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Report

Record attendance underlines ACO conference success

08/02/2018By Lewis Williams PhD
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The Australian College of Optometry (ACO)’s National Conference welcomed around 100 delegates to the MCG late last year. LEWIS WILLIAMS was there to document proceedings from a fascinating two days.

According to ACO CEO Ms Maureen O’Keefe, last year’s conference attracted a record number of delegates. Hoping to build on this momentum, the College is set to continue to offer a number of CPD events covering therapeutic and other areas of need in the future.

Furthermore, to address some of the unmet needs of public health eyecare in Victoria and elsewhere, especially Indigenous eye health, the ACO provides eyecare services to those in need. It has collaborated with four other organisations to land a $4.8 million Indigenous eye health contract.

Also referenced were new and ongoing education and research initiatives and an increased emphasis on clinical research.

Following O’Keefe’s brief overview of the ACO’s activities, the program proper was opened with the OPTICARE Keynote Address delivered by Laureate Professor Hugh Taylor AC on the topic of Indigenous eye health.

OCT and glaucoma


Dr Jesse Gale, a NZ ophthalmologist and visiting lecturer at the ACO, demonstrated how OCT scans can complement clinical observations, with special reference to glaucoma.

Gale sees the main roles of OCT as the differentiation of normal from abnormal, progress monitoring, and as an aid to the avoidance of over-treatment or unnecessary treatment. His advice was to scan all glaucoma suspects, paying particular attention to loss of RGCs and RNFL axons or cell bodies.

The optic disc rim thickness assay feature in OCT instruments was also recommended, following the now widely-accepted ISNT order of assessment. Gale believes that OCT findings pre-date perimetric changes leading to the possibility of earlier intervention.

Despite such technical advances, the Australian gold standard remains photographs, especially stereo photographs, of the optic disc and optic nerve head. However, he did state that circum-papillary RNFL scans were good at detecting early glaucoma and helped differentiate suspects from sufferers even better than stereo photographs and devices such as the HRT.

Gale detailed the readily identifiable, OCT landmark, Bruch’s Membrane Opening (BMO) at the disc, noting that while it was readily identifiable in scans, it was not the same as the clinical-discernible disc margin.

Generally, observable structural changes can predict visual field (VF) loss better than other parameters such as photographs, IOP, etc. However, it is possible for structural changes, including progressive changes, to be observed while the VFs remain unaltered.

Gale noted that predicting the future in those cases is “difficult” but ultimately, VF changes were regarded as a more valid measure of the state of play and/or disease progression.

Finally, Gale observed that OCT does not disclose Drance haemorrhages or disc pallor but still has a context in glaucoma care, even if it is not a complete replacement for observation by a skilled practitioner.

MGD and dry eye

Professor Fiona Stapleton, head of the School of Optometry and Vision Science at UNSW, opened her lecture with a concise explanation of the differences between the often-confused terms of incidence and prevalence.

Starting with the 2007 International Dry Eye Workshop (DEWS1) report, she gave the five main considerations as:

  • Female health

  • Symptoms

  • Signs

  • The poor relationship between symptoms and signs

  • Signs of Meibomian Gland Dysfunction (MGD).

Dry Eye (DE) prevalence increases with advancing age. Figures vary between 5–35% in those over 50 years of age depending on gender (two-thirds of sufferers are female), ethnicity, diet, country, environment, etc.

Once the age of 60 is passed, the prevalence of DE symptoms among females greatly exceeds those among males, but the DE signs in those over 60 exhibit less of a difference. However, as far as MGD is concerned, little difference exists between the sexes with females only slightly greater, especially at older ages.

Often, an autoimmune condition is a fellow traveller (co-morbidity) with DE. Female steroids, androgens, oestrogens, progestins, and glucocorticoids, have differing effects on the body and affect the regulation of the ocular surface (OS).

Intracrine synthesis of sex hormones, a normal function in the human body, also affects the OS.

Importantly, the stimulation and process of the pain sensation differs between the sexes. Confounding the data is the greater likelihood that a female will access the healthcare system than a male, tending to skew results toward female prevalence.

Asians have a greater MGD problem (1.5x prevalence, 2.2x signs, 2x signs and symptoms combined) than Caucasian and other groups, but they show little difference been the sexes. Leading the impacts of DE are the symptoms of discomfort and pain, the latter being compared ‘favourably’ with mild angina.

