Ophthalmology

To the Editor: We believe the study by Kirkwood et al,1 investigating the use of nurse-led perioperative cataract clinics, contains flaws, and their conclusions are premature. The authors do not explain the reduction in elective surgery waiting times. Use of a nurse-led clinic should not affect surgical throughput, which is dictated by surgeon and theatre availability. The rate of postoperative complications with cataract surgery is very low.2,3 An assessment of the concordance in management between the nurse practitioner and ophthalmologist would therefore only be possible if a large number of patients were compared, not just the 18 used in the study. The authors do not justify the statements “a nurse practitioner might be more . . . experienced in managing patients with ophthalmic conditions” [than a junior registrar] and “the experienced nurse practitioner might be more efficient in use of consumables and investigations” by reference to their own clinic or the literature. In our opinion, a medical practitioner is best placed to understand and make these decisions. In Queensland, registrars perform or observe most cataract operations done in public hospitals. It is important for their training to see these patients both before and after surgery,4 making the presence of a nurse practitioner unnecessary. If the authors are interested in increasing the efficiency of the process, they could reduce unnecessary clinic visits, which is very relevant here in Australia given that patients may have to travel great distances for operations. The two preoperative visits proposed in the authors’ model could be replaced by one. Standardised referral forms can be used for screening, and facilities can be put into place so that all necessary tests can be performed on the same visit for eligible patients. The 4-week visit can be eliminated if the patient’s dispensing optometrist is aware of the expected postoperative visual acuity and can readily refer back if there are any concerns. Although the model outlined by Kirkwood et al has merits, the conclusions are misleading. Health care providers and governments must find ways to deliver high quality care during this period of workforce shortages. This should be achieved by increasing efficiency, while preserving doctor training opportunities, rather than through role substitution.

Hamish D R McKee · Glen A Gole

In reply: The points made by McKee and Gole are valid. However, the demand for eye-care services is outstripping the ophthalmological workforce. Some task substitution is necessary. The effect of the nurse-led cataract clinic has been largely to increase patient access to outpatient appointments — it helps deal with a large hidden waiting list (time to first clinic appointment), and frees up ophthalmologists to spend more time in the operating room. Registrars in training are not likely to cope with an increasing demand for services. The number of trainees is determined by the Royal Australian and New Zealand College of Ophthalmologists. Flinders Medical Centre sees 15 000 eye outpatients a year and does 1500 elective procedures — and has been allocated one first-year trainee. The nurse practitioner is more experienced and does not rotate to another hospital every few months. Nurse practitioners may not be the preferred substitute for ophthalmologists. The employment conditions of nurses can be restrictive, and senior nurses are expensive to employ compared with other professionals, such as orthoptists and optometrists. Perhaps McKee and Gole are more comfortable with the use of professionals other than nurses, as they advocate the involvement of optometrists to decrease the load on outpatient clinics.

Bradley J Kirkwood · Konrad Pesudovs · Paul Latimer · Douglas J Coster

Primary care ophthalmology. 2nd ed. David A Palay, Jay H Krachmer. Philadelphia: Elsevier Mosby, 2005 (xvi + 395 pp). ISBN 0 323 03316 4. I was pleasantly surprised at the balanced approach achieved in this book by its American ophthalmologist authors. As a reference book, it delivers as much detail as most primary care practitioners would seek, without getting bogged down in minutiae. At about 400 pages, lightened by abundant photographs, Primary care ophthalmology goes a bit beyond being just a primer. Many of the segments invite browsing, whereas others would only be consulted for a specific topic. There is an emphasis on management at a general practice level, together with clear guidelines on when specialist referral is needed. The urgency of timing of referrals and the frequency of specialist reviews often seems a bit excessive, but this may reflect the American environment. Similarly, the range of medications reflects availability there, especially in antibiotics. The initial sections on examination, differential diagnosis, and the acute red eye are well presented and would also be useful to medical students. Skills varying from as mundane as everting eyelids up to applanation tonometry are clearly described. Much of the rest of the book is anatomically arranged, with brief anatomy refreshers and then succinct disease descriptions, each with differential diagnoses, investigation, treatment and follow-up recommendations. Ophthalmology has not completely seceded from the rest of medicine, and the excellent section on systemic disease reflects this. The systemic drug toxicity segment is clearer than I’ve seen anywhere else. Another highlight is the chapter on the manifestations of ocular trauma and its management. Overall, this is a very useable, good-value and readable reference with good photographic illustrations. Its main role would be in general practice, but emergency departments would also find it useful. The limitations of the American pharmacopoeia don’t really take away from the book, and I don’t think it will date quickly. Malcolm J BurvillOphthalmologist, Mount Lawley, WA

