Ophthalmology

A 22-year-old man presented to our accident and emergency department an hour after a motor vehicle accident. He had no history of seizures. On examination, he was alert, haemodynamically stable and his Glasgow Coma Score was 15/15. Both pupils were normal in size and reacted to light. His left eye was slightly protruded, and a rigid radio antenna about 12 cm long emerged from below the left lateral canthus (Figure 1). His visual acuity was normal, and he had no diplopia. Skull x-rays showed the antenna in the left anterior fossa (Figure 2). A computed tomography scan showed it traversing behind the left globe (Figure 3) as far as the left anterior cranial fossa, with the tip embedded in the region of the left sylvian fissure. There was minimal subarachnoid haemorrhage over the surface of the temporal lobe. The patient underwent emergency left frontotemporal craniotomy. At surgery, the antenna was seen to penetrate just lateral to the superior orbital fissure and reach the dura and the temporal lobe (the left sylvian fissure). The antenna was removed, and the patient was discharged from hospital several days later without any visual or neurological complications. Penetrating intracranial foreign bodies at low velocity characteristically enter via the orbital roof, the temporal squama or the cribriform plate. In this case, the antenna penetrated the orbital roof — one of the thinnest areas of cranial bone — without injury to the globe of the eye, or any neurological complications. We recommend that in cases such as this, with minimal external findings and normal neurological examination, simple external traction should be avoided.

Hossein Sanaei-Zadeh MD · Kamran Aghakhani MD · Mansour Parvaresh MD

Despite well publicised claims of the therapeutic value of dietary supplements and other new treatments, the evidence for their effectiveness is modest The distinction between conventional and alternative medicine is often based on the presence or absence of scientific evidence. However, this evidence is expensive to gather, and often difficult to interpret and reduce to practical advice. Age-related macular degeneration (ARMD), the dominant and rapidly increasing cause of permanent visual loss in Australia, is an important case in point. Its prevalence rises from 0.7% in the 65–74-years age group to 5.4% at 75–84 years and 18.5% in people over 85.1 Definitive treatment does not yet exist. While we have some knowledge of risk factors, this knowledge is imperfect and has recently been muddied by well publicised claims (discussed below) that, although evidence-based, are preliminary and need to be interpreted with caution. The early signs of ARMD include hypo- or hyperpigmentation of the retina and large yellow drusen (> 63 μm) or soft drusen with indistinct margins.2 A few small hard drusen can be found in almost everyone over 50 years of age, and, in contrast to large or soft drusen, do not appear to progress with age.1 Loss of vision from ARMD occurs either as a result of choroidal neovascularisation with exudation and haemorrhage (the “wet” form) or by slow atrophy of the retinal-pigment epithelium and overlying receptors (the “dry” form). Wet ARMD is twice as common as the dry type and causes rapid vision loss. About 10% of patients with wet ARMD who present early with distorted vision and an eccentric neovascular lesion can be treated successfully with laser photocoagulation.3 However, the recurrence rate is over 60%, and further vision is then usually lost. Another small proportion of patients can be treated with photodynamic therapy (involving low-intensity red laser treatment after intravenous verteporfin infusion), but the functional benefit is usually modest.4 There is no treatment yet for the dry form of ARMD. Elderly people fear blindness and the loss of independence greatly, and the prevalence of ARMD is rising dramatically. It is no surprise that recent studies of possible risk factors have attracted a lot of public interest. People with an ARMD-affected first-degree relative have a 50% lifetime risk of experiencing advanced ARMD and vision loss, and tend to develop it earlier.5 Smoking is associated with a fourfold increase in the risk of ARMD and visual loss and, again, tends to promote earlier occurrence.6 Weaker associations have been found with obesity, hypertension, macro-vascular disease, raised cholesterol and fibrinogen levels, cumulative light exposure and cataract surgery. Dietary associations have also been found both with the signs of ARMD and with progression to vision loss.7-9 In a well conducted, prospective study, dietary fat intake was systematically analysed after correcting for other risk factors.9 Vegetable fat intake had the strongest relationship with ARMD progression, with a relative risk of 3.82 for the highest fat-intake quartile compared with the lowest quartile. Higher intakes of total fat and of saturated, monounsaturated, polyunsaturated and transunsaturated fats all raised the relative risk of ARMD progression about twofold. Weekly fish intake and eating nuts two to three times a week were mildly protective. The implication is that a large shift away from vegetable oils, margarine and fat-containing processed foods might reduce this epidemic of blindness in the elderly. Some of these measures conflict with conventional advice on controlling cardiovascular conditions and need further research.10 Definitive evidence for the effectiveness of certain interventions might be obtained by randomly assigning those in the top quartile of risk to receive either a diet with low vegetable fat, fish, nuts and fruit, or a normal diet. There is also evidence from a randomised controlled trial that high-dose dietary supplements of the antioxidants vitamin C, vitamin E, beta-carotene and zinc can reduce the risk of progression from large or soft drusen to advanced ARMD and visual loss by about 20% compared with controls over 6 years.11 However, high-dose zinc can cause gastric irritation or anaemia, and beta-carotene may possibly be associated with an increased risk of lung cancer among smokers. Uncontrolled studies suggest the antioxidants selenium, lutein and zeaxanthin, which localise in the normal macula, may also help. There are as yet no studies to show whether dietary supplements are protective in patients with only small drusen or in the 20% of patients who are at genetic risk. It is not yet known whether major dietary adjustment and/or introduction of dietary supplements for large numbers of elderly people will be justified in terms of preventing blindness. On present evidence, we should identify people at increased risk of ARMD (ie, those with a family history, large or soft drusen, or vision loss in one eye from ARMD), encourage them to stop smoking, and promote a diet that includes vegetables, fish and nuts and reduces fatty foods laced with vegetable oils. Antioxidant supplements should be recommended if a fresh diet is impractical and if retinal signs of progression are present. For people of advanced age with a lower risk of ARMD, we might compliment them on reaching seniority and note that, in the dietary supplement study mentioned above,11 only 1.3% of patients with small drusen experienced ARMD progression over a 6-year period. Retinal images showing age-related macular degeneration (ARMD) A. “Dry” ARMD. Large soft macular drusen, signifying a high risk of progressive visual loss. B. “Wet” ARMD. Arrowed area delineates advanced wet macular degeneration with subretinal exudation and neovascular scar tissue. These changes result in blindness.

Ian J Constable FRANZCO, FRACS, FRCS

Tarney J Spencer,* Ben Clark† * Ophthalmology Registrar, † Ophthalmologist, Geelong Hospital, Ryrie St, Geelong, VIC 3228. drtarnAThotmail.com To the Editor: We are concerned about the recent number of patients presenting to our hospital after accidentally applying superglue to their eyes. Of the four cases in February and March 2004, two arose from patients mistaking cosmetic nail adhesive for their regular ocular lubricant, and applying it to the inferior ocular fornices, creating a tarsorrhaphy. Superglues are cyanoacrylate derivatives. Those used domestically are lower-alkyl derivatives than those designed for medical use and have higher tissue toxicity. The two patients who mistook nail glue for ocular lubricant both required surgical separation of the upper and lower eyelids, and both had significant corneal abrasions, periocular dermatitis and temporary loss of lashes as a result of the reparative surgery. Both were treated with chloromycetin ointment until the abrasions had healed. We examined the bottles containing the nail adhesives. They were remarkably similar to many ocular lubricant bottles, with no significant difference in size, colour or feel (Box). As both products are often kept together in a cosmetics area of the bathroom, accidental ocular application can occur. Similar cases have been reported in other countries over the past 20 years.1-3 The risk of accidental ocular (or potentially aural) application could be reduced by changes to bottles containing superglue, including: childproof cap to prevent conventional opening of the bottle; colour coding of the bottles; different bottle shape; and distinctive odour and/or colouring of the glue. Superglue and eye lubricant bottles Examples of bottles of synthetic nail adhesive (two on left) and eye lubricant (two on right), showing similar appearance and feel.

Tarney J Spencer · Ben Clark

Bruce Hadden President, Royal Australian and New Zealand College of Ophthalmologists, Eye Institute, 125 Remuera Road, Auckland, 1005, New Zealand. bruceATeyeinstitute.co.nz To the Editor: The article by Brooks contains valuable forward-thinking for future healthcare management of the increasing burden of chronic illness.1 However, Brooks’s suggestion that non-medical practitioners might perform cataract extraction shows his lack of knowledge of the complexity and potential complications of modern cataract surgery. Modern cataract surgery is the most commonly performed major operation, and one of the most rewarding in lifestyle improvement. It is done under local anaesthetic with almost no discomfort, and recovery is rapid. Thus, the patient sees it as being simple. However, it is far from simple for the surgeon. The small-incision, phacoemulsification technique has made the operation more demanding than ever before. The learning curve is both long and steep. Posterior capsule rupture during phacoemulsification is an ever-present threat, and if it occurs, the sight-threatening complications of cystoid macular oedema, retinal detachment and endophthalmitis all become more likely. The modern, highly technical procedure that Australians demand and deserve is comparable with coronary artery bypass and joint replacement surgery in terms of the skill required. There are three reasons that non-ophthalmologists think cataract surgery is simple. First, it is simple from the patients’ perspective. Secondly, cataract extraction can be done relatively cheaply in developing countries. However, the operation done in those countries is a different procedure, and comparisons are not valid. Thirdly, some unscrupulous ophthalmologists themselves have trivialised the procedure as a means of self-promotion. Brooks and others would pay the operation much more respect if they took the trouble to view a few procedures in real life.

