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SCC7 entrenches conference’s reputation as a leading event

03/12/2018By Lewis Williams PhD
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The Specsavers Clinical Conference continues to expand and attract increased delegate numbers. LEWIS WILLIAMS canvasses the highlights from what was a diverse and extensive program.

The 7th Specsavers Clinical Conference was held at the Melbourne Convention and Exhibition Centre over the weekend of September 8–9. Over the years, the conference has expanded to occupy almost two full days of presentations and courses by leading academics and practitioners drawn mostly from ophthalmology and optometry.

As has been the trend since SCC1, this year’s delegate numbers rose again to around 750 making it one of the biggest, if not the biggest, optometry conference in the country. It will be interesting to follow the numbers that result from the revamped SRC/ODMA conference starting in 2019. However, the latter’s biennial timeline will make direct comparisons of delegate numbers difficult.

Opening address

Head of optometry Dr Ben Ashby began by summarising results from more than 2.7 million eye exams Specsavers had performed. They included 40,000 cases with glaucoma, only half of whom were aware of that fact; 200,000 with diabetes with some 50,000 exhibiting some form of diabetic retinopathy; and 150,000 with AMD, some 15,000 of whom had reached a neovascular stage.

In AMD cases, data relating to the presence or absence and type and size of drusen were used to determine the type of treatment to follow. He revealed that on average, Specsavers optometrists were referring about 20 patients a month for follow-up with appropriate professionals, usually ophthalmologists, which is within the range of current expectations (18–22).

Ashby then posed the question, ‘just what should the referral rate be?’, before revealing that Specsavers had already initiated a research project to answer that very question in association with Glaucoma Australia.

That project follows the agreed RANZCO Glaucoma Guidelines and was dependent secondarily on the Specsavers-wide rollout of Topcon’s Triton S-S OCT instrument, now well underway across Australia. Ashby characterised the study as part of Specsavers’ way of ‘transforming eye health’, a phrase that became the theme of SCC7.

Managing glaucoma

Glaucoma and cataract ophthalmologist Dr Simon Skalicky paid special attention to the role of the optometrist in clinical practice in his presentation on the 2018 standards in clinical glaucoma care.

He described glaucoma as a progressive, irreversible, optic neuropathy in which the intraocular pressure (IOP) might be elevated.

He added that it was a multifactorial disease, and that some of its effects were the result of altered optic nerve perfusion complicated by vasospasms in nocturnal hypertension.

Despite the fact that IOP is not elevated in all cases of glaucoma, e.g. normal-tension glaucoma, IOP remains the only modifiable/treatable factor.


"There is no shame in frequent reviewing, if unsure."
Colin Chan, Sydney-based ophthalmologist

Skalicky noted that care had shifted to a patient-centric model, nutrition and lifestyle are now factored in, and Glaucoma Australia has assumed a leading role in patient education, motivation, and care.

He characterised collaborative care as putting the patient first, including the patient in the professionals’ communication loop, supporting the patient actively to provide a positive and supportive environment, all care to be adapted to the individual, the encouragement of self-monitoring, and seeking the continuous improvement of all aspects of care.

An ophthalmological examination every 2 years was recommended for early to moderate glaucoma cases already under routine care. He also recommended support services, patient monitoring and counselling services, such as those offered by Glaucoma Australia, due to the limits of just how much information the average patient can absorb.

In discussing the relative merits of ongoing eye drop therapy versus a surgical intervention such as SLT, Skalicky sits firmly in the surgical intervention camp. His reasons were: decreased OSD issues meaning fewer dry eye cases subsequently, no eye drop toxicity, more likely to be able to continue to wear CLs that might have been in use for many years, no ongoing treatment costs and compliance issues.

Generally, SLT and similar treatments target the pigmented cells in the trabecular meshwork. Usually, he treats only 180° of the meshwork in the first sitting and treats the remaining 180° 2 weeks later. He estimated that SLT was 70–75% efficient and a 20% lowering of IOP is expected.

He rated OCT as the best means of early detection, as it provides earlier warning than visual field defects becoming apparent, Drance haemorrhages becoming apparent, or IOP increases being detected. In his view, ongoing monitoring of the glaucomatous eye is as important as treatment.