DE sufferers are also more than 2–3x more likely to report poor or reduced vision including at near, when using a computer, and while driving, to the extent that their quality of life is impacted adversely. The latter is linked strongly to depression, and medications confound the issues involved.

It has been estimated that up to 20% of eye hospital outpatient visits and 11–26% of optometric examinations are DE-related. Those figures translate to about $1,000 per patient per year. Overall, patient symptoms are reported to be severe on as many as 200 days per year.

The dominant DE subtype (<65%) is evaporative dry eye/MGD (EDE/MGD) as disclosed by poor expressibility of the meibomian glands and telangiectasia. Expressibility, MG dropout, poor meibum quality, and age-related changes are all signs of EDE/MGD.

CL wear exacerbates MGD by 5.6%, decreases gland expressibility, and increases gland dropout. The longer CLs are worn, the greater the dropout.

Significantly, there is little difference between modern RGP and soft CLs. Overall, the effect of CL wear is to bring forward the signs of MGD by around five years compared with non-wearers.

Therapy for MGD includes: eyelid hygiene (also serves as a preventative measure), ocular lubricant (preferably, unpreserved), essential fatty acids in the diet, topical azithromycin, and oral tetracyclin.

The DEWS II (2017) report recommended that ocular homeostasis be restored as closely as possible first, while it also found it important to determine if the condition presenting is aqueous-deficient DE (ADDE), EDE, or a mixture of both.

In terms of treatment, it was suggested that a rigid step-wise approach be avoided in favour of simple approaches, that use more than one treatment at each stage as necessary.

The inheritability of DE is unclear but could be as high as 30–45%, and those with chronic blepharitis and poor Schirmer’s Tear Test results are more likely to develop DE later in life. Emerging risk factors include climate changes and extensive use of screen-based digital devices of all sizes.

The protective pathway is to treat MGD, alter the environment favourably, and instigate changes that increase the essential fatty acids ingested.

KEYNOTE SPEAKERS

Daniel Chiu

Hugh Taylor

Maureen O'Keefe

Marcel Mikulka

Fiona Stapleton

Jesse Gale

Neovascular AMD

Keynote speaker Dr Daniel Chiu, focused his presentation on non-anti-VEGF treatments of neovascular AMD (nAMD).

According to Chiu, the durability of the effect of anti-VEGF injections to treat nAMD is linked intimately to the individual’s response to the treatment.

Factors affecting that response include molecular factors such as drug half-life, individual affinity of the drug to its target, transretinal transport, the effects of the vitreous, extracellular matrix differences, alterations to the neovascular architecture, and an increase in the tolerance and tachyphylaxis – a diminishing response to successive doses of a drug that can be confounded by local increases in VEGF expression, decreasing the efficacy of the therapy. Sometimes, taking a break from treatment can restore efficacy, at least temporarily.

Other factors affecting the outcome of treatment include the amount of drug reaching the target, increases in drug clearance, and neutralising antibodies (e.g. 1–6% develop immunoactivity to ranibizumab after 12 months of monthly dosing). In some cases, changing the drug used can improve the efficacy of anti-VEGF therapy.

Usually, efficacy of therapy is based on the amount of IRF or subretinal fluid (SRF), central retinal thickness (CRT), the condition of the inner retinal complex (IRC), and VA.

Chiu suggested that anti-VEGF treatment be held back in cases of recent or frequent stroke. Quoting the 5-year CATT study, he reported the onset of geographic atrophy (GA) in some cases while on anti-VEGF treatment for two years, due to the deprivation of VEGF from the choriocapillaris layer (VEGF is essential to maintenance and survival of the capillaries in the layer).

In summarising the risks of anti-VEGF therapy, Chiu listed the frequency of visits, the lifelong commitment required (both patient and practice), and the small but real risk of infection from repeated injections.

Designs for Vision
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While still an uncommon disease, 90% of endophthalmitis cases (often due to aggressive Streptococcus spp.) are now anti-VEGF injection-related. Figures suggest the rate is 1:1,500 patients or 1:4,000 injections, which is similar to endophthalmitis resulting from intraocular surgery.

Seeking to avoid the disadvantages of current therapies, alternative strategies are under investigation.

