The main programme on the second day of SCC6 featured a variety of presentations from respected researchers, which focused mainly on the major causes of blindness in Australia – glaucoma, age-related macular degeneration, and diabetic retinopathy. Both domestic experts and international guests related findings from their research, and delivered advice on the latest techniques for best-practice treatment of the diseases.Collaborative glaucoma careSydney ophthalmologist, Dr Mitchell Lawlor, gave the opening lecture on Sunday. He provided an update on the collaboration between ophthalmology and optometry, with specific reference to comprehensive glaucoma care. Some 500 plus delegates were in attendance for the all-day programme, 150 of which were independent, i.e. not aligned with the Specsavers group.{{quote-A:R-W:450-I:18-Q: Diabetes is a coming health tsunami fuelled by an ageing population and the obesity epidic. -WHO:Dr Peter van Wijngaarden, Ophthalmologist and medical researcher from Melbourne}}Arguably, Lawlor’s presentation was the pick of the day as he achieved a balance between the breadth and depth of the information delivered, all done with competence and confidence in a flowing, logical presentation. His opening line was that glaucoma is approximately 50% underdiagnosed in Australia, which translates to about 150,000 people.The basis of his presentation was Oculo, the referral and information-sharing portal used by 115 Specsaver stores currently (the Oculo website claims 1,400 optometrists and 400 ophthalmologists overall), the OCT in-store pilot project run by Specsavers head office using the Topcon Maestro, and the 2016 RANZCO MoU with Specsavers.As of July 2017, 224 extra glaucoma referrals resulted from the OCT pilot study revealing suspicious signs of glaucoma. To streamline interactions further, Oculo integrates seamlessly with Specsaver’s own in-house practice managent software, Socrates. He described the collaboration model as outcome-led eyecare. The co-operation of Alcon, BOC, Hilco, and Zeiss was also acknowledged.{{image2-a:r-w:200}}According to Lawlor, about 3% of the general population have glaucoma and the prevalence is increasing. In the 20 years between 1996 and 2016, the prevalence in the over-65 age group rose from 12% to 15.3%, and in the over-85 age group the prevalence doubled. He also repeated the message that glaucoma and raised IOP were not synonymous.Lawlor’s simplified description was cupping of the optic nerve head accompanied by matching visual field defects. The latter was typified by a superior nasal step in the visual field. He also recommended the use of gonioscopy to investigate the possibility of angle-closure glaucoma.{{image3-a:r-w:200}}One of the main reasons for steering practitioners away from the 1970s concept of IOP’s central role in glaucoma is the significance of normal-tension glaucoma (NTG) which, according to North American and European figures, accounts for up to 40–50% of glaucoma cases at the time of their diagnosis. In Asia, the NTG rate can be as high as 80–90%.Although primary open-angle glaucoma (POAG) cases outnumber primary angle-closure glaucoma (PACG) by about 3:1, their respective vision losses are about the same. Because some countries and ethnic groups have large PACG probls, it is necessary to assess possible cases comprehensively to rule out the possibility.{{image4-a:r-w:200}}Without a family history of glaucoma, the incidence is 3%, but once a first-degree relative is diagnosed, that figure jumps to 6%. However, in cases of PACG, close family have a 50% chance of having the same probl eventually.Lawler gave a mean central corneal thickness of 540 microns (range 510–580) as being ‘normal’ and for which no IOP/tonometer correction factor was valid. The glaucoma risk is known to be raised outside that thickness range (i.e. thinner and thicker).{{image5-a:r-w:200}}In cases of pseudoexfoliative glaucoma (PxF) and pigment dispersion syndrome (PDS), Lawlor noted that while it was possible to have a normal looking optic disc in PDS, if PDS-glaucoma is diagnosed, the disc appearance is usually abnormal. Rapid changes in IOP are possible in PxF leading to a recommendation of 6-monthly examinations.Describing gonioscopy as a learned skill, Lawlor recommended inexperienced gonioscopists start with myopes (deeper ACs), and determining trabecular meshwork and scleral spur visibility as starting points. He gave the van Herrick anterior angle assessment trigger point as <15% of central corneal thickness, estimating its sensitivity as being 85% in PACG.{{image6-a:r-w:200}}CP8: Assess the peripheral retinal fully in all diabetics, as up to 10% of cases have significant (or even severe) peripheral retinal issues that are easily missed and not always easy to see even if pursued carefully.CP9: Consider the use of special optics and OCT technology in hard-to-examine patients. Some patients with small pupils, poor co-operation, media opacities, vitreous haorrhages, asteroid hyalitis (more common in diabetic patients), etc. present a challenge to the examiner. Usually, an Optos UWF instrument and an OCT can get around asteroid hyalitis.AMD Diagnosis{{image7-a:r-w:200}}Confounding the GA/CNV divide is the possibility that either can convert to the other form. Furthermore, according to Guymer, early and intermediate AMD are not ‘dry’. In Guymer’s experience, the natural progression is for drusen to tend towards GA ultimately, but in some patients along the way they mount a response that causes neovascular complications, including scar formation.The drusen sizes were selected pragmatically to represent retinal vein calibre after four bifurcations (63 microns) and vein calibre at the optic disc (125 microns), so that approximations were easy to make in vivo.