If doubts arise in an optometrist’s mind in a glaucoma case (suspected or established), Skalicky urged them to call the ophthalmologist involved or to whom they refer their glaucoma cases and with whom they have established a working relationship, rather than assume that it’s OK or can wait for another day. He also cautioned that the usual optic disc rim thickness (width) order of ISNT (I≥S, S≥N, N≥T) can sometimes present in SINT configuration in some myopes.

Diabetic eye disease

Brisbane ophthalmologist Dr Erwin Groeneveld reported that the prevalence of diabetes among Australians is around 8%, with about half of those undiagnosed and unaware. He estimated that around 25% of all diabetics have signs of diabetic retinopathy and a significant proportion of those will progress to develop a vision-threatening stage of the disease.

Quoting world figures, he gave the prevalence of diabetes in 1985 as just 30 million a figure that had blown out to 135 million just 10 years later. By 2012 it was 382 million, and it’s predicted to reach almost 600 million cases by 2035.

It’s estimated that 280 patients are diagnosed with diabetes in Australia every single day. That amounts to 100,000 new cases per year maintaining a pool of cases of around 1.1 million.

That number is largely Type 2 diabetes (956,000), Type 1 (120,000), and around 23,600 gestational cases. Once patients, family members/carers, healthcare staff, and others affected directly and indirectly by diabetes are factored in, it’s estimated about 2.2 million Australians are affected by the disease in some way or another – just short of 10% of the entire population.

The main threats to the eye, and vision subsequently, are non-proliferative (NPDR) and proliferative diabetic retinopathy (PDR), diabetic macular oedema (DMO), and retinal ischaemia.

DMO results in fluid leakage that swells the macular and causes central vision loss. Fundus fluorescein angiography (FFA) can reveal lipid residues and drusen.

Signs of pre-PDR include: cotton wool exudates, venous calibre irregularities, dark blot haemorrhages, and IRMA (intraretinal microvascular abnormalities). Diabetic retinopathy remains the most common complication of diabetes.

The top three diabetic risk factors for adverse outcomes are the duration of the disease, increased HbA1c levels, and elevated blood pressure. A dyslipidaemia can also result.

Some ethnicities are at greater risk, such as Indigenous Australians and Pacifica/Polynesian races. If the duration has been <10 years, 18% of cases will develop DR, if the duration is 10–20 years, that figure increases to more than 51%. However, the risk changes little (>52%) in cases of >20 years.

Unfortunately, once DR has commenced, it’s likely to progress and about 30% have PDR by 6 years. HbA1c level is the most important modifiable risk factor, to the extent that each 1% increase in HbA1c increases the DR risk significantly and if it exceeds 10% (<7% is desirable), it will accelerate the rate of diabetes-induced changes.

Vascular hypertension increases the risk of DR. Decreasing the level of blood LDL cholesterol is also a target, as excessive amounts of the light/fluffy LDL component damages the walls of the small blood vessels. Although statins can reduce the LDL levels overall, it’s the proportion of the light/fluffy to dense fractions that is more important.

Mild cases of NPDR are likely to be accompanied by microaneurysms. Groeneveld made the point that DR is ‘non-linear’, i.e. the signs and the contributing factors do not march in lockstep. He gave the mechanisms of vision loss as: retinal ischaemia due to capillary drop-out, macular oedema (which is aggravated by cataract surgery), vitreous haemorrhage (can cause proliferation or vitreous traction) and epiretinal membrane formation (ERM). Retinal detachment (traction or rhegmatogenous [RRD]), neovascular glaucoma, cataract, optic nerve ischaemia, were also listed as other mechanisms of vision loss.

If a laser is used to treat any of the above, its use can cause a rhegmatogenous detachment or, more directly, destruction of retinal tissue such as photoreceptors, resulting in a predictable visual field defect.

Other effects include high blood-sugar levels, which affect retinal capillary leakage; the loss of microvascular pericytes and vascular endothelial cells that lead to a breakdown of the blood-retina barrier; and cataract surgery, as it can stimulate the up-regulation of growth factors that can also increase capillary leakage. The latter can lead to NPDR and vision loss if the macular is involved.