Malcolm J Burvill

Age-related macular degeneration (AMD) is the leading cause of irreversible blindness in Australia and other Western countries. As there is no cure for AMD, and treatments to stop its progression have met with limited success, there is an interest in identifying modifiable risk factors to prevent or slow disease progression. To date, smoking is the only proven modifiable risk factor for AMD. Other factors under study include (i) cardiovascular risk factors such as hypertension, body mass index, and atherosclerosis; and (ii) dietary risk factors including fat and antioxidant intake, but so far these studies have produced conflicting results. Dietary fat in relation to AMD has recently attracted media attention. Despite very limited work supporting an association between vegetable fat and AMD, widespread publicity advocating margarine as a cause of AMD and encouraging use of butter instead has caused confusion and anxiety among sufferers of AMD and the general public, as well as concern among health professionals. The antioxidant carotenoids — lutein and zeaxanthin — found in dark green or yellow vegetables exist in high concentrations in the macula and are hypothesised to play a protective role. Of nine controlled trials of supplementation with carotenoids and other antioxidants, three suggested that various combinations of antioxidants and carotenoids were protective. While a low-fat diet rich in dark green and yellow vegetables is advocated in general, any specific recommendations regarding certain fats or antioxidant supplementation and AMD are not based on consistent findings at this stage.

Robyn H Guymer RANZCO, PhD, MB BS · Elaine Wei-Tinn Chong MB BS

Objective: To describe the implementation of a nurse-led preoperative cataract assessment and postoperative care clinic and to assess the safety, efficacy and outcomes.Design, setting and participants: A prospective study involving 185 public patients (221 eyes) referred to the Department of Ophthalmology at Flinders Medical Centre for cataract surgery. The study was conducted between February 2003 and August 2004.Interventions: Patients were assessed in the nurse-led preoperative assessment clinic. Those deemed suitable for cataract surgery were also assessed by an ophthalmologist and underwent cataract surgery if appropriate. The nurse managed postoperative care.Main outcome measures: Concordance between nurse practitioner and ophthalmologist assessments; waiting times for first clinic appointment and surgery; visual acuity and degree of visual disability; patient satisfaction.Results: 114 patients (61.6%) were assigned to see the ophthalmologist for cataract surgery. Median waiting times fell from 115 days (range, 23–268 days) to 21 days (range, 9–43 days) for initial clinic appointment, and from 44 days (range, 5–148 days) to 29 days (range, 14–154 days) for surgery. All 114 patients were listed for cataract surgery, and surgery had been performed on 121 eyes by the end of the study. After surgery, visual acuity improved by a mean of 0.45 logMAR (logarithm of the minimal angle of resolution) (SD, 0.24; range, 0.08–1.32). All patients had improved visual ability and high levels of satisfaction. Three quality assurance evaluations demonstrated full concordance between nurse and ophthalmologist assessments.Conclusions: Implementing a nurse-led cataract assessment clinic improved access to care for public patients with cataracts. The safety and efficacy of the program and its excellent visual and patient-centred outcomes commend its adaptation and implementation to other ophthalmology departments.

Bradley J Kirkwood MA · Konrad Pesudovs PhD · Paul Latimer FRCOphth · Douglas J Coster FRANZCO, AO