Bruce Hadden

In 1978, when I was a Fellow in Ophthalmology at the Johns Hopkins Hospital in Baltimore, I went to a seminar given by one of the senior faculty (Maurice Langham) about work he was doing on an unusual disease called onchocerciasis. Although I must have learnt about onchocerciasis at medical school and during my ophthalmology training, it was such an esoteric tropical disease in small print that it had made no perceptible impact on me. Actually, onchocerciasis is a fascinating disease. It is also called river blindness, as those who are affected live along rivers and streams. It affects about 20 million people; 99% of these live in Africa, with a few in Latin America (see Box 1).1 In endemic areas, half will become blind before they die and, at any one time, some half a million people with onchocerciasis are blind. Onchocerciasis has had a devastating impact in Africa. All but the poorest of the poor have abandoned the endemic areas. In the worst affected villages, everyone is infected by the age of 14 or 15 years.1 People go blind in their 20s and 30s, just when these subsistence-farming families are raising children. Once blind, parents often need to be led to their fields by their young children. This has a devastating effect on all aspects of the villagers’ lives. There have been various attempts to treat and control onchocerciasis. During the Second World War, tens of thousands of Australian and American soldiers fighting in the Pacific islands were afflicted with lymphatic filariasis. Wartime drug development led to the discovery of diethylcarbamazine (DEC) that would halt the progression of, and sometimes cure, filariasis. After the war, DEC was tried on some people with onchocerciasis and was found to have a temporary holding effect.1,2 DEC was better than nothing, but its use was limited, as many infected people had a severe reaction to the treatment caused by the sudden death of billions of microfilariae, the so-called Mazzotti reaction.3 Sleeping sickness or trypanosomiasis is almost invariably fatal. During the First World War a drug called suramin was developed in Germany that could save some people with sleeping sickness, although it was very toxic. It was tested and found to be effective against onchocerciasis, but 2%–3% of those treated died and so it was not widely used.4 The World Health Organization had started a major program to control onchocerciasis by spraying breeding sites to control the black fly vectors. This program started in 1974 in 11 countries in West Africa. Breeding sites in rivers and streams were “bombed” each week with the aerial application of larvicide. This was an effective, if slow and expensive, method of controlling the disease in open savanna but, because of problems with aerial access, it could not be used in rainforest areas. This was the state of play as I listened to Langham in Baltimore describe the human studies to treat onchocerciasis he had recently done in Africa. After the lecture, I suggested some clinical trials he could do. It seemed so simple to me then: get a small team of two or three people and a bit of equipment to examine people and do a prospective randomised trial. I had had great lab training at the Royal Melbourne Hospital under Peter Morris (later Professor Sir Peter Morris), and I had had an extraordinary experience of working in the field with Professor Fred Hollows when I travelled throughout outback Australia on the National Trachoma and Eye Health Programme. I little suspected how much I still had to learn, but Langham proposed that I should do the study and offered to help me put it together. Within a few months I was starting a study in Liberia and another in Guatemala. I teamed up with a young infectious diseases doctor, Bruce Greene, who was at Hopkins and later went to Case Western University in Cleveland. This was the start of a very successful collaboration. As there were only a few ophthalmologists working on onchocerciasis, I was soon appointed to a WHO Scientific Working Group on Filariasis that included onchocerciasis. In the 1970s, WHO had started a drug-screening program under their Special Programs for Training and Research in Tropical Diseases. Pharmaceutical companies could send interesting compounds to be tested in WHO-supported laboratories in selected universities to see if their new drug had an effect against some of the targeted tropical diseases. In 1983, I was asked to chair a new WHO Scientific Working Group on Onchocerciasis Chemotherapy. Since the Second World War, major drug companies have scoured the world looking for new antibiotics, many of which came from fungi. In 1978, a Japanese scientist collected a fungus species that was to revolutionise the treatment of onchocerciasis from beside a golf course in Kawano, Japan — I have been told it was from beside the fifth fairway. This fungus made a compound that was called in the lab MK 933. Later, it was called ivermectin. It was not good as an antibiotic, but it was a very potent killer of parasites. It went to a WHO test laboratory where it created some interest, but then it disappeared. It was the pharmaceutical firm Merck and Co. that developed ivermectin and started to market it for veterinary use. It is now a worldwide product used to treat heartworm in dogs, and a whole range of parasites in sheep, cattle, horses, pigs and other animals.5 Dr Mohammed Aziz worked for Merck. He was originally from Bangladesh, and had worked in Africa with WHO where he learned about onchocerciasis. He insisted that MK 933 be tried in onchocerciasis. Once the veterinary product was successfully launched, he got his way, and he did a small pilot study in Senegal.6 The results were published in the Lancet and picked up by the New York Times, Le Monde and other newspapers. This was the first time that I, and others in the field, had heard of this drug. The study was somewhat unusual. The results seemed to be too good to be true. How could any drug kill the microfilaria without producing the intense Mazzotti reaction we saw with every other drug that killed microfilaria? This did not fit with any conceivable clinical, laboratory or theoretical explanation at the time. Besides, the study patients were only lightly infected, the investigators had not worked on “oncho” before, the study was funded by a drug company, and it was published simultaneously in the newspapers and the scientific literature. Maybe it was just wishful thinking, or artefact. Soon a series of parallel, randomised clinical trials were planned to more fully evaluate this very exciting new drug. These studies started after some further patients were treated in an open dose-ranging study. Bruce Greene and I undertook a study in Liberia. We treated men who had become heavily infected with onchocerciasis while working as rubber tappers on a plantation. In this controlled trial, 10 men received ivermectin, 10 received DEC, and 10 took placebos. We were very anxious for the first few days, as we expected to see similar reactions to those seen in patients treated with DEC. Some animal studies suggested even worse reactions were possible with ivermectin. Maybe some people would even die. We were elated six months later when our results showed that ivermectin was at least as effective as DEC, but safer.7 The two other parallel studies came up with similar results.8,9 Subsequently, one partial answer emerged for the lack of a Mazzotti reaction. It seems that, rather than killing the microfilariae in the tissues, the microfilariae are paralysed and then pass through the lymphatic system and die in the lymph nodes. We went back to Liberia and this time treated 300 people, men and women, to test different doses. We followed this group for 2 years. A tiny tablet of ivermectin cleared the microfilariae almost completely and people’s skin and eye signs improved dramatically.10,11 The adult worms were not affected, so ivermectin needed to be given once every year. By August 1987, Merck had enough data to register ivermectin for use in onchocerciasis. The chairman of Merck, Dr Roy Vagalos, announced that his company would provide the drug at no cost to treat anyone with onchocerciasis, anywhere in the world, for as long as it was needed.12 This was an unprecedented and extraordinarily generous and courageous decision. Although Merck was selling huge amounts of ivermectin to treat animals, there were some 20 million people with onchocerciasis, and maybe 40 million who would need treatment. Treatment had to be continued for at least 10 years. This was a huge commitment when each pill was worth US$3. However, Vagalos knew that if Merck did not do something, this breakthrough treatment could never be afforded by those who lived beyond the end of the road, the poorest of the poor. Ivermectin was now freely available. But how could it be distributed to the millions who needed it? There were other questions to be answered: for example, would ivermectin have rare but serious side effects? And what would happen if pregnant women inadvertently took a tablet? We then started another study of 30 000 people in Liberia to assess the community acceptance and safety, and to work out distribution strategies. We monitored every person, every month, investigating and documenting all births and deaths. We kept track of people as they moved, we caught and examined the biting black flies, and we thoroughly examined all the children. This huge study was very successful and confirmed the safety of ivermectin: it could be distributed to nearly everybody in the community.13,14 We showed that by treating the whole community we could reduce transmission and the incidence of new infection in children.15 Initially, the dose of ivermectin was adjusted for each individual’s weight, so everyone had to be weighed, but later work showed that height could be used instead.16 If children could walk under the stick, they got one pill; if they were too tall, they got two. By 1989, when our last Liberian study was finishing, several government and non-government organisations coordinated by WHO had started delivering ivermectin in pilot projects. Although Merck would deliver boxes of ivermectin to the national port, it still cost between 5 cents and $5 a tablet to get the ivermectin up-country and into people’s mouths. A lot of work was done to develop cost-efficient ways of community-based distribution. To supervise the distribution of the donated ivermectin, Merck created the Mectizan Expert Committee.1,17 This joint committee was based at the Jimmy Carter Presidential Centre in Atlanta and included representatives from WHO and Merck, and other experts. I had the privilege to serve on this committee in the early 1990s. In 1990, a Houston software developer, John Moores, read an article about ivermectin in the Houston Chronicle. He was so taken by this story that he started a foundation to support this work. I was also fortunate to be on the Board of the River Blindness Foundation and eventually John Moores gave US$25 million to the Foundation. It became clear that a lot more money would be needed to distribute ivermectin in the 28 African endemic countries. The River Blindness Foundation, the Carter Centre and other non-government organisations convinced the World Bank to start a special program to distribute ivermectin in Africa, worth about $300 million.18 Another smaller program was set up for the six endemic countries in Latin America. In 2002, nearly 50 million doses of ivermectin were given away free: over four million doses a month, treating about 100 people every minute. Despite local disturbances and civil war, ivermectin distribution programs are active in 25 of the 27 endemic countries and currently reach 45% of the “Ultimate Treatment Goal”, the total number of people required to be treated (see www.mectizan.org). The number treated each year continues to increase at an almost exponential rate, and progress is closely monitored by the Mectizan Expert Committee, WHO and non-government organisations. The commitment and strategies are in place to reach everyone who needs treatment and to eliminate onchocerciasis by the year 2020. Success has many parents, and failure only one. Obviously, many people were involved in the ivermectin story, but it has been a great thrill to be one of them and to have been a part of what must be one of the most significant breakthroughs in tropical medicine in the past 25 years. 1: Onchocerciasis endemic areas Two onchocerciasis control programs provide onchocerciasis control in 30 endemic countries in Africa. (OCP — Onchocerciasis Control Program — initial area of vector control; APOC — African Program for Onchocerciasis Control — World Bank and WHO supported ivermectin distribution; OPEA — Onchocerciasis Elimination Program for the Americas — ivermectin distribution in Latin America). Reprinted from Reference 19 with permission. 2: Onchocerciasis fact file Cause Onchocerca volvulus, a filarial worm. Transmission Various biting black flies. Main African vector is Simulum damnosum. The flies breed along the river banks and in the rapids and fast-flowing streams. A female fly bites an infected person to take a blood meal, and becomes infected with a tiny microscopic worm – a microfilaria – that is less than a third of a millimetre long. Over a week or so, these microfilariae develop into infective larvae and can be transmitted when the fly bites another person. Life stages After entering the body, the infective larvae grow to become adult male or female worms. The males are only 5 cm or so long, but the females may be up to a metre long. The adult worms are wrapped together in a nodule like a ball of string. The worms reproduce sexually and the female releases tens of thousands of microfilariae every day. As the female can live for 10 years or so, she literally releases millions and millions of microfilariae. The microfilariae migrate throughout the host’s body, especially to the skin and the eye. In the skin they wait to be taken up by another black fly to continue the life cycle. If this does not occur within 18 months or so, the microfilariae die. There is no inflammatory response to live microfilariae, but dead or dying microfilariae provoke an intense local response. Disease manifestations Subcutaneous nodules (adult worms often attach to bones or joints) Skin changes: severe pruritus and rash, maculopustular reaction, pigmentary changes, atrophy Eye changes: microfilaria in cornea, anterior chamber and retina; uveitis; sclerosing keratitis; chorioretinal atrophy Liberian rubber tappers from one of the early onchocerciasis drug studies. Bruce Green (left) and Hugh Taylor standing at the back.

Hugh R Taylor AC, MD, FRANZCO

Graeme H Johnson*, Donna B Mak†; *Acting Public Health Medical Officer; †Former Public Health Medical Officer, Kimberley Population Health Unit, Derby, WA 6728. graeme.johnson@health.wa.gov.au To the Editor: In their study of a SAFE-style trachoma control program (which included Antibiotic treatment, Facial cleanliness, and Environmental improvement, but not Surgery) in a remote Australian community, Ewald et al suggest that no systematic SAFE trachoma control program exists in Australia.1 In the Kimberley region of Western Australia, the Kimberley Public Health Unit (KPHU) has coordinated a trachoma control program since 1989. The World Health Organization SAFE strategy has been implemented since 1996, as described in the Kimberley regional trachoma control guidelines and a peer-reviewed publication.2,3 The trachoma control program in the Kimberley has been delivered by a variety of environmental health, health promotion, community and clinical health professionals employed by State and local governments, and by community-controlled and other non-government organisations. We believe a coordinated regional approach is mandatory, because of the numerous organisations involved in program delivery. The trachoma control program in the Kimberley continues to achieve good results. The prevalences of follicular trachoma during annual screening of school-aged children in the Kimberley have been published annually in the KPHU Bulletin.4 Since 1996, in accordance with the WHO SAFE strategy, communities with trachoma prevalences of less than 5% were not screened in subsequent years and did not contribute to regional prevalence data. Thus, the observed decrease in trachoma prevalence between 1996 and 2001 is likely to be greater than that shown in the Box. We believe the Kimberley region is well placed to achieve the WHO aim of eradicating blinding trachoma by 2020.5 However, it is a concern that other regions of Australia with endemic trachoma infection may not conduct disease control activities in a coordinated manner because of lack of leadership in trachoma control or insufficient resources, or both. The community described by Ewald et al borders the Kimberley region and has strong cultural links with several Kimberley groups. The achievements in trachoma control in the Kimberley cannot be sustained in the long term without a nationally coordinated approach. We believe that it falls within the statutory responsibilities of State and Territory departments of health to ensure that environmental and clinical health services are coordinated to achieve trachoma control in Australia. Trachoma in Kimberley children Point prevalence of follicular trachoma among children in the Kimberley region aged 5–15 years at annual trachoma screening, 1991–2002

