ODMA’s CPD return to Sydney mostly welcomed

This year’s incarnation of ODMAFair, ODMA17, was held at Sydney’s redeveloped International Convention Centre (ICC) in Darling Harbour from July 7–9. The first day of the event had the regular trade exhibition running in parallel with a Vision Summit, an all-day CPD event that ran from 8am–6pm with a two-hour lunch break.{{image2-a:r-w:400}}Unfortunately for the exhibitors, many delegates to the Summit were at ODMA17 for just that one day which meant that their exposure to the trade’s offerings were limited to the two hour lunch period reduced, in most cases, by the time taken to consume food.Given the number of competing CPD-eligible events, especially offered in the Sydney area, a reasonable question to ask is why a trade association representing the supply side of an industry, assumes the role of being a CPD supplier to its professional ‘customers’, especially given the many other organisations that provide CPD.Regardless of the answer, the quality of what was offered as CPD was beyond reproach and well in keeping with the high standards set by similar CPD days accompanying previous ‘ODMAFairs’, especially the last two events held in Brisbane.Paradoxically, the Brisbane CPD events attracted much greater delegate numbers than the recent Sydney event, for reasons unknown.Dry EyeProfessor Fiona Stapleton, head of UNSW’s School of Optometry and Vision Science, launched her dry eye presentation by stating that the real prevalence of the condition is not really known because figures depend largely on rubbery criteria, such as measuring methods, age, sex, ethnicity, and geography.Crucially, another factor is the definition or definitions, and who’s applying th. Diagnostic criteria now in use are based on the Women’s Health Study (WHS), symptoms, signs, or a combination of those, or signs of MGD.While a diagnosis of DED might be made at a certain point in time, the onset of the condition is gradual. Figures available suggest that between 5–35% of sufferers are over 50 years of age, however, youths are not expt and even the very young can be affected. About two-thirds of all cases are fale and the risk increases further after menopause. Ironically, the use of HRT increases that risk further.Giving figures somewhat lower than US-based ophthalmologist Dr Rolando Toyos, who spoke earlier in the day, Stapleton estimated that 65% of DED cases also had MGD, although about two-thirds of MGD cases rain symptom-free.CL wearers are in further difficulty because CL wear decreases both the number of functioning meibomian glands and the function of those glands raining. Following an assessment of blocked gland orifices and the difficulty of expressing meibum, it has been estimated that experienced CL wearers have the glands of non-wearers who are five years older.Apart from the obvious discomfort and pain of DED, DED cases are 2–3x more likely to have poorer vision, especially at near, and are more likely to suffer from depression. Those effects have cost and productivity downsides. DED cases account for 20% of eye hospital outpatient clinic appointments, 11–26% of optometric consultations, and an estimated individual overall treatment cost of around $1,000 per year. To underline the seriousness of the issue, it has been estimated that DED accounts for up to 50% of genuine absenteeism.Most sufferers report that their perception is that the symptoms change very little with advancing age. However, statistically, MGD or blepharitis result in worsening symptoms with age. Studies of mono and dizygotic twins have shown that DED is around 71% environmental, while blepharitis signs are about 78% genetic.Meanwhile, Sjögren’s syndrome patients have been found to have increased hypomethylation of the IL-12A gene, among others. Perhaps fortunately for ophthalmic practice, MGD’s signs occur before symptoms are reported, giving a suitably-equipped, vigilant practitioner time to initiate treatment before their onset.MGD is believed to have a 30–45% genetic component to its causation. The significant and frustrating disconnect between signs and symptoms, eg, few signs accompanied by big symptoms and vice versa, is still a stumbling block to routine, timely, and preventative care of DED, MGD, and blepharitis patients.


Fiona Stapleton Gerald Liew Minas Coroneo Peter McCluskey Rolando Toyos Stephanie Watson