John Colvin made an outstanding contribution to ophthalmology in Australia. He also (with the technical assistance of spectacle maker Martin Hogan) played a role in the successful US Apollo space flights and extended the flying time of Royal Australian Air Force (RAAF) and civilian airline pilots. Born on 14 January 1929 in Hobart, John was educated mainly in Queensland. After graduating in medicine at the University of Queensland in 1953, he spent 5 years in England training in ophthalmology, spending part of that time at the Leeds General Infirmary. Returning to Melbourne in 1961, he entered private practice and was appointed to the honorary staff of the Royal Victorian Eye and Ear Hospital. On Saturday mornings at the hospital he gave free lectures to medical students (whose attendance was voluntary). He estimated that, over a period of 37 years, he gave 1000 lectures to 12 000 students. In recognition of this unique service, the hospital’s management committee named the John Colvin Clinical School in his honour. John joined the University of Queensland Air Squadron in 1950 and gained a pilot’s licence in 1954. As an RAAF reservist, John became consultant ophthalmologist to the RAAF, serving for 45 years and reaching the rank of group captain. He designed spectacles that allowed presbyopic Air Force and airline pilots to read instruments above their line of sight, thus enabling them to continue to meet visual standards. He also designed spectacles with polycarbonate lenses that could withstand high gravitational forces, as well as an anti-glare docking aid, that were adopted by the US National Aeronautics and Space Administration (NASA) for its astronauts. He was invited to be a keynote speaker at an aerospace conference in Las Vegas, and visited NASA at Cape Kennedy. For 25 years, John gave honorary service to Royal Flying Doctor Service clinics from Broken Hill to the Queensland border. A dedicated teacher, he lectured to the Royal Australian College of General Practitioners, the College of Pharmacy, the Mobile Intensive Care Ambulance Service, and dental and nursing students. He was also a visiting speaker in New Zealand, Fiji, New Guinea and Vietnam, where he advised Air Vietnam on the selection of pilots. His pamphlet “Golden eye rules” was distributed to hospitals and general practices, and was translated into many languages. His article “Effective management of penetrating eye injuries in remote Australia”1 became the basis of standard practice. In his spare time, John enjoyed watching football. He was a supporter of the Hawthorn Football Club and its honorary ophthalmologist, and received the Club’s Service Award. Disabled by a stroke in 1995, John died on 7 August 2005 after a long period of failing health. He is survived by his wife Sylvia and their three children, David, Alan and Andrea.

Derek Meyers MBBS, MD, FRACP

An ophthalmologist who made an enormous contribution to improving eye care in Central Australia, Wilfred Win Law died suddenly on 11 October 2005 as the result of a stroke. Wilfred was born on 11 June 1930 in Rangoon, Burma. He graduated from Rangoon University in 1955, after which he received postgraduate training in ophthalmology in London. After working at the Royal Victorian Eye and Ear Hospital, Melbourne, in 1977, he spent 6 years in Hong Kong before moving to Alice Springs in 1984 to take up the position of Senior Specialist Ophthalmologist at Alice Springs Hospital. For the next 21 years, until his death, he devoted himself to establishing a sustainable eye care service in Central Australia — a service that was badly needed. Through his considerable energy and dogged persistence, Wilfred built up a substantial ophthalmology service based in Alice Springs. Recognising the paramount need to achieve a sustainable pattern of activity, he committed himself to stay for the long term. He realised that a resident specialist would always be able to achieve more than a visitor. He also recognised the value of teaching and training the next generation. Like all good teachers, he was a generous man, prepared to pass on in a few minutes something that he may have taken decades to learn. He also had a well developed sense of responsibility. This he attributed to his traditional oriental upbringing. He felt he was fortunate to have been given the talent to study medicine and the opportunity to do so. In recognition of this privilege, he chose to practise medicine for as long as he could do it well — and he did, until the day he died. Wilfred taught not by preaching but by example. If he was consulted by junior emergency staff, even in the middle of the night (as was often the case), he was always prepared to attend the hospital — replete in coat and tie. The junior staff loved him for his generosity, wisdom and after-hours support. To them he was more a mentor than a clinical supervisor. Wilfred is survived by his wife Elizabeth, children Justus and Maria, and two much-loved grandchildren.