Graeme H Johnson · Donna B Mak

Andrew C Laming,* Bart J Currie† * Advisor, Federal Minister for Health and Ageing, Parliament House, MG 48, Canberra, ACT 2600; † Professor in Medicine, Northern Territory Clinical School and Menzies School of Health Research, Darwin, NT. andrew.lamingAThealth.gov.au To the Editor: The important article by Ewald et al shows that offering azithromycin treatment to 70% of a remote community may be inadequate to control hyperendemic trachoma, even when combined with a health promotion campaign.1 Yet, significant short-term gains in similar locations have been achieved with as little as 20% of the population receiving azithromycin, where administration to children with trachoma and their household contacts was directly observed by health staff.2 In that study,2 we reported a 6-month follicle resolution rate in schoolchildren of 72%, followed, however, by a return of trachoma prevalence towards baseline levels over 12 months. The critical factors for short-term success with azithromycin appear to be appropriate selection of cases and contacts, plus, where possible, directly observed therapy to minimise reinfection from untreated cases. Sustainability of initial reduction in trachoma prevalence is problematic, and issues of how extensively and how often to screen and/or treat need to be determined in the Australian context. Similar sustainability considerations have arisen in community scabies programs.3 Ewald et al are correct to identify population mobility as a major issue, with trachoma likely to be reintroduced by untreated children entering a community where a treatment program has occurred. Hence the need for a coordinated regional approach. However, a regional approach to trachoma control does not necessarily mean a uniform approach, and it is vital to tailor programs to suit the capacity of communities and their degree of commitment to labour-intensive treatment and health promotion. Our study suggested that directly observed twice-yearly azithromycin therapy, with a health promotional component, is likely to be preferable to an annual program.2 Mathematical modelling supports this more frequent dosing and, unlike in Africa, the cost of azithromycin should not be a constraining factor in Australia.4 Regardless of the strategy selected, if, after treatment, the prevalence remains hyperendemic (> 20%), then the outcomes from concurrent health promotion are compromised. Appropriately targeted and directly observed azithromycin therapy can help create conditions favourable for health promotion campaigns, which in turn prolong those gains by reducing trachoma transmission.5 Major issues for trachoma control in Australia are (i) who to screen and treat (with directly observed azithromycin therapy); (ii) how often to screen and treat; (iii) how to plan trachoma programs as regional initiatives; and (iv) who will fund, coordinate and implement trachoma programs.

Andrew C Laming · Bart J Currie

Dan P Ewald,* Gillian V Hall,† Christine C Franks‡ * Senior Research Fellow, Centre for Remote Health, Flinders University, PO Box 4066, Alice Springs, NT; † Lecturer, National Centre for Epidemiology and Population Health, Australian National University, Canberra, ACT; ‡ Educator, Health Development, Health and Community Services, Alice Springs, NT. dan.ewaldATflinders.edu.au In reply: These letters reinforce a number of important points about control of trachoma (and other endemic infections) in Australia. The questions of whom and how often to treat need refining through Australian experience. Long-term control needs multifaceted, intersectoral collaboration to alter environmental and behavioural conditions against disease transmission. Strategies should be sustained, regional (large as practicable); acknowledging, and guided by, Aboriginal kinship networks; and recommend observed drug treatment (which was negotiated for the final treatment in our study). A non-uniform approach could include more frequent treatment in hyperendemic communities, probably leading to less net use of antibiotic treatment. Reports from the Kimberley Population Health Unit show a very mixed picture, with wide year-to-year fluctuations in prevalence in many communities. While hyperendemic communities remain in a region, the prevalence of trachoma may increase unnoticed in communities no longer screened because their prevalence has dropped below 5%. If not looked for, it is unlikely to be noticed. Further analysis, such as the graph provided by Johnson and Mak, is to be applauded in the context of a thorough analysis. When this happens, it will greatly strengthen the case for active trachoma control in other regions. For trachoma prevention, and for many other reasons, we believe environmental health interventions are critical. These remain difficult to evaluate given the high mobility of people in Aboriginal communities. Reliable, long-term, regional environmental health and mobility data are needed as part of this broad issue.

Dan P Ewald · Gillian V Hall · Christine C Franks

A 71-year-old man with a past history of right-sided, renal cell carcinoma presented with a recurrent, right upper eyelid lesion (Box, Figure A). The initial biopsy showed Bowen's disease, but review after Mohs micrographic surgery revealed focal sebaceous differentiation suggestive of in-situ sebaceous carcinoma. A diagnosis of Muir–Torre syndrome was suspected, and the patient was referred for genetic counselling and targeted cancer surveillance. This led to the discovery of multiple dysplastic colonic adenomas and a left renal cell carcinoma (Box, Figure B). Muir–Torre syndrome is an autosomal-dominant genodermatosis characterised by cutaneous sebaceous neoplasia and one or more visceral malignancies. Diagnostic criteria include at least one sebaceous gland adenoma, epithelioma, or carcinoma, and at least one internal malignancy. The diagnosis of sebaceous carcinoma can be difficult, particularly in the periocular region, where it often masquerades clinically as blepharoconjunctivitis or recurrent chalazia. Furthermore, sebaceous carcinoma often displays only focal differentiation and, as seen in our patient, may be histologically misdiagnosed as squamous-cell or basal-cell carcinoma. A history of internal malignancy in patients presenting with sebaceous gland carcinoma should raise the possibility of Muir–Torre syndrome. Correct diagnosis in this case enabled early detection of dysplastic colonic polyps and renal cell carcinoma. A: Clinical photograph showing induration and ulceration of the central right upper eyelid margin. B: Computerised tomography scan showing a left renal mass (arrow) confined to the capsule.

Celia S Chen MB BS · Lindy Loweinstein · Shyamala C Huilgol FACD · Dinesh Selva FRANZCO · Craig James FACPA

An ophthalmologist remembers his time spent at a mission hospital in Pakistan After September 11, 2001, TV bulletins about attempts to destroy al-Qaeda and the Taliban featured footage of Quetta, a city in Pakistan on the fabled North West Frontier, just south of Afghanistan's Kandahar (see Map in Simpson). The news recalled memories of the weeks I'd spent there, 42 years previously. More came flooding back as I leafed through the pages of my photo album. From Karachi to QuettaAlmost naked, I sweated on a Karachi hotel bed, the ceiling fan spinning above me. What had I let myself in for? Disconsolate, missing my wife and new firstborn son who were already back home in Australia, I could well understand why Somerset Maugham's expatriate Englishmen took to drink in the equatorial Empire. It was the northern spring of 1959, and I was overnighting in Karachi, then Pakistan's capital, en route to Quetta, near the border with Afghanistan. After three and a half years away from Australasia gaining specialist ophthalmic training in England and the USA, I'd allowed an American colleague to entice me to detour on my way home — for a 10-week stint at Quetta's Church Missionary Society Hospital. I hadn't thought of arranging professional indemnity insurance (!), and I'm not even sure travel insurance would have covered all the potential risks. The next morning, I boarded my train to the north. In addition to my ticket, I'd purchased, on advice, my personal air conditioner — a 30kg block of ice in a tin tub placed under my seat for the 24-hour trip. As we journeyed through the Desert of Sind, on the strategic railway built by the British in 1895, stories of the British Raj, India's frontier, the Khyber Pass, the Bengal Lancers and Gunga Din ran through my head. The last remnants of my ice block were melting away as the train chugged up the final slope of the Bolan Pass to enter the Quetta plateau. Missionaries among the militaryThe city of Quetta is a hill-station, about 1700 metres above sea level, in a valley ringed by snowy mountains rising to about 2500 metres. In spring, the valley floor is lush and productive, but the overgrazed hillsides are always bare. The city was rebuilt after being destroyed by earthquake in 1935. Low-rise to the eye, Quetta was, to me, reminiscent of an Australian country town. The population was about 30 000 in winter, doubling in summer. Quetta has long-standing military connections, beginning with its name — derived from "kuwetta", meaning "fort". In the centre of town, on a hillock, is the famed Red Fort antedating British rule. The British arrived in about 1876, encountering tribal groups of Brahuis and Baluchis, as well as the Pathans, the Pashtun nomads. Fearing Russian encroachment via Afghanistan, the British military commanders of the day considered the chain of missionary hospitals positioned along the frontier, including the one at Quetta, to be the equivalent of several battalions. These missions, in effect, garrisoned the border with Afghanistan, supplementing the forts along the thousand miles from Iran to China. During the Second World War, although not an active theatre of war, this garrison town was the second-largest military establishment in the British Empire, after Aldershot. Quetta's military cemetery holds the graves of soldiers from all over the old Empire, from many cultures and religions. In 1959, Quetta still retained the Commonwealth Staff College founded at the height of Empire in 1907. Security was still a concern and became evident to me in a personal way. One day, when I'd cycled out of town to photograph the scenic city and surrounds, two policemen pounced on me and confiscated my camera film — India and Pakistan were already battling over Kashmir and there had been recent bomber activity at the Indo-Pakistan border. Western medical outpostQuetta's mission hospital was originally established in 1886, and had been rebuilt after the earthquake. In the courtyard there were small cottages forming the caravanserai where patients were nursed by relatives who also took care of food and cooking. Throughout the day, electric amplifiers and loudspeakers alerted us to the call of the muezzin, reminding our Christian medical island of the dominant culture that lapped against the walls of the hospital compound. Purdah (seclusion) and veiling were still upheld in Quetta despite its cosmopolitan community. The hospital had a segregated women's section, the zenana wards. The hospital served the city and the region, catering particularly to the trans-border nomadic Pathans who moved down through the Bolan Pass to the southern plains during the winter, returning to the hills of Afghanistan during the summer. Accordingly, these tribal nomads had two opportunities each year to benefit from Western medicine. Cataracts and neglected chronic diseases were common presentations, as was diarrhoea. I myself suffered diarrhoea on several occasions and progressively lost weight during my stay. Faecal tests positive for blood and/or amoebae sentenced one to amoebicides; negatives dictated sulfas, to which my bugs responded. The diarrhoea was surely related to the town's contaminated water supply. Irrigation water from the city's reservoirs flowed through the streets alongside the footpaths. Using removable paddles, the waterman selectively diverted the flow into separate open channels for individual sections of the town on given days. Not surprisingly, the water reaching our vegetable gardens in the hospital compound was murky. This public health issue didn't seem to agitate either the city authorities or, in general, the Western doctors! In winter, the hospital ran an outreach clinic at Shikarpur, 200 miles to the south. Many such clinics, known as "cataract camps", were held on the Indian subcontinent under missionary auspices, foreshadowing the Fred Hollows Foundation. Cataract surgery and other proceduresEvery operation began with a Christian prayer. For the anxious patient, this was extra premedication. Local anaesthesia was used for cataract operations — patients' eyelids were kept open during the procedure with a pair of locally made fork retractors, handheld by the assistant, one of the male nurses trained in the hospital's own program. Graefe section with conjunctival flap was standard, progressing to intracapsular extraction. I carried out over 100 cataract procedures in my 10 weeks, and many plastic operations on eyelids and tear ducts. I treated one patient with retinal detachment. I also assisted at numerous general surgical procedures and outpatient clinics. The hospital's surgeons — Pakistani Christians as well as English — were skilled in all aspects of surgery (ophthalmology included). I saw many cases of advanced cancers of the head and neck such as I'd never before witnessed that were managed with massive excisions and repairs. Radiotherapy was available in the form of radium needles. When two of those valued needles were mislaid, many of the hospital staff devoted the day to search for them — they turned up when an American geologist scanned the rubbish tip with his Geiger counter! A social summerThe social atmosphere throughout my stay was memorable. I was made to feel one of the family by the hospital's director, Dr Ronnie Holland, son of a previous director, Sir Henry Holland, who had been knighted for heroism in the 1935 earthquake. His wife, Joan, was a remarkable woman who, while pregnant, had survived near-fatal polio, being kept alive with manual resuscitation until an iron lung could be procured and repaired. She now worked from her wheelchair, as nurse-anaesthetist. Sunday was a real day of rest, commencing with chapel and then a relaxing picnic lunch on the English lawn of the hospital gardens, next to a rich and varied orchard. It was here that I became partial to green tea. At the Hollands' table, I met intriguing characters from many cultures. They included the indigenous Bishop of Karachi, Chandhu Ray — an amiable man with whom to exchange philosophies; Parsee merchants, who were the first to tell me that their dead were disposed of on special towers, for the vultures; and American scientists working for United Nations agricultural or prospecting agencies. Among other social engagements were invitations to dinner with Australian army officers at the Staff College. When it came time for the Hollands to open the hospital's summer cottage in the hill-station of Ziarat, 70 miles east, and elevated some 900 metres above Quetta, I accompanied them. We set off for the weekend through a narrow defile to a higher plateau before climbing the dusty hills on one side of the broad valley. As I swallowed the dust and, terrified, looked over the rim of the snaky alpine tracks, I was told that Alexander the Great had passed along the valley below after conquering Swat, in the border regions near China. At various points in our passage, we came across clusters of flags on poles like those marking golf holes, but twice as tall — markers of nomad graves. At 630 metres above sea level, juniper trees suddenly appeared on the valley walls, creating a new demarcation line between the bare slopes below and the trees, which only thrived above this height. The mountain air was laden with the scent of thyme, as well as juniper. ReflectionsAt the end of my adventure, returning to my hotel in Karachi, I was surprised to find that Bishop Ray had left a message for me. He invited me to lunch with him, and then came to the airport to see me off. His touching courtesy prompted me to ponder the situation of the Christian minority and its missionary doctors, whose lives I had shared. My missionary friends were not confounded by their inability to care for everyone, everywhere in the region. They were realists, content to do all they could to meet local needs. To them, their calling didn't involve self-sacrifice (although a young English nurse did die suddenly during my visit). Perhaps the missionary urge, previously a preserve of the Christian medical missionaries, can be best illustrated by paraphrasing Sir Henry Holland: Our aim is to care for the whole person, body, mind and spirit. Our healing is like a sermon in the ward. It's not bait to lure the people. It's delivered in dedication to our calling, undaunted by dangers and difficulties. Today, the North West Frontier is an even more dangerous place than it was in 1959. Opposition to the presence, and even to the work, of medical missionaries has intensified. I reflected on what the hospital and I had provided for each other. I'd assisted slightly with the patient load. Quetta gave me the benefits of concentrated experience with advanced, neglected, untreated disease; further medical and surgical insight; and the privilege of working with admirable colleagues dedicated to the impressive people native to this frontier. I'd learnt much more in Quetta than surgery alone.