Some target an increase in the duration of the action (fewer injections) while other possibilities include: the DARPin molecule (small molecules derived from natural ankyrin repeat proteins), cell-based therapy, gene transfer/use of a viral vector, slow-release formulations, investigations into CNV pathogenesis, further investigations of angiogenesis, uncovering additional targets within the retina, and endogenous anti-angiogenesis inhibitors.

Multi-target and combination therapies are also under active investigation.

Despite the success of the last decade in treating AMD, many challenges still exist, with sustained increases in VA still regarded as the main game. However, with the amount of funding at stake and the potential income from a successful product or technology, further advances are highly likely.

A different type of TED talk


Melbourne ophthalmologist, Associate Professor Alan McNab, spoke about thyroid eye disease (TED), a disease of orbital and paraorbital tissue involving the orbit, eyelids, and lacrimal system.

TED is an autoimmune disease and, despite the telltale sign of protrusion of the globe (exophthalmos) in TED, the exotropia depicted in many photographs, skits, and comedy routines, is actually uncommon.

The inflammatory process is a result of circulating autoantibodies and while acute initially, the condition usually settles into being a chronic inflammation process. That process results in the deposition of very hydrophilic glycosaminoglycans (GAGs) in the orbit, producing a significant increase in the volume of orbital fat and exophthalmos.

Later, fibrosis occurs leading to the formation of scar tissue. Despite a detailed understanding of the process, the condition remains unexplained largely. Likewise, the higher prevalence in females (5:1) remains unexplained.

Some of the extraocular muscles are affected more than others (IR>MR>SR>LR>obliques) and smoking is known to exacerbate the problem. Patients complain of sore, gritty, watery eyes, eyelid swelling, an altered appearance (prominent eyes), disturbances of vision, ocular surface drying, diplopia (especially on eye movement due to globe movement restriction), optic neuropathy, and, uncommonly, strabismus.

Treatment for mild disease is largely supportive, e.g. elevated bed head (to decrease oedema accumulation), sunglasses, smoking cessation, prescribed prisms, the use of diuretics (only in some cases), and an increased intake of selenium in the form of a handful of Brazil nuts daily.

Moderate disease adds oral or intravenous steroids, orbital radiation, and possibly surgery to the treatment schedule. Severe disease adds immunosuppression and cytotoxins, radiotherapy, orbital decompression, and possibly monoclonal antibodies. Radiotherapy requires the concurrent use of corticosteroids to reduce its effects.

Strabismus and lid-retraction surgeries may also be required but if possible, surgery should only be undertaken when the disease is inactive. Furthermore, orbital decompression should be performed before strabismus surgery.

Optic neuropathies secondary to TED are a direct result of orbital apical overcrowding and can result in changes in VA, VFs, colour vision, pupil behaviour, the optic disc, and contrast sensitivity. However, vision loss is unlikely.

In something of a worst-case scenario, balanced orbital wall removal may be required to alleviate overcrowding and pressure issues, and to decrease the possibility of induced strabismus.


Indigenous eye health

Professor Taylor is a former head of ophthalmology at the University of Melbourne (UniMelb), founder of the Centre for Eye Research Australia (CERA), recipient of the Companion of the Order of Australia (AC, 2001), and the author/co-author of more than 700 published papers.

Currently, he is the president of the International Council of Ophthalmology, and a member of the Board of Trustees and deputy chairman of Vision 2020 Australia.

Commencing in 2008, the Minum Barreng (literally: tracking eyes) national Indigenous eye health survey was rolled out from the Indigenous Eye Health Unit, UniMelb with the expressed aims of ‘closing the gap’ between Indigenous and non-Indigenous levels of health and healthcare.

Taylor reported that Australia’s first people start with the best vision in the world, a situation that, unfortunately, often does not last their lifetimes. He gave figures of 55% of males and 45% of females having 6/2.4 VA or better, with the best result recorded of 6/1.4 (European figures are 32% and 8% respectively).

As well as better vision, Indigenous Australians have much lower levels of myopia and no high myopia (≥5 D). However, they do not escape the universal curse of presbyopia.

The earlier Melbourne Vision Impairment Project found that for the decades after 40 years of age, there is a 3x increase in vision loss and blindness among Indigenous peoples for each subsequent decade.