Douglas J Coster

The public image of psychiatry could be better. Just three of the perceptions held by the community are that psychiatrists are loopy, that their treatments are ineffectual, and that the profession is too removed from mainstream medicine. Turning around such strong public opinion is no easy task, and possibly unachievable. Or so I thought until earlier this year. Saturday 21 May dawned a crisp and clear day, albeit a little breezy. A quick shower and breakfast, then I was out the door with my son Adam for his Under 8 soccer match. After a wind squall midway through the first half of a gripping encounter, one of Adam’s team mates, Brad, suddenly clutched his right eye and began to scream, then ran towards his mother on the sideline. The match was temporarily suspended, and parents from both sides formed a huddle around Brad and his distraught mum, the sense of helplessness profound. Little did anyone know that, over 20 years ago and before commencing psychiatry training, I had spent a term at Sydney Eye Hospital and that, despite limited opportunities since, I still fancied my skills in this area over the next person. I decided to intervene. Brad’s right eye was swollen and watering profusely. “Is the pain worse when you blink?” I enquired. Brad nodded, sobbing. Without further ado, I gently pulled his right upper eyelid towards me by its lashes and slowly everted it. The sight of the lid’s inflamed inner conjunctival surface caused some parents to step back, others to look away and many to wince, but my focus was now on a speck of dirt, trapped under the lid, that beckoned, seductively, “Garry, I’m yours”. Without averting my gaze, I requested a clean tissue and an onlooker obliged by inserting one into my free outstretched hand. A deft dab saw the foreign body gone and Brad once more a “happy camper”. For the hero, of course, the trick on such occasions is to give the impression that these actions are all in a day’s work by making no fuss, by politely shrugging off backslappers, and by quickly resuming one’s previous activities. Accordingly, when the game restarted, I was the first to recommence barracking: “In there, Adam!”, “Defence! Defence!”, “Nice tackle Kevin!”, and so on. At the same time, I was very mindful of the sorts of conversation taking place nearby: “They say he’s a psychiatrist.” “Surely not?” “Yep, a shrink.” “You don’t say . . . Wow!” Now a psychiatrist’s self-esteem and the public image of a profession should never hinge on a fortunate turn of events, as occurred during Round 7 of the 2005 Under 8 Ku-ring-gai District Soccer Competition. Nevertheless, while I do not pray that a gale blows during every soccer game in which my son plays, I confess to now following the weather forecast more closely and to not minding the occasional stiff breeze on match days. I even keep a box of tissues handy. I have also recently reminded myself how to reduce a dislocated shoulder. Just in case.