Ivan Cher FRACS

More patients than beds. Dr Lion, Dr Kimborarith and Dr Thaly doing ward rounds on the verandah of the Takeo Eye Hospital. Bombed in secret for years by the United States during the Vietnam War, overrun by Pol Pot and his murderous Khmer Rouge, invaded by Vietnam in 1978, blighted by landmines, and lurching through periods of famine, post-colonial political crisis, and intermittent civil war, Cambodia has suffered terribly. Its people are among the poorest in Asia. Aid work commenced by the Maryknoll organisation in 1993 has expanded and been handed over to another Catholic charity, Caritas, supported by funding from Germany and Australia. The centrepiece of the project is an eye hospital in Takeo, 80 km south of the capital, Phnom Penh. Here, services are provided to the poor and local doctors and nurses are trained in the basics of ophthalmology. This is the story of my short time working at Takeo Eye Hospital around Christmas 2001: a day in the life of a volunteer. You can tell that French colonialists were in Cambodia; the bread is excellent and a breakfast favourite at the Café Chisor where I start the day. I hail a prowling motorscooter, because taxis do not exist, and negotiate a price to the Takeo Eye Hospital on the outskirts of this small town. As we bounce and weave along the dilapidated dirt tracks that pass for roads, I notice some causes of the eye trauma that will present to hospital today. Workers threshing rice by hand or angle-grinding in metal shops have no eye protection. Despite the dust and insects, none of the "moto" riders wear goggles, let alone a helmet. The hospital is run by a Dutch ophthalmologist, Dr Franz Lion, and staffed by his three trainees, Dr Eng Kimborarith, Dr Sok Chenda and Dr Poch Thaly, who have come from various distant provinces, leaving their families behind, to attend the 18-month Basic Eye Doctor course. In the high humidity and with a lack of basic hygiene, many injuries from foreign bodies result in corneal ulcers. Pathology services are virtually non-existent and mixed infections are the norm anyway, so ulcers are treated with a combination of antifungals, antibiotics and antivirals. Our day begins with a ward round before 8 am, but the nurses start much earlier, removing dressings and ensuring that the patients' relatives are out of the wards. There are two rooms, each with about 20 wooden platforms making the 40 hospital beds. These are rarely sufficient, and today we have an additional 20 patients who have spent the night on the verandah. Our procession enters each area in turn, led by Dr Lion and his cheery salutation of "Sua s'dei" (an informal "hello"). The patients return the greeting and offer the traditional hands-together gesture of Buddhist greeting. One elderly lady just claps. Brief examinations are undertaken and results of the previous day's surgery are revealed. Patients with corneal ulcers are quarantined in their own ward and it too is full. Carers, who spent the night on the floor beside their relatives, are cooking breakfasts over the fires in the communal kitchen area outside the wards. Other nurses are already assessing new patients, some of whom have travelled great distances and have queued since dawn. To ensure the afternoon's surgery will start on time, nurses will only accept new patients until mid-morning. We join them in the outpatients area; a large room with four small desks, slit-lamps and a few tables for simple procedures. The verandahs are used for assessments of visual acuity, visual fields, eye movements and other basics. A toddler is brought in by her father with a lacerated cornea. Like many locals, he traps wild birds and keeps them at home before slaughter or sale. She has been pecked in the eye and, incredibly, is the third such young patient this week. The injury occurred about a week ago and precious time (and money) has been wasted on "traditional healers" in the interim. She will be properly assessed under anaesthesia this afternoon. A stork tethered outside a Cambodian business. Trapping wild birds for food or sale is common. In my time at Takeo Eye Hospital, I saw three children with eye injuries from being pecked by trapped birds. Another child is screaming inconsolably. He is found to have a small rice grain in the upper conjunctival fornix. I imagine that in future he will not stand so close as his parents bash rice sheaves against the threshing boards. I'm obtaining valuable experience with the slit-lamp in reviewing some of the long-term ulcer patients, but their progress is sometimes discouraging. Every surgery list includes eviscerations of eyes that cannot be saved. One of my patients today is a 10-year-old girl with the classic Khmer smile that the guide books always mention. I've never found out how she lost her left eye; I'm just worried about the persistent ulcer on the right that has her vision down to "count fingers at two metres". Uveitis is a common and painful condition in this community, but in the harvest season only very serious ailments will cause an adult to leave their fields. Advanced cases of uveitis with bizarrely misshapen irides due to lens adhesions are frequent. A steady stream of elderly patients present with glaucoma and cataracts. Lunch is an event I've been enjoying with the local doctors for a few weeks now. One of the cleaners is given funds and goes to the market daily. She returns to prepare delicious traditional meals; like the spicy soup, curried fish, and pickled vegetables which we eat noisily and with gusto, as is the custom. I'm told this feast is only "simple food". It costs me two dollars but that is the daily wage in Cambodia. Everyone who survived the Khmer Rouge has a story, and now that I know them better the trainees are talking about some of these events. Dr Thaly's family were separated to work on different communes for almost the entire four years of Pol Pot's regime. All educated people were considered counter-revolutionaries. Dr Thaly confirms that people were killed simply because they did not have the calloused hands of a peasant, as depicted in The Killing Fields. One doctor in a nearby town survived by passing himself off as mentally handicapped, feigning a twitch and a stammer for four years, and is now unable to cease these behaviours. The afternoons are dedicated to surgery. The operating theatre is airconditioned, but a wardsman armed with a flyswatter watches for intruding insects. Equipment is basic; fragments of razor blades serve as scalpels and haemostasis is achieved with a probe heated in a candle. Adult patients are given a face block and walk in and out of the surgery. Children are anaesthetised with ketamine, and vital functions are monitored by a stethoscope. The eye of our bird-peck girl collapses as the wound is explored and another evisceration is performed. But there are many successful outcomes: tarsal plate rotations for trachoma, trabeculectomy for glaucoma (drugs are unaffordable), lid elevations for ptosis, corrections for strabismus, pterygia removed, and sight restored for many patients by cataract extractions. Last year, this hospital performed 3100 operations. Surgery at Takeo Eye Hospital: barefooted patients and doctors in thongs. In the late afternoon, Dr Lion enthusiastically summons us for a tutorial. Afterwards, I stay back to do some study, but mostly chat, with the trainees. Later, as I'm walking home two nurses on a moto stop and offer a lift. As three is only half the maximum number that I've seen on a Cambodian motorscooter, I feel quite secure. The best place for dinner is back at Café Chisor. This was set up by Dr Lion's wife as a non-profit enterprise to provide employment and training for local women. The food is traditional, wonderful and very affordable, but I have been startled by a scorpion and a snake during meals here, much to the amusement of local patrons. Very few westerners visit Takeo and young Khmers are desperate to learn English, so I am quite popular. I've started giving impromptu lessons to relatives of the cafe's staff and they return the favour in kind. We often end up just laughing at each other. As I return to my room, extinguish the candle (the electricity has failed again) and carefully slither under the mosquito net, I'm very grateful to have learned from the inspirational Dr Lion and other staff, and to have been of some assistance to the needy patients of Takeo Eye Hospital. I hope that this project will one day mean that there are enough Cambodian eye doctors to go around.

