ocular imaging data. Centre for Eye Health is an initiative of Guide Dogs NSW/ACT and UNSW Sydney and has an affiliation with the Macular Disease Foundation Australia.

Acknowledgements: The author thanks Michael Yapp and Professor Michael Kalloniatis for reviewing the manuscript.


1. Neely DC, Bray KJ, Huisingh CE et al. Prevalence of Undiagnosed Age-Related Macular Degeneration in Primary Eye Care. JAMA Ophthalmol 2017; 135: 570-575.
2. Fong DS, Custis P, Howes J et al.   Intravitreal bevacizumab and ranibizumab for age-related macular degeneration a multicenter, retrospective study. Ophthalmology 2010; 117: 298-302.
3. Ho AC, Albini TA, Brown DM et al. The Potential Importance of Detection of Neovascular Age-Related Macular Degeneration When Visual Acuity Is Relatively Good. JAMA Ophthalmol 2017; 135: 268-273.
4. Obeid A, Gao X, Ali FS et al. Loss to Follow-up Among Patients With Neovascular Age-Related Macular Degeneration Who Received Intravitreal Anti-Vascular Endothelial Growth Factor Injections. JAMA Ophthalmol 2018; 136: 1251-1259.
5. Giguere A, Legare F, Grimshaw J et al. Printed educational materials: effects on professional practice and healthcare outcomes. Cochrane Database Syst Rev 2012; 10: CD004398.
6. Ly A, Nivison-Smith L, Zangerl B et al. Self-reported optometric practise patterns in age-related macular degeneration. Clin Exp Optom 2017; 100: 718-728.
7. Ly A, Nivison-Smith L, Assaad N et al. Infrared reflectance imaging in age-related macular degeneration. Ophthalmic Physiol Opt 2016; 36: 303-316.
8. Ly A, Nivison-Smith L, Assaad N et al. Fundus Autofluorescence in Age-related Macular Degeneration. Optom Vis Sci 2017; 94: 246-259.
9. Ly A, Yapp M, Nivison-Smith L et al. Developing prognostic biomarkers in intermediate age-related macular degeneration: their clinical use in predicting progression. Clin Exp Optom 2018; 101: 172-181.
10. Ly A, Nivison-Smith L, Assaad N et al. Multispectral Pattern Recognition Reveals a Diversity of Clinical Signs in Intermediate Age-Related Macular Degeneration. Invest Ophthalmol Vis Sci 2018; 59: 1790-1799.
11. Ly A, Yapp M, Kalloniatis M, Zangerl B. Automated identification of drusen regression. American Academy of Optometry Annual meeting, San Antonio, Texas, 2018.
12. Linden A, Butterworth SW, Prochaska JO. Motivational interviewing-based health coaching as a chronic care intervention. J Eval Clin Pract 2010; 16: 166-174

Mistakes not to make in glaucoma management

Dr Joseph Sowka

OD FAAO Diplomate
Nova Southeastern University
College of Optometry
Ft. Lauderdale, FL, USA


Diagnosing and managing patients with glaucoma can be a challenging task.

Glaucoma can be diagnosed by observations of characteristic changes in the optic disc and retinal nerve fibre layer (RNFL), abnormalities in threshold perimetry, alterations in structure demonstrated on optical coherence tomography (OCT) and assessment of risk factors such as intraocular pressure (IOP) and family history of the disease.¹ Therapeutic intervention is generally straightforward; that is, reduction of IOP with medicines, lasers and/or surgery. However, errors in diagnosis and therapeutics can make glaucoma management an arduous task. Take care not to make these common errors

Mistake #1: Not recognising when the OCT is wrong

There are several issues in imaging that make OCT assessments for glaucoma very suspect and even misleading. A relatively limited normative database (against which the patient’s measurements are compared), signal quality, blinks and saccades, segmentation errors, media opacities and an abnormal axial length can all contribute to induced false measurements on an OCT.