{{image8-a:r-w:200}}A better way to determine the presence of GA is multimodal imaging, such as fundus auto fluorescence (FAF) and fundus fluorescein angiography (FFA), because a normal photo will often not disclose the existence or extent of the probl. Abnormalities of the RPE can result in hyper autofluorescence, a harbinger of GA.GA is often the result of drusen regression – atrophic patches of retina indicate where drusen once were and that have disappeared over time. Nascent GA (nGA) is a result of the subsidence of the retina’s OPL and INL layers due to a loss of photoreceptors that ultimately lead to hyper-reflective and wedge-shaped bands becoming visible. About 30% of intermediate AMD cases have OCT signs of GA.{{image9-a:r-w:200}}If OCT is used as the basis of defining atrophic changes, it is usually based on layers missing from the normal OCT images. In an early 2017 CAM meeting, atrophy endpoints were defined further in terms of missing OCT layers as complete RPE and outer retinal atrophy, including photoreceptor loss (C RORA) or i RORA (incomplete RORA). It is probable that i RORA and nGA are similar stages.Multimodal imaging has revealed new risk factors, especially hyper-reflective foci in OCT in intermediate AMD.{{image10-a:r-w:200}}When attention is drawn away from the macular area, another retinal background feature, so-called reticular pseudodrusen (RPD), can often be seen. The presence of RPD is a risk factor for the development of advanced AMD and GA, and usually starts in the superior retina, then makes its way down.OCT shows th to be stack-like lesions (probably debris) anterior to the RPE, whereas real drusen are under the RPE (posterior).AMD Treatment advances{{image11-a:r-w:200}}Early work attpting to slow AMD’s progression by roving drusen, showed that atrophic patches take their place. Later work (1990s using laser on DR) showed that thermal laser radiation applied to drusen appeared to make drusen disappear without any increase in complications.Those observations encouraged Professor John Marshall (UK) to postulate laser stimulation of RPE cells to produce significant amounts of MMP as a treatment for AMD.That is now being done with a non-thermal laser, the Ellex (Adelaide, South Australia) 2RT Laser, that delivers three nano second, low-dose laser light to the retina with the aim of encouraging RPE reproduction (RPE cells need MMP to divide and slide into position subsequently) and other benefits.{{image12-a:r-w:200}}The energy levels are 500–1,000x less than that required to produce a wound or initiate a wound healing response. Up to 12 spots near the macula are irradiated with the laser and in a pilot study of intermediate AMD cases, about 40% of cases had a reduction in drusen while others showed no change. Improvents occurred over a 3–12-month period.Functional improvents were reported without pain or clinical lesions. Interestingly, there were some improvents in the contralateral eye as well, suggesting an ocular syst or a general systic response. Animal studies by Guymer’s colleague, Professor Erica Fletcher (UniMelb), have also shown encouraging results.{{image13-a:r-w:200}}A newer study, LEAD (laser intervention in early age-related macular degeneration) with a full 36-month follow-up period has commenced. Initial results are expected in April 2018 from more than 150 cases. It is seeking no CNV and no GA outcomes as confirmed by FAF.In a recent article on laser therapy, it was stated that laser irradiation impacted RPE metabolic activity and gene expression producing the proteins, enzymes, and cytokines involved in angiogenesis and vessel leakage regulation. The overall concept is to avoid tissue damage while pursuing the beneficial responses.
| Dr: Diagnosis{{image14-a:r-w:200}}Melbourne ophthalmologist and medical researcher, Dr Peter van Wijngaarden, also tackled DR in his presentation. One of his opening statents was that diabetes is a coming health tsunami fuelled by an ageing population and the obesity epidic.About 9% of all people have diabetes currently, which translates to around 415 million people worldwide. In an Australian context, around 12% of the Australian health budget is spent directly and indirectly on DR alone.{{image15-a:r-w:200}}According to van Wijngaarden, almost half (46.5%) of cases rain undiagnosed, while 50% of the world’s diabetics are located in Australia’s backyard – the Asia-Pacific region.Around 1.2 million Australians are diabetic, and according to figures from the National Eye Health Survey, 13.9% of people over 50 years of age have diabetes, 28.5% of which have DR, and 4.5% have threatened sight. Figures for Indigenous people are worse – 37.1%, 39.4%, and 9.5% respectively.{{image16-a:r-w:200}}Overall, diabetics have a 20x greater lifetime risk of blindness. Van Wijngaarden estimated that 72,000 Australians suffer from DMO and 60% of those have some form of vision impairment (VI). He offered a possible answer to his own question of “why are Australians still losing vision?” – DR is asymptomatic until the disease is advanced and the generally low level of awareness of DR among the population. Both work against good outcomes.NHMRC Guidelines suggest that every Australian have their eyes examined every two years (despite changes to Medicare that only reimburse optometric examinations ever three years for many patients) and for Indigenous people that recommendation is shortened to one year. Currently, only about 50–77% of non-Indigenous, and 20–52% of Indigenous people, are screened adequately.{{image17-a:r-w:200}}Diabetes is significant in that it affects most body systs to such an extent that eyes are not top of the list of significant impacts. Even intensive education of sufferers about their own disease failed to be effective at one year in a rigorous study, as measured by a failure to achieve long-term HbA1c control. Even small reductions in blood sugar levels are known to decrease DR and slow vision loss. Tight control of blood sugar levels leads to a 37–76% reduction in DR risk. |
Sixth Specsavers Clinical Conference Gallery
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