Leo J Ryan LLB(Hons), BSc

Glaucoma is the most common neurodegenerative disease of the optic nerve, with a prevalence of about 3%.1 This means that about 150 000 Australians, about 75% of whom are aged over 70, have glaucoma. This number will double over the next 30 years as our population ages.2 After macular degeneration, glaucoma is the second most common cause of irreversible blindness in our community,3 and the commonest cause of preventable blindness. The basis for the most common form of glaucoma is multifactorial. Genetic linkage analysis has isolated several putative genes for open-angle glaucoma, but these account for only a small percentage of cases. Risk factors for open-angle glaucoma identified in Australian cross-sectional analyses include age and intraocular pressure, family history of glaucoma,4 myopia, systemic hypertension and diabetes.5 In glaucoma there is a relatively slow loss of retinal ganglion-cell axons. Early loss is usually in the mid-peripheral visual field. The disease becomes symptomatic at a relatively late stage when central vision is affected and the visual acuity declines, or extensive loss of peripheral vision leads to problems with mobility. However, because progression of the visual field loss is relatively slow, glaucoma is responsible for a relatively small number of the new cases of visual acuity impairment detected annually.6 Underpinning the treatment of glaucoma is a reduction in intraocular pressure. Recent reports7,8 provide evidence for setting a target intraocular pressure level for each patient, depending on the assessed risk of progressive visual damage, such as extent and rate of prior damage, proximity of the visual damage to the point of fixation (most sensitive central vision), likely number of years of life remaining for the patient, family history, and the level of intraocular pressure at which damage has occurred. Usually, topical drug therapy is used first. Newer drugs such as prostaglandin F2α agonists (latanoprost, travoprost), prostamides (bimatoprost), topical carbonic anhydrase inhibitors (dorzolamide, brinzolamide), β-blockers (timolol, laevobunolol, betaxolol) and α2-agonists (brimonidine, apraclonidine) have tended to replace pilocarpine and adrenalin-related compounds. Since drugs are absorbed directly from the nasal mucosa into the venous circulation with hepatic by-pass, topical agents mimic intravenous drugs — their safety margin can be widened by simple eyelid closure and digital occlusion of the tear duct for at least two minutes after instillation. Non-compliance and difficulties with instillation techniques remain major challenges for the long-term treatment of this incurable and asymptomatic condition. Failure to achieve target intraocular pressures by medical means usually leads to laser procedures. Laser trabeculoplasty techniques offer a 75% chance of helpful intraocular pressure reduction, with a 50% chance of continuing benefit for up to five years. Lasers are also used to achieve peripheral iridectomies for angle-closure glaucoma, and to inhibit aqueous inflow by ciliary-body destruction in blind, painful eyes. If medical and laser treatments fail, incisional surgery is performed to create an alternative pathway for the aqueous humor onto the scleral surface. Augmented with antifibrotic agents (5-fluorouracil, mitomycin-C), a long-term success rate of up to 90% can be achieved. For patients with exaggerated healing responses (glaucoma secondary to uveitis or rubeosis), intraocular pressure reduction can be achieved with plastic tubes draining into plastic reservoirs (there are three types of implants — Molteno [Molteno Ophthalmic, Dunedin], Baerveldt [Pharmacia, Kalamazoo, Mich, USA], and Ahmed [New World Medical, Rancho Cucamonga, Calif, USA]). Beyond intraocular pressure reduction lies the hope of neuroprotection — an attempt to prevent initiation or progression of intracellular processes resulting in retinal ganglion-cell apoptosis (induced cell suicide). A large international multicentre prospective randomised clinical trial of the NMDA [N-methyl-d-aspartate]-receptor antagonist memantine is under way, with results expected in 2006. Our conventional approach of looking for visual field defects, or for their progression, with white-on-white automated perimetry is still the main method of monitoring for glaucoma stability, but a large proportion of the nerve fibres can be lost before an initial defect is seen. (In white-on-white automated perimetry, a white light target is projected into a white background bowl — the patient responds when the light is just seen and its intensity is varied until the threshold for seeing has been crossed, which determines the sensitivity of the retina at that point.) There are now several new techniques for the detection of glaucoma which are specifically designed to detect change at earlier stages of the disease. Psychophysical tests are available which target smaller subpopulations of ganglion cells, such as frequency-doubled perimetry, and short-wavelength automated perimetry (blue target/yellow background). Multifocal objective perimetry, recently developed at the Save Sight Institute,9 records a multifocal visual evoked potential and removes the need for patients' subjective responses. Optic disc and nerve fibre imaging techniques using scanning laser ophthalmoscopes (eg, Heidelberg retina tomograph [HRT, Heidelberg Engineering, Heidelberg, Germany]; GDx Access [Laser Diagnostic Technologies, Jackson, Fl, USA]) or optical coherence tomography can provide objective measures of structural change. Glaucoma blindness is largely preventable. While the visual damage is not reversible, it can usually be arrested. To achieve this, early diagnosis of this otherwise progressive, asymptomatic process is essential. Ninety per cent of the Australian population visits a general practitioner annually, yet 50% of patients with glaucoma identified in population surveys are undiagnosed and untreated.3 Clinically, the first changes occur at the optic disc and it is vital that clinicians look for the characteristic sign of optic disc cupping. Every GP should view a patient's optic disc with an ophthalmoscope from time to time, especially if one or more risk factors are present. Anyone with significant optic disc cupping, or asymmetry between the optic discs of the two eyes, should be referred for investigation.

Ivan Goldberg FRANZCO, FRACS · Stuart L Graham FRANZCO, FRACS · Paul R Healey FRANZCO, BMedSc, MMed

To the Editor: Warfarin is frequently used in the same population that is at risk of age-related macular degeneration (ARMD), the commonest cause of blindness in the elderly. A recent report has suggested that warfarin may cause severe intraocular haemorrhage and loss of vision in the minority of patients who have the neovascular form of ARMD.1 We have also seen this occur in patients taking warfarin. There are methodological imperfections in the report, and the association is certainly not proven. Nevertheless, it would seem prudent to exercise some caution in the use of warfarin in patients who are or may be at risk. Our preliminary recommendations (pending a prospective study) are: If a patient has only one functioning eye (for whatever reason), an ophthalmologist's opinion should be sought as to the risk of neovascular ARMD in the seeing eye before or soon after commencing warfarin therapy. Low-risk patients are easily identified and warfarin use in these patients should have no visual sequelae. In patients considered at high risk of neovascular ARMD, the use of warfarin may carry a (currently unquantifiable) risk of visual loss. Alternatives to warfarin should be considered, and the possible risks of taking, or not taking, warfarin should be discussed with the patient. If a patient has two seeing eyes, the risk of bilateral visual loss from warfarin must be exceedingly small, and indeed there have not even been anecdotal reports of such an event. Warfarin can be used in such patients without regard to ocular status. Ophthalmologists should ask all patients they examine whether they take warfarin and should communicate to the treating doctor the presence or absence of factors that put this patient at high risk of neovascular ARMD.

Lionel M Kowal FRANZCO · C Alex Harper FRANZCO

The major advance in ophthalmology in the past five years has been the findings from two recent epidemiological studies that have indicated the priorities for clinical and public health practice and basic science research in ophthalmology in Australia.1,2 These studies have shown that the prevalence of vision impairment increases threefold with each decade after the age of 40, with almost one in three people over the age of 80 having impaired vision. Prevention. There are five major causes of vision loss: under-corrected refractive error, age-related macular degeneration (AMD), cataract, glaucoma, and diabetic retinopathy.1,2 Of the 400 000 Australians with impaired vision, half have refractive error that is correctable. Almost all of the 9% with cataract will have excellent outcomes from surgery, and a further 8% have preventable vision loss due to glaucoma or diabetic retinopathy. With the ageing of the population, the number of cataract operations (currently about 125 000 a year) will need to double over the next 20 years. By the age of 90, most people will develop cataract and half will have already had cataract surgery. Another key finding of the two Australian studies was that cigarette smoking and ultraviolet-B exposure bring on cataract earlier, but lifetime exposure seems critical. These studies have also reported the impact of vision loss on quality of life. Even relatively minor vision impairment (< 6/12 vision) increases social isolation and doubles the dependency on community services, increases morbidity (with a twofold increase in falls and a threefold increase in depression), and doubles mortality rate. It is critical for healthy ageing that people with impaired vision be referred to vision-related rehabilitation services to reduce the impact of vision loss. Currently, less than one person in three with vision loss has used these services. Within the past few years, simple visual acuity tests have been developed to detect most treatable or correctable vision loss, particularly from refractive error, cataract and AMD. Vision screening targeted at older people (65 years and over) through primary healthcare is both simple and effective. Diagnosis. Although almost one in 10 people will develop glaucoma by the age of 80,3 only half of those with the disease are currently diagnosed. The measurement of intraocular pressure has been shown to be ineffective in detecting glaucoma. Current trials are investigating new screening technologies (frequency-doubling technology and confocal scanning laser tomography) and protocols for community use to detect early signs of damage to the retinal nerve fibre layer. The target group for screening is people with a family history of glaucoma and those over 50 years. Diabetes, associated with a 25-fold greater risk of vision loss, is a rapidly increasing problem. Although tight control of diabetes, blood pressure and blood lipid levels will reduce the development of diabetic retinopathy, the critical issue is its early detection (by screening at least every two years) and timely laser treatment.4 New, non-mydriatic fundus cameras used by non-specialised staff are an effective alternative to dilated ophthalmoscopy. They offer a great advantage in some situations, especially in rural and Indigenous communities. Intervention. Cataract surgery is now extraordinarily successful. The next major development will be an accommodating intraocular lens that will remove the need for reading-glasses after surgery — this is probably 5–10 years away. Ultimately, two in three people will develop AMD and one in four will lose vision. However, a third of AMD incidence is attributable to cigarette smoking.5 Only a few people with AMD benefit from current laser therapy. However, newly developed photodynamic therapy (PDT) can reduce or delay vision loss in selected cases. PDT involves the use of a diode laser with an intravenous light-sensitive dye (verteporfin). The laser photocoagulation of choroidal neovascularisation can reduce the risk of progression of vision loss from AMD. Treatment often has to be repeated three or four times a year and long-term benefits are still unclear. A large randomised controlled trial we completed this year showed that vitamin E supplementation did not protect against either AMD or cataract. The recently completed Age-related Eye Disease Study found that dietary supplements containing high-dose combinations of antioxidants and minerals (vitamins C, E, beta-carotene and zinc) reduced the risk of advanced AMD and vision loss (see <http: //www.nei.nih.gov/amd>). The development of glaucoma, cataract and AMD has been found to have a genetic basis. Genes related to presence and severity of glaucoma have been identified, but candidate genes for AMD are still to be found. It seems unlikely that gene therapy will prevent eye disease in the short term. As the famous baseball player Yogi Berra said, "predictions are always hard, especially when they are about the future". Even though the bionic ear is highly successful, a successful bionic eye is unlikely to be seen in the next 10 years or more.