Diabetic macula oeda and neovascular AMDMedical retina ophthalmologist Associate Professor Gerald Liew provided some astounding figures on the prevalence of diabetes (mostly Type 2), starting with 415 million worldwide in 2015, 145 million of whom have diabetic macula oeda (DMO), and 45 million of whom have decreased vision.Local figures indicate there are more than one million diagnosed and undiagnosed Australian diabetics, some 100,000 of whom have DMO. The risk of DMO is lower for people who have had diabetes for less than 10 years, whereas the risk is high for those who have lived with the disease for more than 20 years. Cholesterol is regarded as a diabetic risk factor.While DMO treatment in the 1970s was laser-based, by the 2000s it had shifted to intravitreal steroids, such as triamcinolone, introduced by Sydney research ophthalmologist Professor Mark Gillies. Currently, treatment has settled on anti-VEGF therapy. The International Council of Ophthalmology’s guidelines for DMO suggest that laser treatment be limited to no-central, mild cases only, and up to 13 letters can be gained through that approach.Additionally, an anti-VEGF drug such as aflibercept can gain 18 letters or more in at least 50% of DMO cases in which the VA is poor to start with. In clinical trials, there were no significant differences between the three mainstream anti-VEGF compounds in common use and the results were sustained over a 2-year period of use. The regimen used was 9–10 injections in the first year and 5–6 injections in the second (a loading dose of three monthly injections is the norm).Although progress is slow in the traditional 1–2-year treatment plan for DMO, as Liew put it, each injection chips away at the oeda. It is not known if injections are required for the rest of the patient’s life, but some studies suggest four years of treatment, using a nine, four, two, one or similar regimen of annual injections, might be the maximum required. Intravenous triamcinolone is the second-best solution to DMO but its use is accompanied by a greater risk of cataract, glaucoma, and infection.According to Liew, there is no need to achieve good glycaic control before commencing anti-VEGF therapy. However, despite the relative success of anti-VEGF treatment, in some cases the DMO can bounce back on a 4–6 week cycle. The use of anti-VEGF is also contraindicated in pregnancy.Switching to neovascular AMD, Liew asserted that it was beneficial to detect AMD early and to instigate long-term anti-VEGF therapy as soon as possible if maximum vision preservation was to be realised. He revealed that currently, 300,000 injections are given annually in Australia, a figure that started at just less than 110,000 in 2010 and which is expected to rise to more than one million by 2020. Many recipients are 80 or older.He summarised the process of ‘wet’ AMD as being one of drusen weakening Bruch’s mbrane, new, abnormal vessels growing through the breach in Bruch’s, and subsequently, those vessels leaking.Classification of CNV was given as:

  • Type 1: sub-RPE spaces shows in angiogram, neovascular mbranes seen sub-RPE – the occult stage
  • Type 2: CNV mbranes located above the RPE having penetrated the retina – the classic stage
  • Type 3: Intra-retinal RAP lesions (retinal angiomatous proliferation) located at the level of the foveal avascular zone (FAZ)
  • Type 4: Polypoidal lesions above and below the RPE – especially in Asian ethnicities (30–40%), 8–12% in Caucasians

Left untreated, neovascular AMD results in disciform scars and polypoidal choroidal vasculopathy (PCV) that is often accompanied by a pigment epithelium detachment (PED). The polyps tend to cluster if left untreated resulting in irreversible vision loss, generally measured at one-line loss at three months, two lines by six months, three lines by 12 months, and four lines by 24 months.Liew described the introduction of anti-VEGF as a true revolution in ophthalmological care, offering between seven letters and 1–2 line gains by two years. Furthermore, severe vision loss (>15 letters) is prevented in more than 90% of cases.After the three monthly-loading doses some practitioners follow a treat and extend protocol, in which 1–2 weeks are added to each injection cycle, with careful VA and OCT monitoring to detect any untoward shortcoming in the regimen. However, intervals longer than 3–4 months are uncommon.Anti-VEGF usage is expected to be life-long once commenced. Australia’s AMD outcomes are better than most world figures, due in part to our relatively generous PBS sche, early adoption of the therapy, and diligence on the part of ophthalmology. For example, Australians undergoing anti-VEGF treatment average a 5.4 letter gain at 12 months, versus the 3.6 letters gained in a comparable US study.Currently, data out to six years is now available that shows good retention of vision, but many expect that it will be difficult to sustain the gains in the longer term. Working against success are geographic atrophy (GA, 39%), retinal fibrosis (33%), structural damage (12%) and infective ophthalmitis (6%).It is known that the GA risk is heightened by continuous monthly anti-VEGF injections, but an as yet unanswered question is: Does anti-VEGF therapy induce GA? Analyses of the long-term safety effects are probably cumulative as follows:Interestingly, although questions have been asked in relation to the systic effects of anti-VEGF on microcirculation and cerebral and cardiac function, no increased risk of cardiovascular disease or stroke has been donstrated.