Garry J Walter PhD, FRANZCP

Clinical records Patient 1 A 30-year-old woman presented to hospital with bilateral hand paraesthesia and a serum potassium level of 2.9 mmol/L (reference range [RR], 3.5–5.0 mmol/L). She denied taking medications and had no significant past medical history. However, 3 months before admission, she had presented to her general practitioner complaining of anorexia, nausea, lethargy, fevers and aches. An erythrocyte sedimentation rate (ESR) of 91 mm/h (RR, 7–18 mm/h) and a serum creatinine level of 0.106 mmol/L (RR, 0.030–0.110 mmol/L) were noted. (Twelve months previously, her serum creatinine level had been 0.073 mmol/L.) Then, 1 month before admission, she had developed blurred vision due to anterior uveitis, diagnosed by an ophthalmologist, and was treated with topical steroids. In the intervening period, she had lost 12 kg in weight. A normochromic, normocytic anaemia was now present (haemoglobin level, 103 g/L; RR, 115–165 g/L), and her serum creatinine level was 0.230 mmol/L. The hypokalaemia was corrected, and she was discharged with a referral to the renal outpatient clinic. In clinic, her blood pressure was 140/85 mmHg, but the physical examination was otherwise normal. Repeat laboratory tests showed: creatinine, 0.250 mmol/L; potassium, 3.1 mmol/L; bicarbonate, 17 mmol/L (RR, 23–31 mmol/L); and phosphate, 0.64 mmol/L (RR, 0.60–1.40 mmol/L). Urine microscopy showed no leukocytes, erythrocytes or casts. Urine pH was 7.0, with glucosuria on dipstick. Protein excretion was 0.9 g/day (RR, < 0.15 g/day). Autoimmune markers were negative, including antinuclear antibody, antineutrophil cytoplasmic antibody, antidouble-stranded DNA antibody, and antibodies to extractable nuclear antigens. Serum calcium and angiotensin-converting enzyme (ACE) levels were normal. A chest x-ray and renal ultrasound were unremarkable. A renal biopsy showed acute interstitial nephritis and chronic renal damage (Figure A). After taking prednisolone 60 mg/day and concurrent phosphate, bicarbonate and potassium supplements for 4 weeks, her serum creatinine level fell to 0.130 mmol/L. The dose of steroids was reduced gradually over 4 months and renal function remained stable. Shortly after stopping prednisolone, her eye symptoms recurred. Ophthalmological examination revealed a bilateral visual acuity of 6/4, keratic precipitates, posterior synechiae and perilimbal injection, consistent with anterior uveitis (Figure B). This responded to topical steroids. Patient 2 A 34-year-old woman was referred to the renal clinic by her general practitioner, with a creatinine level of 0.190 mmol/L, normochromic, normocytic anaemia (haemoglobin level, 110 g/L), and an elevated ESR (120 mm/h). She gave a 1-month history of weight loss (15 kg), with anorexia, nausea, arthralgias, myalgias, fatigue and fevers. She had mild asthma, which was being treated with salbutamol, and took no other medications. Physical examination was unremarkable. Repeat laboratory tests 1 week later showed a serum creatinine level of 0.250 mmol/L. Urine microscopy showed no leukocytes, erythrocytes or casts. Proteinuria was absent and a renal ultrasound gave normal results. A renal biopsy revealed granulomatous acute interstitial nephritis with multinucleated giant cells (Figure C). Her serum calcium and ACE levels were normal, and a chest x-ray was unremarkable. Oral prednisolone 60 mg/day was commenced. One week later, her constitutional symptoms and renal function markedly improved. Repeat tests showed: creatinine, 0.120 mmol/L; potassium, 2.9 mmol/L; and phosphate, 0.40 mmol/L. Glucosuria was detected on urine dipstick analysis. All autoimmune markers and HLA-B27 were negative. Potassium supplementation was commenced. After the prednisolone dose was reduced to 2.5 mg/day over 2 months, she developed bilateral red and painful eyes, photophobia and watery discharge. Ophthalmological examination showed bilateral anterior uveitis, with a visual acuity of 6/9 bilaterally, perilimbal injection, keratic precipitates, anterior chamber cells 3+, and posterior synechiae. The uveitis resolved with topical steroids and cycloplegic agents. Her serum creatinine level remained stable without steroid dose adjustment. A: Renal biopsy specimen (Patient 1) showing an interstitial infiltrate of lymphocytes, plasma cells, histiocytes and eosinophils, without granulomas. There is prominent tubular atrophy and wide separation of tubular structures due to interstitial fibrosis (haematoxylin–eosin stain, original magnification x 200). B: Photograph of the right eye of Patient 1, with the thick arrow showing pupil irregularity and posterior synechiae, and thin arrows showing inflammatory perilimbal injection. Keratic precipitates and anterior chamber cells are best appreciated on slit lamp examination. C: Renal biopsy specimen (Patient 2) showing tubulointerstitial mononuclear infiltrate with non-caseating granulomas and multinucleated giant cells (large arrows) (haematoxylin–eosin stain, original magnification x 200). Inset: Small arrows highlight eosinophils with typical bilobed nuclei (x 400). Tubulointerstitial nephritis and uveitis syndrome (TINU) was first reported in 1975.1 Diagnosis of TINU requires identification of acute interstitial nephritis and uveitis, in the absence of systemic diseases associated with either condition. TINU occurs more frequently in females (3 : 1), with the median age of onset being 15 years, and has no racial association.2 At least 50% of cases are probably idiopathic based on the absence of risk factors for acute interstitial nephritis.2 Associations that have been reported include: drugs (antibiotics, non-steroidal anti-inflammatory drugs), infections (herpes zoster, Epstein–Barr virus, toxoplasmosis), and systemic diseases (hyperthyroidism, hypoparathyroidism, rheumatoid arthritis).2 The main differential diagnosis is sarcoidosis. Although uveitis associated with sarcoidosis is typically granulomatous, uveitis associated with TINU is mostly non-granulomatous. Sarcoidosis rarely causes acute interstitial nephritis and frequently affects the lungs, whereas lung involvement has not been reported with TINU. Sjögren’s syndrome is not a differential diagnosis because patients with Sjögren’s syndrome do not develop uveitis despite having sore eyes (sicca). Neither patient was taking medications known to cause acute interstitial nephritis. There is often a time interval between the diagnosis of uveitis and that of acute interstitial nephritis, making the diagnosis of TINU difficult. In 35% of patients with TINU, ocular findings precede or develop concurrently with acute interstitial nephritis. In 65% of patients, ocular symptoms follow acute interstitial nephritis by a median time of 1 month, but can occur up to 14 months later.2 The most common systemic features are fever, weight loss, fatigue and malaise (50%); and eye pain and redness are the most usual ocular symptoms (77%).2 Acute anterior uveitis is the typical finding (80%) and is usually bilateral. About 20% of patients develop ocular complications, such as posterior synechiae (most common), cataracts and glaucoma. Patient 1 developed recurrence of uveitis despite quiescent renal disease, showing that the course of ocular disease can be independent of renal disease.2,3 Uveitis recurs or becomes chronic in about 50% of patients. It is commonly treated with topical or systemic steroids, and cycloplegic agents. Methotrexate, cyclosporin or azathioprine may prevent relapses in steroid-resistant, recurrent or persistent uveitis, but randomised trials are lacking.2,4 Both patients demonstrated features of proximal tubular dysfunction consistent with Fanconi’s syndrome. This syndrome causes aminoaciduria, glucosuria, metabolic acidosis (bicarbonate wasting), hypophosphataemia, natriuresis, kaliuresis, polyuria and proteinuria. It has been reported in idiopathic interstitial nephritis,3 drug-related interstitial nephritis,5 and TINU.6,7 Incomplete Fanconi’s syndrome and distal tubular defects with hyperkalaemia have also been reported.8 Urinary electrolyte losses can be significant and symptomatic, as in Patient 1. Lessons from practice Beware of red eyes — check for interstitial nephritis and renal failure. In patients with uveitis, acute interstitial nephritis may not develop concurrently and may be asymptomatic. In tubulointerstitial nephritis and uveitis syndrome, complications of proximal tubular dysfunction (leading to metabolic acidosis and serious electrolyte disorders) and chronic renal damage can occur. Potassium, bicarbonate and phosphate supplementation may be needed. Steroid treatment may prevent chronic renal damage. Another complication that has been found is chronic renal damage. Some authors consider renal disease in TINU to be benign,9 but the renal biopsy from Patient 1 suggests that TINU produces chronic damage. Renal failure may resolve spontan-eously and almost always responds to steroids.2 Persistent renal dysfunction occurs in about 10% of patients, with few needing dialysis. Renal biopsy findings are typical of acute interstitial nephritis, with eosinophils seen in 34% and non-caseating granulomas in 13%.2 Granulomas have been described in lymph nodes and bone marrow.1 Despite its propensity to affect the young, TINU is not limited to paediatric patients, as these cases demonstrate. TINU may be underreported, given the frequent temporal dissociation between uveitis and acute interstitial nephritis. Chronic renal damage and electrolyte abnormalities do occur; hence, patients with uveitis should be evaluated for renal involvement. If any abnormalities are detected, a renal biopsy may be indicated. Early detection and steroid treatment may prevent renal complications.