Hugh R Taylor AC, MD, FRACO · Jill E Keeffe PhD

Indigenous Health Trachoma in Australia Hugh R Taylor Australia is the only developed country in the world where blinding trachoma still exists MJA 2001; 175: 371-372 Trachoma is a disease that has been with us from antiquity. It is discussed in ancient Egyptian texts written on papyrus and in even earlier writings from ancient China. Chronic infection with the trachoma organism, Chlamydia trachomatis, can lead to blindness. The disease came to prominence in Europe during the Napoleonic wars, when tens of thousands of British and French troops returned with trachoma after fighting in Egypt. It spread rapidly through the armies of Europe, where the troops lived in crowded and insanitary barracks. Most of all, trachoma was a disease of the urban slums. In Europe, as people left their relatively healthy rural homes they were crowded into the workhouses and tenements created by the Industrial Revolution. Personal and community hygiene fell to an all-time low and the prevalence of trachoma surged. Trachoma was rampant throughout Europe and North America in the 19th century. In addition to tuberculosis and typhus, trachoma was one of the diseases that would-be immigrants to the United States were examined for — if found to have trachoma, they were sent all the way back to Europe. The early European settlers of Australia brought trachoma with them. Whether the Australian Indigenous people had trachoma before colonisation is unclear, but it seems unlikely, as small groups of nomadic hunter-gatherers can maintain good hygiene. However, with the poor housing conditions of the early settlers, and with the heat, dirt and flies of Australia, trachoma (or "sandy blight" as it was often called) became widespread and well known. It even left its stamp on certain place names (eg, Sandy Blight Junction in the Western Desert and the Ophthalmia Ranges in the Western Australian Pilbara). However, by the beginning of the 20th century, hygiene and living conditions in our larger cities had started to improve. In 1901, one of my predecessors at the Eye and Ear Hospital in Melbourne stated he could no longer find cases of active trachoma from Melbourne to teach his students. Instead he had to find people who lived in the Goulburn or LaTrobe valleys in Victoria. But, even in rural Australia, trachoma was disappearing, and by the late 1930s sandy blight had essentially disappeared as most Australians moved into proper housing with separate beds, running water and adequate sewerage and rubbish removal. The same happened in other developed countries. In England, the trachoma schools and clinics closed before World War II, and the last trachoma hospitals in the United States closed just after the war. In the 1950s, trachoma also disappeared in Italy and the Soviet Union. Despite the disappearance of trachoma from most of the Australian population, it has remained prevalent among certain groups of Indigenous Australians. The late Father Frank Flynn, an Australian-born and London-trained ophthalmologist turned Catholic priest, worked as an Army chaplain in Darwin in 1941. He was the first to recognise the frequent occurrence of trachoma among Indigenous people in the Northern Territory, and their welfare became his life's work. After World War II, Ida Mann, an English ophthalmologist who had worked with Frank Flynn in London before the war, moved to Perth. She subsequently conducted extraordinary trips throughout the outback, examining and treating Indigenous people with trachoma. In the 1960s, Fred Hollows took up his position as Professor of Ophthalmology at the University of New South Wales and became aware of the importance of trachoma in Australia. First working with the Gurindji people at Wave Hill in the Northern Territory and then with the people around Bourke in far western New South Wales, he cajoled the Federal Government and the Royal Australian College of Ophthalmologists into establishing the National Trachoma and Eye Health Program (the "Trachoma Program"). From 1976 to 1978, the Trachoma Program teams visited every Indigenous community in Australia (including some groups in large urban centres), examining over 62 000 Indigenous people and nearly 40 000 others (consisting of whites, Asians, etc, in rural and remote areas). It gave a clear picture of the number of people affected with trachoma and its distribution. They also treated nearly 40 000 people for trachoma and set up clear guidelines and recommendations as to what needed to be done to eliminate trachoma.1 In 1996, I was asked by the Federal Minister for Health to prepare a report on Indigenous eye health.2 It was very satisfying to go back to places like Bourke and Broome and find that trachoma had essentially disappeared over the previous 20 years. Clearly, progress was being made — at least in the towns and larger communities. In other areas, although the amount of trachoma had decreased and fewer children were affected, their elders still had scarred eyelids and blindness from the inturned eyelashes caused by trachoma. However, I was devastated to find that in some other communities, such as Jigalong in the Western Desert, and Amata and Fregon in the Musgrave Ranges, the rates of trachoma in children had not changed one jot over the 20-year period. At a meeting of the World Health Organization (WHO) in Geneva a few years ago, we added up the number of countries where blinding trachoma still occurred. We counted 54 — Australia is the only developed country on that list. WHO has launched a special program for the Global Elimination of blinding Trachoma by the year 2020 ("GET 2020").3-5 Its aim is to eliminate trachoma from the poorest areas of Africa and Asia over the next 20 years. My colleagues from other countries turn to me and ask, "How can you possibly still have trachoma in your country?". Fred Hollows once said that trachoma was a disease of the crèche, the preschool childcare group. Studies I subsequently did, both in the laboratory6,7 and in the field,8,9 identified and confirmed the importance of repeated episodes of reinfection by C. trachomatis. Each episode of infection gives more inflammation that leads to more scarring and a greater likelihood of eventual blindness. Endemic trachoma persists in areas where living standards are inadequate, with poor personal and community hygiene that permit the frequent spreading of infected eye secretions from one child to another. To stop trachoma, one needs to stop the transmission by improving living conditions. After all, this is what happened in mainstream Australia 100 years ago. Nowadays, Australians in both urban and rural areas expect to have the basic facilities that are needed for healthy living, such as a house, electricity, clean running water and sewerage, a made road and a rubbish collection facility. We expect them as a right — just recall the outrage in Sydney when the water supply was contaminated in 1998! Nevertheless, the Aboriginal and Torres Strait Islander Commission (ATSIC) has reported that half of the Indigenous people in the Northern Territory do not have adequate housing,10 and one in six communities do not even have potable water. ATSIC estimated that in 1991 there was a $2 billion deficit in funding for basic infrastructure and housing in Indigenous communities. These are services provided by local and state governments to everyone else in Australia. To eliminate trachoma in Australia we need to upgrade the basic services and housing of Indigenous communities in the outback to the same minimal standard that every other Australian enjoys. This is fundamental and can only occur if the Australian community accepts the need and insists that the problem be rectified. We must direct and empower federal, state and local governments to provide the basic community infrastructure and health hardware. This would be a good example of "practical reconciliation" espoused by the Coalition Government. Using research findings of the past decade or so, we have worked with WHO to devise the so-called "SAFE strategy" to eliminate trachoma.5 The SAFE strategy has four components: "S" for surgery (to correct inturned eyelashes); "A" for antibiotics (to eliminate chlamydial infection); "F" for facial cleanliness (to reduce the spread of infection from one child to another); and "E" for environmental improvement (to upgrade community hygiene and living conditions). Some of the recommendations contained in the review of eye health in Aboriginal and Torres Strait Islander communities2 related to trachoma, and the Federal Government accepted the recommendations that included the implementation of the SAFE strategy in all communities where trachoma still exists. In 1997, when he accepted the report, the Federal Minister for Health, Dr Wooldridge, promised to "do whatever it takes". The Prime Minister also supported this work, and on a visit to Nhulunbuy in 1998 announced the provision of azithromycin to treat trachoma in Indigenous communities. However, since then, disappointingly little has happened. In most places, little has changed, even though the problem has been clearly identified, strategies have been carefully laid out, verbal support has been given by leaders and there has been a lot of discussion with bureaucrats. In areas with severe trachoma, one in five of the older people have inturned lashes, and about half of these are either blind already or will eventually go blind. It is a tragedy to see their children or their grandchildren suffering from trachoma infection, because you know that they are on the same escalator and will certainly suffer the same fate if things do not improve. We can stop this if we as a community care. Trachoma is entirely preventable. Although it disappeared from white Australia 100 years ago, it could take another century to disappear from Indigenous Australia if we do not do something about it. We can not wait that long. All Australians have the right to sight. The time to act is now. Do we have the will? References National Trachoma and Eye Health Program. Sydney: Royal Australian College of Ophthalmologists, 1980. Taylor HR. Eye health in Aboriginal and Torres Strait Islander communities. Report of a review commissioned by the Commonwealth Minister for Health and Family Services, the Hon Dr Michael Wooldridge. Canberra: Commonwealth of Australia, 1997. Dawson C, Schachter J. Can blinding trachoma be eliminated worldwide? Arch Ophthalmol 1999; 117: 974. Taylor HR. Towards the global elimination of trachoma. Nat Med 1999; 5: 492-493. World Health Organization. Future approaches to trachoma control. Report of a global scientific meeting; 1996 June 17-20, Geneva, Switzerland. Geneva: WHO, 1996. (WHO Publication 96.56.) Taylor HR, Prendergast RA, Dawson CR, et al. An animal model of cicatrizing trachoma. Invest Ophthalmol Vis Sci 1981; 21: 422-433. Taylor HR, Maclean IW, Brunham RC, et al. Chlamydial heat shock proteins and trachoma. Infect Immun 1990; 58: 3061-3063. Taylor HR, Millan-Velasco F, Sommer A. The ecology of trachoma: an epidemiological study of trachoma in Southern Mexico. Bull World Health Organ 1985; 63: 559-567. Taylor HR, West SK, Mmbaga BBO, et al. Hygiene factors and increased risk of trachoma in Central Tanzania. Arch Ophthalmol 1989; 107: 1821-1825. Water: a report on the provision of water and sanitation in remote Aboriginal and Torres Strait Islander communities. Canberra: AGPS, 1994. Jones R. The housing needs of indigenous Australians, 1991. Research Monograph No. 8. Canberra: Centre for Aboriginal Economic Policy Research, Australian National University, 1994: 149-151. This is an edited version of a talk presented on the ABC Radio National program Ockham's Razor, 1 July 2001. Authors' details Centre for Eye Research Australia, East Melbourne, VIC. Hugh R Taylor, AC, MD, FRACO, Professor of Ophthalmology. Reprints: Professor H R Taylor, Centre for Eye Research Australia, Locked Bag 8, East Melbourne, VIC 8002. h.taylorATunimelb.edu.au Make a comment