  • 0.04% risk per injection of endophthalmitis infection
  • 0.01% risk per injection of endophthalmitis non-infective
  • 0.33% from other intraocular surgery
  • 0.02% risk per injection of a retinal detachment
  • 0.04% risk per injection of a RPE tear

St cellsThe Save Sight Institute’s Professor Stephanie Watson spoke about st cells (SCs), one of her main research interests. Generally, SCs renew thselves as well as become the source of other cell types by a process of differentiation. Limbal SCs (LSCs) have a turnover rate of about seven days. A LSC deficiency can follow significant mucous mbrane damage, severe Pseudomonas aeruginosa infections, CL-induced anterior eye probls, burns, etc.If the damage is serious enough and a SC deficiency induced, the damaged corneal surface can become conjunctivalised, with obvious vision ramifications. LSCs reside in the Palisades of Vogt, an ocular anatomical feature that has a wide variety of appearances in normals, where they are less exposed to UV and possible physical injury.Recent research at Moorfields Eye Hospital in London suggests that melanocytes wrap around SCs, affording th a measure of radiation protection. Corneal SCs divide into daughter cells that are shed on a 7–10-day cycle. Recent research by Professor Nick Di Girolamo at UNSW suggests that SC colonies can actually provide different types of SCs.The earlier use of the expedient ‘impression cytology’ technique of sampling eye cells for research and biopsy purposes has been abandoned, because recent findings show that the technique can lead to permanent surface defects at the sampling locations. An ongoing probl in the laboratory has been the difficulty of identifying SCs with certainty.In LSC deficiencies, the medical managent of the condition includes optimising the ocular surface, ocular lubricants, and the use of retinoic acid and autologous blood serum. If a LSC transplant becomes necessary, SiHy CLs seeded with SCs have met with up to a 70% success rate. Experimentally, SCs have been used in paediatric cataract cases to regrow crystalline lenses, donstrating up to 20 D of accommodation. Corneal, limbal, and conjunctival cells can be derived from LSCs.Future research is directed towards finding and isolating SCs with greater certainty, gaining a better understanding of their behaviour, and the development of an economic and effective method of SC production.

Main applications for corneal crosslinkingWatson gave pellucid marginal degeneration, keratoconus (KC), and post-LASIK kerectasia as the main applications for corneal crosslinking (CXL), as they benefited most from the resulting increase in corneal strength. CXL adds to the natural bridging of the stromal lamellar layers or, in KC, replaces some of the lost bridging inherent in the disease.{{image9-a:r-w:400}}Most CXL follows the so-called Dresden Protocol or a variant of it. That protocol uses 0.01% riboflavin in a 20% dextran vehicle and UV exposure. Indications for CXL include changes in at least two of the following: steepening of the anterior corneal surface, steepening of the posterior corneal surface, or a significant change in VA. As KC stabilises by around 30 years of age, CXL usage is more likely in younger patients.If a young patient is progressing but their spectacle VA rains good, CXL can be considered as a means of stabilising and maintaining that situation. Importantly, they must be advised to keep their hands off their eyes (no eye rubbing) and any atopic factors likely to induce eye rubbing need to be reduced as much as practicable.Research on the protocols used, including the pursuit of epithelium-on application, is ongoing. To that end, the Save Sight Institute’s KC and CXL registry (Fight Corneal Blindness) has amassed 1,719 eyes from 888 patients over 7,339 patient visits in Australia and New Zealand since it commenced in October 2015.Data suggests that CXL improves VA, donstrates some corneal thinning at 12 months, and shows few differences between 10 minute (more intense) and 30 minute (less intense) procedures. The registry provides graphical output when enough data is available and also tracks adverse events and outcomes as part of its ‘learning’ rit. These events include: corneal haze, scarring, microbial keratitis (MK), and corneal infiltrates.However, outcomes can still be variable and as with experiences outside ANZ, Kmax can either decrease or increase. Additionally, some vision loss can occur (about 3% of cases can lose two or more letters of acuity), and some cases continue to progress especially if their original Kmax was very steep. Haze can involve up to 60% of the corneal depth and can be permanent in some cases.Although MK can be a complication of CXL, CXL can also be used to treat MK because of its ability to inactivate bacteria. There is now some evidence supporting the belief that CXL can make the cornea more resistant to MK, just not in all cases.However, the use of CXL in herpetic corneal disease is not possible due to the possibility of inducing a corneal melt. The use of CXL has seen reductions of up to 50% in the number of penetrating keratoplasties and there is more to go as the procedure is still evolving and further improvents are expected.

More reading: Special Report Part 1: ODMA CPD returns to Sydney

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