Diabetic vision screening should include an assessment of the VA, a DFE (the use of a non-mydriatic fundus camera or wide-field fundus imaging instrument is satisfactory), looking for other signs of diabetes and DR, and the involvement of other relevant professionals, e.g. the patient’s GP, ophthalmologist, and endocrinologist.

Complicating all the foregoing is the ability of Type 2 diabetes to remain active but asymptomatic and therefore undetected for years. Groeneveld recommended the use of a slit-lamp and a Goldmann contact lens to detect macular oedema.

He stated that, generally, vision loss can be prevented and that exercise and diet were important. He also noted that the use of fenofibrate, a lipid-modifying agent used to reduce cholesterol levels, improved DR outcomes significantly with reductions between 31–40% reported.

KEYNOTE SPEAKERS

Ben Ashby

Colin Chan

Chameen Samarawickrama

David Mackey

Erwin Groeneveld

Simon Salicky

Corneal lesions

Western Sydney ophthalmologist Dr Chameen Samarawickrama gave what was, in my opinion, probably the best presentation of the conference.

Samarawickrama observed that the knowledge base relevant to medicine was expanding exponentially, making staying up-to-date difficult. He preferred a first principles approach based on lists, tables, flowcharts, etc., all of which can be maintained and, if necessary, generated electronically.

He likened clinical care to a continuous loop encompassing investigations, treatment options, follow-up and re-evaluation, knowledge, and clinical acumen. When a differential diagnosis is required the considerations are: the possibilities, the most likely, and the worst-case scenarios.

Treatment options include: the medications for each disease, their possible side effects, possible drug interactions, the possibility of antibiotic resistance, and the Herxheimer Effect (a reaction to endotoxin-like by-products released by dead or dying pathological micro-organisms during antibiotic use).

Another question that also needs to be asked is “Can the signs and/or symptoms be indicative of another condition?”. Finally, decisions need to be made in relation to when to investigate, what to test for, how and when to taper treatment, and when to cease treatment altogether. It’s also prudent to look for recurrences subsequently to confirm that the problem has been resolved successfully.

Three corneal conditions – microbial keratitis (MK), marginal keratitis, and peripheral ulcerative keratitis (PUK) need to be differentiated. Focusing on just MK and marginal keratitis, the latter is accompanied by blepharitis and can be peripheral or nearer the centre of the cornea.

Pain and photophobia are not useful differentiators as both are about the same. However, marginal has no epithelial defect whereas MK can have an abscess, infiltrates, uveitis, and/or hypopyon. Lesion size too is useless as they both start out small.

Marginal cases are likely to demonstrate a Type 3 hypersensitivity to Staphylococcus spp. and ‘sterile’ infiltrates located where the open eyelid touches the cornea. Chloramphenicol was suggested as first line treatment.

Causative agents of MK include Acanthamoeba spp., acid-fast Gram + or Gram – bacteria, or one of the two great mimickers – HSV (syphilis is the other). Australian MK cases can have Gram + or – bacteria or fungi as aetiological factors.

The incidence of MK can also be modified by external risk factors such as location or climate – rural cases are more likely to be fungal in origin and winter cases are more likely to be Streptococcal in origin. Other risk factors are: trauma, CL wear (now the most common cause in which overnight CL wear increases the risk by 6x), OSD, and HSV.

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A CL-related MK is most likely due to Pseudomonas aeruginosa (>50%) but Samarawickrama noted that CLs can introduce new pathogens to the list of causative agents, such as Microsporidia spp., a group of spore-forming, unicellular parasitic fungi or fungi-like organisms.

The filamentous fungi Fusarium spp. was singled out for special mention because of its ability to penetrate as deeply as Descemet’s membrane. Acanthamoeba spp. infections are noteworthy for the disconnect between symptoms and signs (symptoms usually >> signs) and the alarming statistic that the protozoan can remain viable in the dehydrated state for up to 18 years.