Vision impairment (VI) doubles the risk of falls, increases the risk of hip fractures by 4–8x, triples the incidence of depression, and increases the chance of admission to a nursing home 3x earlier than other health causes.

Furthermore, the social aspects are significant, as assistance is often required to complete otherwise simple tasks such as going shopping or visiting a medical practitioner – the latter being required twice as often as for other causes. Taylor also gave data that showed that those with <6/12 VA who were more than 50-years-old are twice as likely to die compared with others with similar health levels but normal vision.

Furthermore, established research has shown that the return on each $1 spent on vision care, equates to $5. By his estimates, Taylor believes that about 80% of vision loss is unnecessary.

Leading causes of Indigenous VI/blindness are cataract, refractive error, some optic atrophy, trachoma, and diabetic eye disease. About 94% of such vision loss is preventable or treatable and therefore unnecessary, and more than one-third of those afflicted have never had an eye exam.

Vision loss explains 11% of the health gap between Indigenous and other Australians and, while not the greatest contributor, it is the most ‘treatable’.

To illustrate what can be achieved, Taylor reported that there were 15,000 Indigenous people with poor vision in 2010. If nothing was done that would double to 30,000 by 2030 but, if proper measures were undertaken, the figure would fall to below 2,000 by 2030.

Compounding the problem, only 20% of Indigenous adults have glasses and 40% cannot read N5. Despite having a similar cataract development profile as other Australians, aboriginal people are 12x more likely to present with cataract because they are not getting the surgery they need.

The Indigenous surgery rate is 1/7th that of the mainstream and compounded with much longer waiting times (>1 year) – seven years being the longest in one Brisbane case. About 37% of Indigenous adults have diabetes (type 2) and without treatment, all will go blind or end up severely VI.

Taylor then detailed trachoma, noting that it is dependent on repeat trachoma infections (150–200 to lead to blindness) to take hold in an eye. Most initial infections occur early in life (around 8–10 years) and are dependent on the repeated transfer of infected eye secretions from one child to the next, a life-cycle stage that can be eliminated relatively easily with a ‘clean face, clear eyes’ program in the affected communities.

Antibiotics are not the answer despite being about 95% effective as they only reduce, but do not eliminate the problem. Health promotion material targeting aboriginals using the Melbourne Football Club (a team with several Indigenous star players acting as trachoma ambassadors) as the vehicle has proved to be successful. From a figure of 21% in 2008, the trachoma prevalence in 2015 was estimated to be about 4.5% of the Indigenous population, nationwide.

An ongoing barrier to suitable eyecare is the general unwillingness of Indigenous people to utilise private eyecare services because of cultural and other concerns. The availability of the Aboriginal Medical Service (AMS) for example, made a large difference in the numbers seeking healthcare generally. If trust can be built, that situation can change somewhat.

Describing the system as ‘leaky’, Taylor identified 42 ‘leaks’ in the system that prevented aboriginal people from seeking or getting suitable health/eyecare. For a population of say 10,000 people, Taylor’s research estimates that one full-time equivalent optometrist, a 0.3 FTE ophthalmologist, and 8.3 clinical support staff (excluding surgical support staff) would suffice.

Moving to DR, he recommended that prevention is what is required. Suitable measures include: weight loss, exercise, control of blood-sugar levels, control of blood serum lipid levels (high cholesterol levels double the risk of type 2 diabetes), and control of blood pressure.

About one-third of those with DR develop sight-threatening levels of the condition. When Taylor started his involvement in aboriginal eye health more than 40 years ago, the diabetes rate was about 10% of the mainstream.

While the mainstream prevalence has doubled, the Indigenous rate is now 5x that of the mainstream making it a real healthcare problem. Because of those figures, he recommended an Indigenous eye examination every 12 months, as opposed to the standard 24 months for mainstream Australians.

To assist practitioners interested in the issues involved, online DR grading training (and referral recommendations) is offered on the UniMelb website.

The Closing the Gap program halved the Indigenous blindness rate between 2008 and 2016 from 6x that of the mainstream to 3x the mainstream. However, Taylor described the latter as “still totally unacceptable!”

In summary, he described vision loss as bad for the individual and costly for the community, and his goal is still to close the gap by 2020.

 

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