Hugh R Taylor

Editorial "Smoking is a major cause of blindness" A new cigarette pack warning? MJA 1999; 171: 173-174 Health warnings on Australian tobacco products have been mandated through federal legislation since 1973, being updated in 1987 and 1995. Issue of the current warnings followed a detailed study examining the likely impact of prototypes, particularly on youth.1 The warnings address general health ("Smoking kills"), lung cancer, heart disease, addiction, low infant birthweight, and harm to others through passive smoking. The adoption of health warnings was vigorously opposed by the tobacco industry, whose internal research indicated that many smokers disliked their prominence and more detailed content.2 Internationally, the track record of the tobacco industry has been to oppose more "hard-hitting", specific warnings in favour of blander, more general warnings such as "Smoking reduces your fitness". We propose a new "hard-hitting" cigarette pack warning. Recent population-based cross-sectional data from four countries3-6 including Australia,7 together with data from two large cohort studies,8,9 have consistently identified smoking as the strongest environmental risk factor for age-related macular degeneration (AMD), the leading cause of blindness in Australia.10,11 All of these studies have shown that people who currently smoke are two to five times more likely to develop AMD than non-smokers or past smokers, and several have demonstrated a dose-response relationship with pack-years of smoking,6,8,9 and a decreased risk with longer duration since cessation.4 Evidence of a gradient between amount smoked and AMD severity has also been shown.4,7 Based on data from two large population-based Australian studies,12,13 there are currently around 34 500 Australians aged over 50 years with legal blindness (ie, they qualify for blind pension benefits because visual acuity in both eyes is reduced to < 6/60). In over 80% of these people, blindness is due to AMD.12 Two late stage AMD lesions causing visual loss have been defined: "neovascular AMD", characterised by macular haemorrhage and scarring (responsible for two-thirds of cases), and "geographic atrophy", an atrophic macular lesion which accounts for the remaining third.11 Increasing age is the strongest risk factor for AMD, with the prevalence of late stage lesions rising from under 1% in people aged less than 70 years to over 10% in over-80-year- olds and more than one third in over-90-year-olds.12 To date, longitudinal data relating smoking to the incidence of AMD are less conclusive than cross-sectional population-based studies. Both the Nurses' Health Study8 and the Physicians' Health Study,9 however, relied on self-reported diagnosis of AMD. The Macular Photocoagulation Study report14 did not find an association between a history of current smoking at the start of the trial and incidence of AMD, but there may have been selection bias in the recruitment of patients to a laser treatment trial. Follow-up examinations have now been performed in three of the four population-based cohorts3,4,7 to assess risk factors for AMD. Of these, the Beaver Dam Eye Study is the only cohort yet to report incidence data.15 This study found that, in both men and women, smoking was related to the incidence of large drusen, the principal precursor lesion for late stage AMD lesions.16 Individually, each of the three studies has relatively low statistical power to examine risk factors for incident late stage AMD lesions, so that pooling of data may be useful. Despite the present lack of firm incidence data, all of the recent cross-sectional studies show a consistency of findings that is difficult to ignore. We estimate that there are currently almost 100 000 people with late stage AMD in Australia, of which around 20 000 may have AMD directly attributable to smoking. Further, we estimate that there are currently more than 8200 Australians whose blindness from late stage AMD can be attributed to smoking. These estimates, shown in the Table, are based on Australian data collected in the Blue Mountains Eye Study. Population-attributable risk estimates were derived from odds ratios adjusted for age and sex.7 We repeated the calculations using risk ratios from the Beaver Dam and Rotterdam studies,3,4 and these separately provided evidence that around 10 000 Australians are currently likely to be blind as a result of smoking. As our population ages, the prevalence of AMD and age-related blindness will increase. At present, the only preventable confirmed risk factor for AMD is smoking. We estimate that smoking may now be responsible for around 20% of all cases of blindness in Australians over the age of 50 years. As 80%-90% of blindness in Australia occurs in those over 50 years, there is a similar overall proportion of people blind as a result of smoking. Most Australian smokers are aware that smoking is harmful to health. However, knowledge of the role of smoking in causing many specific diseases is unacceptably low. For example, a Victorian study found that the percentage of smokers able (unprompted) to nominate specific conditions linked to smoking was 54% (lung cancer), 38% (emphysema), 38% (heart attack), 20% (unspecified cancer), 17% (asthma), and 22% (bronchitis/respiratory problems).17 While research has shown dramatic increases in recognition of cigarette pack warnings, only 66% of Australian smokers say that they "at least sometimes notice" the current warnings.18 There is clearly room for improvement. Pack warnings that are novel and targeted at the concerns of specific population subgroups are likely to have greater impact than blander, older and more general warnings.19 As further epidemiological evidence becomes available on the role of smoking in causing specific diseases, it is important that this is reflected in public information campaigns and warnings. For example, on 5 November 1998, the Thai government required "Smoking causes impotence" to be included among the mandated warnings appearing on cigarette packs. There is no treatment for the majority of AMD cases, and support services for blind people are very costly. The eyes are popularly venerated as "mirrors to the soul" and blindness is greatly feared. Everyone can imagine what it would be like to be blind. If "Smoking is a major cause of blindness" were added to the current Australian set of health warnings, some smokers might reconsider their continued tobacco use. Paul Mitchell Associate Professor, Department of Ophthalmology University of Sydney, Sydney, NSW Simon Chapman Associate Professor Department of Public Health and Community Medicine University of Sydney, Sydney, NSW Wayne Smith Senior Research Fellow National Centre for Epidemiology and Population Health Australian National University, Canberra, ACT Email: paulmiATwestmed.wh.su.edu.au Acknowledgement: The Blue Mountains Eye Study was supported by the National Health and Medical Research Council and the Save Sight Institute, University of Sydney Borland R, Hill D. The path to Australia's tobacco health warnings. Addiction 1997; 92: 151-157. <http://www.pmdocs.com/getallimg.asp?DOCID=2504091432/1443> and <http://www.health.su.oz.au/tobacco/Ozdocs.html#Plain packaging> Klein R, Klein BE, Linton KL, DeMets DL. The Beaver Dam Eye Study: the relation of age-related maculopathy to smoking. Am J Epidemiol 1993; 137: 190-200. Vingerling JR, Hofman A, Grobbee DE, de Jong PT. Age-related macular degeneration and smoking. The Rotterdam Study. Arch Ophthalmol 1996; 114: 1193-1196. Klaver CC, Assink JJ, Vingerling JR, et al. Smoking is also associated with age-related macular degeneration in persons aged 85 years and older: The Rotterdam Study [letter]. Arch Ophthalmol 1997; 115: 945. Delcourt C, Diaz JL, Ponton Sanchez A, Papoz L. Smoking and age-related macular degeneration. The POLA Study. Arch Ophthalmol 1998; 116: 1031-1035. Smith W, Mitchell P, Leeder SR. Smoking and age-related maculopathy. The Blue Mountains Eye Study. Arch Ophthalmol 1996; 114: 1518-1523. Hankinson SE, Willett WC, Colditz GA, et al. A prospective study of cigarette smoking and risk of cataract surgery in women. JAMA 1992; 268: 994-998. Christen WG, Manson JE, Seddon JM, et al. A prospective study of cigarette smoking and risk of cataract in men. JAMA 1992; 268: 989-993. Cooper RL. Blind registrations in Western Australia: a five year study. Aust N Z J Ophthalmol 1989; 107: 875-879. Mitchell P, Smith W, Attebo K, Wang JJ. Prevalence of age-related maculopathy in Australia. The Blue Mountains Eye Study. Ophthalmology 1995; 102: 1450-1460. Attebo K, Mitchell P, Smith W. Visual acuity and the causes of visual loss in Australia. The Blue Mountains Eye Study. Ophthalmology 1996; 103: 357-364. Taylor HR, Livingston PM, Stanislavsky YL, McCarty CA. Visual impairment in Australia: distance visual acuity, near vision, and visual field findings of the Melbourne Visual Impairment Project. Am J Ophthalmol 1997; 123: 328-337. Macular Photocoagulation Study Group. Risk factors for choroidal neovascularization in the second eye of patients with juxtafoveal or subfoveal choroidal neovascularization secondary to age-related macular degeneration. Arch Ophthalmol 1997; 115: 741-747. Klein R, Klein BE, Moss SE. Relation of smoking to the incidence of age-related maculopathy. The Beaver Dam Eye Study. Am J Epidemiol 1998; 147: 103-110. Klein R, Klein BE, Jensen SC, Meuer SM. The five-year incidence and progression of age-related maculopathy: the Beaver Dam Eye Study. Ophthalmology 1997; 104: 7-21. Mullins R, Morand M, Borland R. Key findings of the 1994 and 1995 household surveys. Quit Evaluation Studies Number 8, 1994-1995. Melbourne: Centre for Behavioural Research in Cancer, 1996. Borland R. Tobacco health warnings and smoking-related cognitions and behaviours. Addiction 1997; 92: 1427-1435. Fischer PM, Krugman DM, Fletcher JE, et al. An evaluation of health warnings in cigarette advertisements using standard market research methods: what does it mean to warn? Tob Control 1993; 2: 279-285. Reprints: Professor P Mitchell, Department of Ophthalmology, University of Sydney, Hawkesbury Road, Westmead, NSW 2145. Projected estimates of age-related macular degeneration (AMD) and blindness in Australia due to smokingSmoking prevalence §Sex, Age (years)Population at risk (1999)*Estimated no. of AMD cases †Estimated no. blind from AMD ‡FormerCurrentF, 55-59461 6001 385023.5%20.5%F, 60-69728 0204 25930423.8%14.5%F, 70-79601 48019 5476 03128.2%11.6%F, 80+352 52047 09219 20621.1%4.0%M, 55-59476 1600037.7%25.5%M, 60-69714 6201 980055.3%16.5%M, 70-79493 44010 5571 98757.1%13.0%M, 80+189 78014 0912 87434.1%4.5%Total4 017 62098 91130 402Estimated risk of AMD in smokers compared with never smokers (odds ratio) §Sex, age in (years)FormerCurrentAttributable risk for AMD in (former and current) smokers ¶Estimated no. of AMD cases due to smoking**Estimated no. blind from smoking**F, 55-591.25.653.0%7420F, 60-691.25.644.6%1 898136F, 70-791.25.640.1%7 8482 410F, 80+1.25.619.6%9 2253 765M, 55-591.63.161.0%00M, 60-691.63.168.1%1 3470M, 70-791.63.147.0%4 958933M, 80+1.63.125.6%3 610992Total20 4038 236 * Estimated Australian Population in 1999 interpolated from 1996 Census and 2001 projected population. † Based on Blue Mountains Eye Study prevalence estimates,11 using 5-year age-specific prevalence rates. ‡ Based on Blue Mountains Eye Study visual impairment data,12 assuming that 88% of age-related blindness is caused by AMD. § Based on Blue Mountains Eye Study smoking prevalence data.7 ¶ Calculated using formula: (smoking prevalence) x (odds ratio 2 1) {1 + (smoking prevalence) x (odds ratio2 1)}. ** Calculated from estimated numbers (AMD and blind) multiplied by percentage attributable risk. 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Paul Mitchell · Simon Chapman · Wayne Smith

Telemedicine ophthalmology consultation in remote Queensland Nikki A M Blackwell, Graeme J Kelly and Lee M Lenton MJA 1997; 167: 583-586 Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - ©MJA1997 Abstract Objective: To assess the use of remote telemedicine ophthalmology in patients presenting to an emergency department with acute eye problems. Design: A prospective review from 1 December 1996 to 28 February 1997 of referral patterns and telemedicine consultations, comparing referral patterns with the same period one year before. Participants and setting: 24 patients presenting to the emergency department of a remote base hospital in Queensland with an acute ophthalmological problem requiring a specialist opinion. Main outcome measures: Clinical outcomes; use of the Patient Transit Scheme for isolated patients; acceptability to patients and doctors; and ophthalmologists' opinions of the system. Results: No adverse outcomes were identified. Patients transferred for urgent assessment fell from 17 for the corresponding period in the previous year to four during the study period, while respective numbers of patients requiring non-urgent transfers (for surgery or postoperative review) during the same periods were 41 and 30. Both patients and staff (including the ophthalmologists) found the telemedicine facility very acceptable. Conclusion: Ophthalmology is well suited to telemedicine for the diagnosis and management of acute conditions and postoperative assessment of patients in remote areas. It offers considerable potential benefits to patients, and enhances the skills of local practitioners. Introduction Telemedicine is "the use of transmitted images, voice and other data to permit consultation, education and integration in medicine over a distance".1 This technology is increasingly viewed as a means of improving specialist services to rural and remote parts of Australia,2 but there are few published studies about the clinical outcomes of telemedicine services.3,4 Critics often cite inability to examine the patient as a reason why telemedicine does not substitute for face-to-face specialist consultation.5 However, in medical specialties that depend heavily on visual observation, such as dermatology or radiology,3,4,6 telemedicine has been shown to be an effective means of providing accurate specialist opinion. Ophthalmology is another specialty which lends itself well to televised con sultation, and acute problems in ophthal mology are an area where telemedicine may augment existing specialist services. Many ocular conditions present acutely and require immediate specialist referral. While the remote town of Mt Isa, in central Queensland, has a visiting specialist ophthalmology service, the clinics are too infrequent to be useful for acute problems. Consequently, patients with acute ocular disease often require transfer to Townsville, 900 km away, for specialist consultation. In 1996, Mt Isa Base Hospital transferred 196 ophthalmology patients, representing almost 25% of the total patients transported under the Patient Transit Scheme in that year. Based on the cost of a return flight to Townsville of $500, and not allowing for the costs of patient escorts or accommodation, the cost to the hospital was approximately $100 000. Following the generous donation to Mt Isa Base Hospital of a slit lamp with a camera facility by OPSM (Optical Prescription Spectacle Makers Industries Limited) in October 1996, we conducted a three-month evaluation of remote consultation for ocular conditions. Our aim was to examine clinical outcome, the effect on Patient Transit Scheme use and expenditure, acceptability to both patients and doctors, the ophthalmologist's evaluation of the transmitted slit-lamp images, and any problems encountered with the system. Methods All patients presenting to Mt Isa Base Hospital (i.e., a non-metropolitan hospital serving a number of smaller health care facilities) with acute eye conditions from 1 December 1996 to 28 February 1997 were assessed by the Emergency Department Director. Patients with a clear indication for immediate referral (e.g., penetrating eye injury) were transferred to Townsville as usual. For those requiring specialist ophthalmological opinion, a telemedicine consultation was arranged during normal working hours within 24 hours of presentation. Each patient was examined by slit lamp at Mt Isa Base Hospital, while a high resolution televised image was assessed simultaneously by the specialist in Townsville, in voice and visual contact with the patient and local practitioner (see Figure). After the consultation, the recommended treatment was initiated and local follow-up was arranged as necessary. Patients could be discharged, referred to the visiting ophthalmology clinic, or transferred to Townsville if necessary. In addition, the ophthalmologists arranged for patients who required routine postoperative review during the study period to be assessed on the telemedicine link rather than having to travel to Townsville for an outpatient consultation. To gauge the impact of the telemedicine system on use of the Patient Transit Scheme by ophthalmology patients presenting to the emergency department, the study period was compared with the corresponding three-month period in the previous year. Acceptability of the telemedicine system to patients and doctors was assessed informally by staff in discussion with patients. Results During the three months of the study, 264 patients presented to the emergency department with an acute eye condition, of whom 24 (or 9%) were considered to require specialist ophthalmology referral, which was then carried out by telemedicine. By comparison, 315 patients had presented in the corresponding period in the previous year, with 17 (or 5.4%) having been transferred urgently to Townsville, and a further 5%-10% being managed after a telephone consultation with an ophthalmologist, without the use of telemedicine. Patient outcomes Our experience with the 24 patients who had telemedicine consultations (31 consultations in all) is shown in Box 1. No patient had an adverse clinical outcome as a result of being assessed by telemedicine rather than face-to-face in Townsville. For the first six patients in Box 1, management was altered as a result of the consultation, and transfer was avoided. For the next 12, management was continued locally as planned and transfer was avoided. For the next four patients, treatment was altered and urgent transfer arranged. For the remaining two patients, treatment was unchanged after telemedicine consultation. Patient transfer Box 2 shows number of ophthalmology patients transferred urgently and non-urgently (for surgery or postoperative review) during the study period and the corresponding period in the previous year. Overall, four patients were transferred for urgent assessment during the study period, compared with 17 for the corresponding period in the previous year. Another four patients were referred to the next local visiting ophthalmology clinic as their problems were not urgent. Comparing the numbers of patients requiring urgent transfer for the two periods (4 v. 17), and based on the costings described above, the hospital saved $6,500 over the three months of the study. In addition, five patients were reviewed locally after surgery (the two children with strabismus correction were seen twice) instead of returning to Townsville, representing a total saving to the Patient Transit Scheme budget of approximately $10 000 over the three months. Acceptability Frail elderly patients who had undergone cataract extractions were happy to avoid a further trip out of Mt Isa. Similarly, the patients who had strabismus correction were all young children with siblings, and it was very convenient for them to be seen locally. Indeed, as previously documented,7-9 all patients seemed to respond well to the new technology, with no patient refusing a teleconsultation, and all saying that in the future they would prefer such a consultation over travelling to Townsville for review. Medical and nursing staff in Mt Isa were enthusiastic about the new facility, often arranging their work so that they could be present at a teleconsultation. The ophthalmologists in Townsville found that the quality of the transmitted slit-lamp image was of sufficiently high quality to allow definite diagnosis in all cases. Discussion Our pilot study indicates that ophthalmology by telemedicine can provide a clinically effective and resource- efficient means of augmenting a specialist service in a rural area. There were no adverse outcomes related to the use of the technology. Indeed, the service for patients seemed to improve, with specialist consultation being provided within 24 hours, allowing appropriate management to be promptly initiated. The ophthalmology telemedicine system, which could be applied across rural Australia, needs local practitioners willing to acquire basic expertise in eye examination, and use of the slit lamp and tonometer. Successful use of the technology requires skilled practitioners at both ends of the transmission10 generating and interpreting slit-lamp images. Yellowlees and Kennedy have identified several key ingredients for successful telemedicine systems.2 Many of these already existed in Mt Isa: an ISDN (Integrated Services Digital Network) videoconferencing system had been in place for two years; many medical and nursing staff had received training in the use of the system; telemedicine remains an initiative strongly supported by the hospital executive; there was enthusiasm for the project in both Mt Isa and Townsville; and Mt Isa Base Hospital employs an Information Technology Coordinator. The success of this new service relied heavily on the enthusiasm and commitment of all involved to ensure that the time of specialists (who donated their services) was not wasted, and that busy practitioners could rely on agreed appointments reflecting accurately the timing and duration of consultations. We found proper notekeeping to be of major importance. Unlike Kavanagh and Yellowlees, who provided case management referral letters after televised psychiatry interviews,11 we have not yet been able to organise specialist letters after ophthalmology teleconsultation because of time, cost and reimbursement issues. Hence, it was the responsibility of the local practitioner who attended the consultation with the patient to document the diagnosis and management plan. The fact that telemedicine is not covered by Medicare is likely to act as a barrier to its widespread development. This has been shown to be the case with several telemedicine applications in the United States.2,11-13 While the ophthalmologists involved in this study donated their time, the question of remuneration must ultimately be addressed. The great sense of camaraderie generated by the improved contact between health professionals was an unexpected benefit of the telemedicine system. As has been suggested,2 the use of telemedicine may decrease the professional isolation of rural doctors by providing an interactive medium for medical education focused on immediate clinical management. The telemedicine facility at Mt Isa Base Hospital will continue to be used for informal ophthalmology teaching, with medical and nursing staff encouraged to attend consultations. In addition, a telemedicine link to a day surgery unit in Townsville is currently being used to train theatre staff for the planned introduction of cataract surgery to Mt Isa. Finally, all users of telemedicine should be encouraged to evaluate their services to ensure that they are meeting a clinical need and not just being driven by the technology. Users should be mindful of the lessons from the extraordinary growth of laparoscopic surgery,14 where practitioners have only recently begun to address clinical outcomes after laparoscopy in appropriately designed studies. Rather than being seduced by the promise of the new, technology must be harnessed to help improve patient care. Acknowledgements We thank Shaun Anderson and OPSM for donating the equipment. Disclaimer of conflict of interest: The authors declare no conflict of interest. OPSM donated the equipment, but had no part in planning the study, analysing the results or preparing the manuscript. References Merrell RC. Telemedicine in the 90's: Beyond the Future. J Med Sys 1995; 19: 15-18. Yellowlees PM, Kennedy C. Telemedicine: here to stay. Med J Aust 1997; 166: 262-265. Warren FM, Lesher JL, Hall JH, et al. Telemedicine. J Family Practice 1995; 41: 17-20. Ferrer-Roca O, Diaz-Cardama A, Pitti S, et al. Tele- medicine in the Canary Islands. Lancet 1995; 345: 1177-1178. Appleby C. Telemedicine -- a prison plugs in. Hosp Health Netw 1995; 69: 56. Binkhuysen FH, Ottes FP, Valk J, et al. Remote expert consultation for MRI procedures by means of teleradiology. Eur J Radiol 1995; 19: 147-150. Bergman R. Letting Telemedicine do the walking. Hosp Health Netw 1993; 67: 46-48. Harrison R, Clayton W, Wallace P. Can telemedicine be used to improve communication between primary and secondary care? BMJ 1996; 313: 1377-1380. Telemedicine: fad or future? [editorial]. Lancet 1995; 345: 73-74. Wootton R. Telemedicine: a cautious welcome. BMJ 1996; 313: 1375-1377. Kavanagh SJ, Yellowlees PM. Telemedicine -- clinical applications in mental health. Aust Family Physician 1995; 24: 1242-1247. Grigsby J. Current status of domestic telemedicine. J Med Systems 1995; 19: 19-27. Puskin DS. Opportunities and challenges to telemedicine in rural America. J Med Systems 1995; 19: 59-67. Johnson A. Laparoscopic surgery. Lancet 1997; 349: 631-635. (Received 17 Apr, accepted 29 Jul 1997) Authors' details Mt Isa Base Hospital, Mt Isa, QLD. Nikki A M Blackwell, MRCP(UK), Director of Emergency Department. Hyde Park Centre, Woolcock Street, Hyde Park, Townsville, QLD. Graeme J Kelly, FRACO, FRACS, Ophthalmologist; Lee M Lenton, FRACO, FRACS, Ophthalmologist. No reprints will be available. Correspondence: Dr N A M Blackwell, Director of Emergency Department, Mt Isa Base Hospital, Mt Isa, QLD 4825. - ©MJA 1997 Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