Andy K H Lim MB BS · Vicki Levidiotis MB BS, FRACP, PhD · Matthew A Roberts MB BS, FRACP · Troy Lim Joon MB BS, FRANZCO, FRACS

Stephen E Cains Medical Director, The Fred Hollows Foundation, Locked Bag 3100, Burwood, NSW 1805. scainsAThollows.org To the Editor: I read with interest the personal perspective by Baker, describing her recent visit as part of an ophthalmic surgical team.1 Such teams from Australia have a long and creditable record of service in the Pacific, and their work has been of great value to the people in the countries involved, and of considerable personal satisfaction to those who have taken part in them. The experience of ophthalmic surgeons working with The Fred Hollows Foundation in developing countries certainly confirms Baker’s observations that the density of the cataracts found in these circumstances commonly makes them unsuitable for phacoemulsification. This does not, however, lead to the conclusion that modern small-incision surgery is not suitable for cataract patients in the developing world. Sutureless small-incision cataract surgery (SSICS) by manual means has been practised in many parts of the developing world for many years, with a range of techniques being used to extract the nucleus without phacoemulsification.2,3 Such techniques have been shown to give better uncorrected vision when compared with standard extra-capsular surgery, and are quick4 and economical, with fewer problems requiring follow-up than extracapsular surgery.5 The Fred Hollows Foundation, along with many other non-government organisations and authorities, is actively teaching and promoting the use of SSICS in its programs as the operation of choice for cataract extraction in the developing world. In light of this, I was surprised to see mention of the introduction of phacoemulsification to the Solomons by the team. Not only is this procedure not suitable for a large proportion of the presenting cataracts, but the cost of equipment and consumables in phacoemulsification is several times that of SSICS, and the time taken for surgery is often longer. In an environment where people suffer vision impairment simply from lack of glasses, and where surgeons are available who can perform modern small-incision sutureless cataract surgery, I wonder if this is an appropriate technology to introduce to the region.