Although bacterial keratitis accounts for 95% of corneal infections, the remaining 5% are due to fungi, Acanthamoeba, or other organisms. If the patient reports swimming in a creek recently, Acanthamoeba should be suspected first.

When confronted with a corneal condition, Samarawickrama’s recommendation was to scrape the lesion, examine the cornea with a confocal microscope (Acanthamoeba spp. are visible), and subject biopsy material to PCR analysis. He recommended against commencing antimicrobial treatment without identifying the infective agent(s).

More than 90% of infections are caused by common organisms (in Australia they are most likely to be bacterial). For reasons of minimal side effects, his preferred agent is ofloxacin applied hourly for 48 hours (no sleep possible) to ‘sterilise’ the cornea, hourly during the day for days 3 and 4, every 2 hours for days 5–7, and four times daily for days 8–14. Generally, his advice was to over-treat and be aggressive.

However, if the condition was showing little or no improvement by day 5, alarm bells should ring.

PUK is a relatively uncommon inflammatory disease, has variable presentation, and results in peripheral corneal thinning. Some 34–42% of cases are associated with rheumatoid arthritis (RA) and the presentation is usually crescentic. If associated with a corneal melt, an autoimmune condition is likely involved and if RA is that condition, the RA must be treated first as immunosuppressive therapy may be required. As a connective tissue disorder might also be involved, an ophthalmological referral was recommended.

According to Samarawickrama, CLs took over from trauma as the most common cause of keratitis in early 2005, with Pseudomonas aeruginosa the leading cause.

Red eye

Sydney-based ophthalmologist Associate Professor Colin Chan tackled the seemingly simple topic of red eyes and succeeded in showing that it can sometimes be anything but simple.

He suggested to the audience that they should use their gut instinct on the topic generally, but any “bad” red eye should be referred to an ophthalmologist without unnecessary delay. Ideally, the practitioner first consulted should take an ‘expect the worst and hope for the best’ approach.

Unfortunately, almost anything can lead to an acute red eye, making an early diagnosis unlikely unless the history offers strong hints or the cause is obvious, e.g. a penetrating injury.

First tier causes include: acute angle-closure glaucoma, endophthalmitis, MK, orbital cellulitis, chemical injury, ocular trauma, and penetrating injuries. Second tier causes include: uveitis and iritis, HSV keratitis, diffuse lamellar keratitis, and corneal graft rejection.

If acute angle-closure glaucoma (AACG) is the cause, action must be taken in well under 24 hours if the worst outcome is to be avoided or at least minimised. In the case of MK, any delay greater than 24 hours increases the likelihood of a poor or poorer outcome.

Cases of endophthalmitis must be treated early if a catastrophe is to be avoided. Chan advised the use of ciprofloxacin early in cases of MK as there was little downside to its use. However, he cautioned that MK cases had to be differentiated from peripheral marginal ulcers, an inflammatory disease that is more likely to be associated with autoimmune disorders than an infective agent and hence will not respond to ciprofloxacin usage.

Although it can take time to determine, the truth is often in the evolution of the disease process. If the process does not follow the textbook-described path then it’s likely that the initial path is not optimum or simply incorrect. In such cases, more frequent reviewing was suggested by Chan: “There is no shame in frequent reviewing, if unsure.”

If simple initial treatment such as Chlorsig fails, the cause of the problem is probably not bacterial.

If synechiae have formed already they can be difficult to break while significant inflammation is still present. Sometimes the inflammation needs to be decreased before breaking is successful, but time remains a factor in their consolidation. His advice on treatment tapering for red eye was simple, “don’t taper too soon and certainly not as soon as an improvement is noted.”

Those comments also apply to the use of steroids but with the additional rider that IOP must be monitored frequently.

Any red eye appearing within 2 weeks of significant eye surgery should be assumed to be a case of endophthalmitis until proved otherwise.

If a red eye is suspected to be a case of rebound uveitis/iritis (inflammation), the patient should be reviewed the following day to confirm. While many cases only need Plan A to be enacted, he advised the audience to have Plans B, C, and D ready, with a reasonable idea of what the trigger points for each plan were in case they needed to be invoked quickly.