Graeme J Kelly · Lee M Lenton

Visual impairment: a correctable global problem For many in developing countries, treatment may be as simple, and as difficult to obtain, as spectacles MJA 1997; 167: 351-352 Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au/>". - - ©MJA1997 Preventable blindness is one of our most tragic and wasteful global problems, restricting the employment and life prospects of otherwise healthy people, and placing unnecessary strain on families and social welfare systems. Blindness and uncorrected low vision affect every aspect of the social and economic welfare of people and countries -- they impede learning in children and may prevent adults finding employment, in turn adding to the burden on welfare resources. Although it may be relatively simple to correct a visual defect, vision restoration is often not a priority in countries where major life-threatening illnesses are common health care problems. The most wasteful problem in vision restoration is the lack of refraction and spectacles for those who need them Over the past few years, great advances have been made in this area by the alliance of non-government organisations (such as the Partnership Committee of Nongovernmental Organizations), government agencies, private organisations, the World Health Organization, and the World Bank Development Agency. Programs have now been put in place to tackle blindness and visual rehabilitation in a systematic, cost-effective way. Typical of one such effort is the Nepal Prevention and Control of Blindness Project. The high prevalence of cataract blindness in Nepal sparked development of a program to replace cataracts with intraocular lenses. The combination of overseas experts to provide surgical expertise, training, planning and coordination, together with low-cost intraocular lenses from the Fred Hollows Foundation manufacturing facility in Katmandu, have dramatically reduced cataract blindness in Nepal (Dr Ram Prasad Pokhrel, President, Asia-Pacific Academy of Ophthalmology, personal communication). The problem: However, in many areas, such as the Indian subcontinent, it is extremely hard to keep pace with eyecare needs because of rapid population growth, maldistribution of ophthalmic personnel and the difficulty in recompensing ophthalmologists for dealing with the massive backlog of cataract blindness, the major type of preventable blindness today.1 In Asia, the number of eyecare practitioners (all professions, including ophthalmologists, optometrists and opticians) is only 12 per million population, and in Africa it is only three per million, and even worse in many rural areas.1 Ratios are slightly better in the Middle East (47), South America (88) and Eastern Europe (108). In contrast, the ratio of eyecare practitioners per million population in developed countries ranges from 151 (Western Europe), to 245 (Pacific region), 262 (North America) and 444 (Japan).1 The lack of practitioners and services is the main reason for the high prevalence of blindness and other vision problems in many developing countries. The prevalence of blindness in Africa is 1.4% of the population, seven times greater than in developed countries, while in the Middle East it is 1.2%.1 However, about 90% of the vision problems in the world today are treatable or preventable (see Figure). The intervention of a trained eyecare professional can stop disease progression, correct defects or restore sight by surgery. Figure: Major causes of visual impairment worldwide1 (figures refer to millions of people). The most wasteful, and certainly the most common, problem in vision restoration is the lack of refraction and spectacles for those who need them. Most of those with impaired vision worldwide simply require correction of refractive errors, but for many in developing countries this is either not available or inadequate. Even presbyopia becomes a debilitating condition for the aged. The lack of vision care services was highlighted by the recent estimate that half the children in blind institutions in Africa were there because they had never been refracted (Dr Allen Foster, International Centre for Eye Health, Institute of Ophthalmology, London, personal communication). In fact, they were found to be reading Braille by seeing the dots up close rather than by feeling them! Low vision is less known in the community as a cause of debilitation compared with blindness, and funding for its alleviation is more difficult to obtain. However, international agencies are increasingly emphasising the need for commitment to this area. Institutional low vision clinics, which can provide low vision aids (such as magnifiers and telescopes), as well as refraction and spectacles when appropriate, need to be established throughout the developing world, especially in Africa. These could meet local needs by harnessing the skills and knowledge of experts in this area. What needs to be done? Crucial to improving eyecare in developing countries is the provision of well balanced eyecare teams that can effectively deliver quality care. A current model of such a community eyecare team, used by the L V Prasad Eye Institute in Hyderabad, India, provides one ophthalmologist, four optometrists, eight eyecare workers, eight ophthalmic assistants, and 16 ophthalmic nurses per 500 000 people. The number of trained eyecare practitioners in developing countries must be increased. To this end, the World Health Organization has set regional targets for ophthalmologists and optometrists.2 While making practitioners available on a part-time or temporary basis in outreach clinics is an important immediate measure for improving eyecare, long term improvement requires that they be permanently available to the community. To achieve this level of practitioner availability, high quality training programs must be established to produce new eyecare practitioners and enhance the knowledge and skills of existing practitioners. These programs should include continuing professional education to ensure that practitioners are kept up-to-date with the latest techniques and equipment. Infrastructure to support these training programs must be established which includes local institutions, associations, industry and service groups. It is also important that practitioners be widely distributed throughout the countryside. In many developing countries, most practitioners work in the capital cities rather than rural areas. Another essential strategy is the education of eyecare educators. Teaching teachers and providing them with educational resources will ensure the continuation and development of eyecare education in developing countries. These educational initiatives will help improve delivery of eyecare to the population, not only in the form of initial diagnosis and treatment, but in ongoing patient support. Ultimately, education is the means to prevent blindness worldwide. Brien A Holden Professor and Director, Cooperative Research Centre for Eye Research and Technology, University of New South Wales, Sydney, NSW Gullapalli N Rao Director, L V Prasad Eye Institute, Hyderabad, India President, Asia-Pacific Division of the International Agency for Prevention of Blindness Kylie M Knox Manager, Cooperative Research Centre for Eye Research and Technology University of New South Wales, Sydney, NSW Sylvie M Sulaiman Director of Education, International Association of Contact Lens Educators Delegate to the WHO Partnership Committee of Nongovernmental Organizations for Prevention of Blindness International Association of Contact Lens Educators. IACLE demographics report, 1995. Sydney: IACLE, 1996. Partnership Committee of International Non-Governmental Organizations dedicated to the Prevention of Blindness and the Education and Rehabilitation of the Blind. World Health Organization global initiatives plan for prevention of blindness. Geneva: WHO, 1997. ©MJA 1997 <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

Brien A Holden · Gullapalli N Rao · Kylie M Knox · Sylvie M Sulaiman