When interpreting an OCT printout, ensure that the quality score (as indicated for each specific proprietary device) has been met at a minimum. Look to see that there is proper illumination and clarity of focus and the optic disc image is properly centred with no missing data. Inspect the scan for signs of eye movement. Look to see how the device has segmented the individual layers to ensure that no artificial errors have been introduced. Posterior vitreous detachments and other vitreal issues may confuse the device and make it seem that it is measuring tissue that isn’t really there. Finally, if using any macular scans or ganglion cell analysis measurements, ensure that there is no concurrent macular disease. If there is, then do not use this potentially misleading information.²-⁴ (Figures 1 and 2.)

Figure 1. Abnormal OCT due to missing data from blink. Note how the RNFL thickness superiorly drops to ‘0.’ This never happens anatomically and is a result of the missing data rather than true glaucomatous loss.


Figure 2. Abnormal ganglion cell analysis OS due to epiretinal membrane and macular pseudo-hole. Such images of concurrent disease should not be used in glaucoma analyses.


Mistake #2: Treating ‘red disease’

Most OCT printouts colour-code results as to degree of statistical significance. Common coding uses green to connote the patient’s measured data to be within 95 per cent confidence intervals, red to indicate when findings would occur normally in just one per cent of the population, and yellow to indicate all intervening values with borderline significance. In that each OCT manufacturer employs a relatively limited normative database to compare against, there commonly will be situations where a patient’s measured data falls outside the device’s normative database, yet the patient may be completely healthy and normal. Just because a patient’s measured information falls outside the 99 per cent level doesn’t mean that there is disease present. In this instance, much of the printout will be coded as abnormal in red, yet there is truly no disease present. This is commonly referred to as ‘red disease.’⁵

The use and overemphasis of imaging technology to the exclusion of additional clinical findings and assessment of risk will put patients in peril. All imaging technology must be interpreted in context with other clinical findings and when the OCT results do not fit with known correlates of glaucoma, the results should be interpreted with caution (Figure 3).

Figure 3. Left superior temporal OCT abnormality in an eye with a robust OCT thickness map, normal visual field, and ophthalmoscopically normal optic disc and RNFL as an example of ‘red disease’


Mistake #3: Not treating ‘real disease’

Similar to red disease discussed above, there may be instances where patient data may fall within the OCT normative confidence interval with results printed in green, yet have clinically, ophthalmoscopically visible damage to the RNFL and functional loss on threshold perimetry.⁶ This commonly occurs when inspecting the quadrant and clock hour graphs on OCT. When the RNFL analysis is divided into four quadrants or 12 clock hours, it must be remembered that considerable area is being averaged to give these sector values. A focal RNFL defect may be present ophthalmoscopically, but when averaged in with adjacent healthy tissue on OCT, the value may fall within the device’s normative database. Thus, everything is printed in green, giving a false sense of security in an eye that truly has structural damage. Thus, it is important to weigh the OCT results against the optic disc photographs and clinical examination to ensure that “green disease” is not missed⁷ (Figure 4).

Figures 4. A: An ophthalmoscopically visible RNFL defect. B: A normal OCT with all data falling within the device’s normative database in a classic example of ‘green disease.’


Mistake #4: Changing therapy based upon one bad IOP reading or one changed visual field

Intraocular pressure measurements and visual field results can be variable, especially when one considers patient compliance with medications and the psychophysical responses in threshold perimetry. Patients often overstate adherence to medical therapy. Even when not trying to be intentionally misleading, many patients may not correctly remember if they used their medication properly immediately before the examination. Medicines don’t fail overnight. A medically adherent patient will not have an IOP of 15 mmHg on one visit and 30 mmHg on the next visit due to medicine failure or progressing trabecular dysfunction.

There will be a slow, progressive upward drift of IOP in cases where medicines are failing to control IOP. Always insist at least two IOP readings above target (and preferably three) before making any therapeutic changes. Similarly, visual field changes occur frequently, but shouldn’t be considered progression unless the change is verified in a subsequent (and preferably two) visual fields. Over 80 per cent of abnormal visual fields noted in the Ocular Hypertension Treatment Study were not verified on repeat testing.⁸ Always look for a sustained decrease in visual field results before changing therapy.