Chan said such an approach eliminates the main surprises that might occur down the track, while the lateral thinking helps to reassure patients. He also suggested that practitioners be alert to the possibility of diffuse lamellar keratitis, which can occur on average about 4 days after LASIK refractive surgery.







Systemic disease

Melbourne-based ophthalmologist Dr Xavier Fagan’s presentation addressed metabolic disease (e.g. diabetes), cardiovascular disease, infections (e.g. herpetic, syphilis, and problems in those immunocompromised), and neoplasia.

Because of the number of diabetics in Australia, Fagan stated bluntly that even with the likely number of ophthalmologists and optometrists involved and available, diabetes is bigger than both professions combined.

Of those diabetics 40 years of age and older, 4.5% have a vision-threatening condition, predominantly peripheral retinopathy, with 10% located in the extreme periphery. Those extreme location cases also have a worsening rate 3x that of other cases.

Retinal signs such as ‘white’ blood vessels indicate a lack of blood flow that can be accompanied by neovascularisation adjacent to the termini of the no-blood/blood zones and an increased risk of proliferative disease. Other than white blood vessels, other appearances include: deep, blotchy haemorrhages; bland fundi despite long-duration diabetes with poor control; and vitreous haemorrhages without any obvious signs of neovascularisation.

Anti-VEGF injections can improve VA by an average of 2.6 letters and reduce vitreous haemorrhages, but usually with worse visual field losses. The downsides of injections are the number of appointments necessary, the cost, and the poorly understood long-term ramifications. As a result, laser therapy is still relevant.

At 5 years after diagnosis, over a third of patients are lost to follow-up, most have no VA difference, the number of injects being given has decreased, and some visual field losses will have occurred (peripheral ischaemia?). Inadequate treatment or worse, no treatment, can lead to iris rubeosis, retinal detachment, and reduced vision. Fagan believes laser is still ‘king’.

Diabetic retinopathy signs can include: intra-retinal hyper-reflective foci (found to be lipids), cystic spaces (macular oedema), and visible lamina of microaneurysms. He also described DRIL (disorganised retinal inner layers), a result of the loss of boundaries between the inner retinal layers, and diabetic optic neuropathy – a non-arteritic, anterior, ischaemic, optic neuropathy (NAAION) characterised by dilated capillaries over the surface of the optic disc. Cystic changes can also occur in areas of vessel abnormality.

Fagan cautioned against trying to gain glycaemic control too rapidly as it can have worse outcomes than a more gradual approach. That outcome is partly due to the ability of the ischaemic retina to convert glucose for its own purpose(s), something that is countered by aggressive treatment. A possible sequel to stopping anti-VEGF therapy is the return of rubeosis.

PAMM (Parecentral Acute Middle Maculopathy) is a vascular disease in which little oxygen remains in peripheral vasculature. It’s an OCT finding of unknown aetiology that laser treatment makes worse.

Fagan’s next offering was ocular ischaemic syndrome, a whole of eye problem in which veins are dilated but not tortuous; the arteries are attenuated; blotchy, mid-peripheral haemorrhages can be seen in about 80% of cases; and the IOP can be normal or even lower. Unfortunately, the 5 yr mortality rate is 40%.

Malignant hypertension is a medical emergency and retinal haemorrhaging can occur even in the absence of vessel tortuosity.

Syphilis was almost eradicated by 2000 but between 2008–2016 it staged a comeback, with the incidence increasing fourfold. It can result in posterior uveitis (55%), panuveitis (25%), or anterior or intermediate uveitis (20%). Syphilis is the great mimic and syphilitic vitritis can masquerade as optic neuritis, vasculitis, or retinitis. Treatment is still penicillin.

In the case of herpetic infections, Fagan recommended transillumination of the iris, measurement of the IOP, and detection of possible uveitis (intermediate or posterior).

Behçet’s disease is a whole of body problem with a probable autoimmune component, whose symptoms vary widely between sufferers. The main ocular ramification is uveitis, but it’s also possible to have an hypopyon in an apparently quiet eye.