Stephen E Cains

John L Szetu Ophthalmologist, Vanuatu National Eye Care Program, Port Vila, Vanuatu. fhfvaneyeATvanuatu.com.vu To the Editor: I am the ophthalmologist from Vanuatu referred to in Baker’s recent article, Sight-seeing in the Solomon Islands,1 who teamed up with the Pacific Islands Project surgeon in Honiara. I am currently working in Vanuatu with the Fred Hollows Foundation (New Zealand) and the Ministry of Health, developing a national eye care program, and continue to make two Fred Hollows Foundation-funded ophthalmic service trips annually to the Solomon Islands. At the end of this year, I will be returning to Honiara to help set up a regional ophthalmic training centre, and again manage and develop the national eye program. The article’s title, while aimed at highlighting the rehabilitation of vision resulting from the visit of a Pacific Island Project ophthalmic team, points ironically to the problem of “medical tourism”. Medical tourism is common in the Pacific, and I speak for many indigenous Pacific doctors when I say that we are trying to discourage the practice because of the patient expectations it raises that cannot be fulfilled, the opportunity cost, and the post-visit cleanup that is often required. Medical tourism is usually well-intentioned and can be seen by those involved as a well earned break from private practice at home. However, it is often not anchored to the real needs and conditions of the countries in which it occurs. The use of phacoemulsification for cataract extraction, as reported in Baker’s article, is a case in point. With due respect, the Pacific Islands Project (PIP) surgeon managed to perform fewer than three phaco-emulsifications, while I did 116 “low technology” manual small-incision cataract surgeries during the 3 days available to us in Honiara. The appropriate backup was not available for “high technology” phacoemulsification. The unit could not be made fully functional, and the surgeon eventually resorted to a manual technique. While quantity is important, so is quality of outcome, for which there is no long-term difference between the high and low technology techniques used in Honiara. Before the civil unrest, the Solomon Islands Eyecare Program was a Pacific leader in terms of facilities, mid-level (nursing and refraction) human resources and overall productivity. I had trained a network of 14 ophthalmic nurses. These workers have held services together in my absence, and been largely responsible for “screening” and organising patients to be seen by visiting teams (PIP), New Zealand-based Volunteer Ophthalmic Services Overseas, and Surgical Eye Expeditions from the United States) and myself. Credit should also go to these workers and the other teams. Medical team visits are valuable, but many Pacific Island nations now see that resources could be better used if they targeted appropriate development of eye care systems and programs, and built local capacity (such as the Solomon Island ophthalmic nurses) rather than delivering services in an ad hoc manner. Visiting service teams need to become aware of this, be prepared to take direction from local authorities, take responsibility for monitoring and evaluating their own clinical activities and outcomes as they would at home, and contribute in an organised and agreed manner to building local resources.