Mistake #5: Not getting enough pre-treatment… and post-treatment IOPs

Unless a patient presents with very high IOP (above 45 mmHg) or has advanced disease (with loss of central visual acuity or relative afferent pupil defect in an eye), there is generally no need to rush to treat chronic open angle glaucoma. It is very beneficial to get several IOP readings (at least two and preferably three) before initiating treatment of any kind. At one visit, the patient may be exhibiting a peak IOP or a trough reading. Knowing the range is very important.⁹ Similarly, one should never prematurely judge efficacy of treatment based upon the IOP reading immediately after initiation of therapy.

Even if the first IOP measurement after initiating therapy isn’t impressively lowered, consider leaving therapy unchanged and check at least one more time before deciding if a medication is truly efficacious or not. In the example here, there was an abrupt IOP drop after the initiation of therapy. However, it is notable that there are several pre-treatment IOPs that are nearly identical to the post-treatment IOPs, indicating that the prescribed medication, while overall effective, doesn’t consistently give the robust pressure reduction initially seen (Figure 5).

Figure 5. IOP curve before and after treatment initiation for glaucoma. Several pre-treatment IOPs were nearly identical to post-treatment IOPs, raising questions about the effectiveness of the chosen therapy.


Mistake #6: Not recognising a neurologic visual field in a glaucoma patient

One of the most insidious situations in eye care occurs when a patient with glaucoma manifests a neurologic disease concurrently. While glaucoma causes arcuate visual field defects that respect the horizontal meridian and neurologic conditions cause hemianopic defects that respect the vertical meridian, such patterns can get lost within the same patient. There are two ways to discern these differences. First, a glaucomatous visual field can be predicted by the optic disc and RNFL appearance. When the field loss is greater than expected and, often in an area not anticipated based upon the optic disc appearance, one should look for the neurogenicity by examining carefully both visual fields. Additionally, the greyscale printout is exceptional at identifying visual field defects which respect the vertical meridian while the pattern deviation can be quite poor. Further, while glaucomatous and neurologic damage can occupy the same quadrant, neurological defects may actually manifest a deeper scotoma within a glaucomatous defect.


A 74-year-old female previously diagnosed with glaucoma had optic nerve and RNFL damage consistent with glaucoma. However, observation of the grey scale showed bitemporal visual field defects that respected the vertical meridian. The fields were repeated and the pattern persisted. Ultimately, she was diagnosed with a pituitary macroadenoma and scheduled for neurosurgical intervention (Figure 6).

Figure 6. Superior bitemporal visual field defect in a patient with both glaucoma and pituitary macroadenoma. Note that the neurologic field is better appreciated on the grey scale than on the pattern deviation.


A second patient, a 65-year-old female also previously diagnosed with glaucoma exhibited bilateral inferior defects on visual fields. The left visual field matched extreme superior disc damage in that eye. In the right eye, her superior field defect matched optic disc and RNFL damage, but there was no structural abnormality to explain her inferior visual field loss. Most notable was the fact that the right inferior visual field defect stopped at the vertical meridian on the grey scale in the right eye. While the left eye had a significant inferior arcuate scotoma, it was notable that the left inferior nasal defect was absolute and much deeper than the remainder of the field loss. This led to the observation that she had not only glaucomatous arcuate visual field defects, but also a superimposed right inferior quadrantanopia. Subsequent neuroimaging revealed an ischemic cerebral infarct (Figure 7).

Glaucoma diagnosis and management can be quite challenging. It is important to be aware that there are common errors that can make glaucoma management much more challenging.

Figure 7. Right inferior quadrant defect hidden beneath the glaucomatous losses. Note that the neurologic field is better appreciated on the grey scale than on the pattern deviation.



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