Patients exhibiting choroidal metastases present a challenge to ophthalmology and oncologists alike as it’s not always possible to determine the location or type of the primary lesion(s) in a timely manner.

In closing Fagan emphasised the importance of history, a knowledge of current medications, and the usefulness of ocular findings to both identifying the root cause as well as monitoring the effectiveness of treatment. He also suggested that optometrists involve themselves in showing patients the consequences of their actions and informing them of the options regarding modifiable risk factors in systemic disease.

Optic nerve diseases

The outgoing managing director of the Perth-based Lions Eye Institute, Professor David Mackey, opened his lecture with the statement that 30–40% of Australians don’t get regular eye examinations. He then proceeded to explain that while some 2–3% of Australians have glaucoma, about 1 in 20,000 have some other type of optic nerve disease.

Some optic disc features are inheritable, and GWAS (genome-wide association studies) have detected ATOH7 as the major gene determining optic disc size. Genetic explanations are now being sought for optic disc cup area, IOP, optic disc area, primary open-angle glaucoma, and vertical cup-disc ratio.

Around 100 genes have already been identified as contributing to IOP, probably meaning that gene therapy would be difficult, if not impossible.

Recent developments in AI and deep learning have seen machine vision being able to detect glaucomatous disc equal to or better than trained specialists. However, Mackey observed that optic disc observation alone was poor at glaucoma diagnosis. Naturally, a history including a family history is important and colour vision tests can also be useful.

The majority of optic atrophy cases are either Leber’s hereditary optic neuropathy (LHON – a mitochondrial defect with matriarchal inheritance) or autosomal dominant optic atrophy (ADOA). Leber’s is not common in Australia, with just 5 new cases a year reported. Presentation is typically a male in their early 20s reporting sudden blindness at least in one eye initially.

While Leber’s cases aren’t completely blind, legally, they are unable to drive, can’t see face detail, can’t read, and usually can’t follow their carer visually. Another condition, Leber’s congenital amaurosis (LCA) is a childhood, retinitis pigmentosa-like disease.

In LHON cases, the affected person is usually 18–30 years of age when the first eye loses vision rapidly. The second eye follows some time later (weeks to months). VA can be as low as 6/60 but recovery to as good a 6/4.8 has been reported (rarely).

A red-green colour vision defect accompanies the disease. The pupil reflexes are spared until the acute stage is reached and a centro-caecal scotoma can be detected. Mild swelling of the RNFL and peripapillary telangiectasia are likely.

Late stage LHON is accompanied by complete disc or temporal disc pallor, but there is no vessel leakage detectable in FFA. About 90% of cases involve mutations of the ND1, ND4, or ND6 gene and recovery is more likely if the patient is young. Male to female ratios depend on the mutation involved, e.g. 3460: 3:1, 11778: 6:1, and 14484: 8:1.

LHON cases rarely use guide dogs, canes, or Braille. The loss of central vision forces the sufferer to use their peripheral vision but some recovery has been reported in young 14484 mutation cases.

An early pharmacological intervention, idebenone, was described by Mackey as “probably ineffective”, although the literature claims that it did halt further progression and preserved colour vision. Another expensive ($80,000 per annum) drug, Catena (Santhera Pharmaceuticals), is also a possibility with some benefits. Mitochondrial donation is now possible in some countries but Australia is still investigating this issue.

LCA cases face even great costs ($1.18 million per pair of eyes) for some benefits from Luxturna (Spark Therapeutics – voretigene neparvovec-rzyl), the first gene therapy for the LCA – RPE65 genetic mutations. It’s applied surgically as a one-time gene therapy.

While no suitable cases have been identified for treatment in Australia, early studies have “yet to deliver” according to Mackey. He also opined that some treatments might never be commercially viable or successful.

Autosomal dominant optic atrophy (ADOA) results in 6/7.5 VA and is accompanied by pale optic discs. It starts in childhood as a result of mitochondrial dysfunction, and DNA testing shows that about 90% of cases involve the ND1 and ND4 genes. Central scotomata and impaired colour vision become apparent as the disease progresses.

The next Specsavers Clinical Conference will be in September 2019.

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