John L Szetu

Michelle L Baker,* Geoffrey T Painter† * Resident Medical Officer, Neurosurgery Department, Royal Melbourne Hospital, 46-58 Drummond Street, Carlton, VIC 3053. † Ophthalmology Coordinator, Royal Australasian College of Surgeons Pacific Islands Project, Melbourne, VIC. michellelouisebakerATyahoo.com In reply: Despite increased efforts over the last decade, the burden of blindness due to cataract is still immense. With over 18 million people in the world blind because of cataract1 there is an obvious need for an affordable and efficient cataract surgery technique. We agree that sutureless small-incision cataract surgery (SSICS) does have an important place in cataract surgery in the developing world. It has advantages over extra-capsular cataract extraction (ECCE) in the longer term, such as decreased cost,2 reduced astigmatism and decreased surgery time.3 There is increasing interest in SSICS among Australian ophthalmologists, and instruction courses are to be held at the forthcoming Royal Australian and New Zealand College of Ophthalmologists meeting. On the other hand, SSICS can be more difficult to learn, and for inexperienced surgeons, there are risks of complications when it is used for a bulky dense cataract.3 ECCE is continuing to evolve, with modern surgical blades giving significantly shelved wounds, which are potentially safer and require fewer sutures, and still has a place. In the Solomon Islands, ECCE and SSICS are the predominant techniques because phacoemulsification is unsuitable for most patients as their cataracts are too dense.3 SSICS was used successfully for suitable cases by Szetu, who is very experienced in the technique. The phacoemulsification machine was brought to Honiara to perform vitrectomy (which the machine is capable of) for diabetic retinopathy in patients who otherwise would have needed expensive treatment in Australia. Phaco-emulsification was purposely used only as a trial (hence, in only three patients), but in the subsequent Pacific Islands Project (PIP) visit, six children with congenital and traumatic cataracts were successfully treated with with phacoemulsification/lensectomy and the insertion of folding intraocular lenses (these were six of a total of 260 operations). In this group it is an ideal technique.4 Currently, it is sustainable to use phacoemulsification because of generous donations. With the advent of low cost phacoemulsification machines (as presented at the Australasian Society of Catar-act and Refractive Surgeons conference in Broome in 2004) and low cost disposables, it is likely the technique will be increasingly used when the backlog of dense cataracts are reduced. Phacoemulsification is the accepted standard of care for cataract surgery in the developed world,2 and there are valid reasons for introducing it into developing countries. Professional development is important, and we must consider the aspirations of our colleagues; the appropriate introduction of phacoemulsification can aid this. We are pleased to hear of Szetu’s return to Honiara, and are sure this technology will have a small, but useful, place in his clinical practice in the future. We cannot agree more strongly that so-called “medical tourism” is wrong. It provides no significant benefit to the community and is disruptive, unhelpful and is, at worst, a burden to the local medical and nursing staff. Unrequested, unhelpful and short-term visits should not be undertaken. The PIP was specifically set up to avoid the abovementioned problems by providing aid that was substantial and well funded (by AusAID), and teaching trips to countries that have made specific requests at the government level for assistance. Such assistance is provided only with the total cooperation and support of local ophthalmic staff, and is run to the highest standards by experienced and committed volunteers. It has been well received in all Pacific countries visited. Ultimately, PIP was intended only as a transitory phase in Pacific development and, as each country achieves self-sufficiency through infrastructure development, visits will be scaled down. We are looking forward to the Solomon Islands regaining the place it once had in Pacific ophthalmology before the civil unrest, and look forward to continuing to help develop the Eye Department in the years ahead. We hope that the close to 1500 operations the PIP team have performed over the eight visits since 2000 have been of help during this troubled time.

Michelle L Baker · Geoffrey T Painter

Umberto Boffa Medical Director, BUPA Australia Health Insurance, 600 Glenferrie Rd, Hawthorn, VIC 3122. umberto.boffaAThba.com.au To the Editor: Taylor and colleagues have provided an excellent analysis of the prevalence and causes of vision loss in Australia.1 However, their conclusion that vision loss in Australia is a much bigger problem than is usually recognised and requires “save your sight” public promotion bears some discussion. The main outcome measure used was impairment in visual acuity. Impairment does not necessarily equate with disability. Disability has been defined as an alteration of an individual’s capacity to meet personal, social or occupational demands, or statutary or regulatory requirements, because of an impairment.2 An impaired person is not necessarily disabled. The study of Taylor et al did not use measures of visual disability, such as the VF-14 (Visual Function Index). Participants were asked to complete a questionnaire that included information about “symptoms of eye disease”, but it is not clear that the questionnaire explored self-perceived problems with vision. Nor does the study seem to have looked at the level of cognitive impairment within this aged population. Tielsch et al, in a similar study,3 made the point that whether people who have both a treatable loss of vision and cognitive impairment should receive ophthalmological intervention depends on the cause and severity of the cognitive deficit. Further, Taylor and colleagues stated that, after undercorrected refractive error, cataract is the most common cause of low vision and is also comparatively easily treated, but they did not objectively evaluate the relative risks and benefits of such interventions. The study provides interesting data on the extent of visual impairment in Australia, but the authors are presupposing that the uncovered prevalence of visual impairment necessarily constitutes a social problem requiring “save your sight” public health measures. Reference should be made to patient goals and needs, and an objective cost–benefit analysis, before such a conclusion can be reached.

Umberto Boffa

Konrad Pesudovs,* Douglas J Coster† * Deputy Director, † Director, NHMRC Centre for Clinical Eye Research, Department of Ophthalmology, Flinders Medical Centre and Flinders University, Bedford Park, SA 5042. Konrad. PesudovsATflinders.edu.au To the Editor: The timely report of Taylor and colleagues of large numbers of Australians suffering visual impairment caused by refractive error raises some important questions.1 Firstly, is it reasonable to assume that visual acuity of less than 6/12 is disabling and demands intervention? The correlation of visual acuity and visual disability is tenuous.2-4 This is not surprising. Visual acuity measures a narrow domain of visual function. Different abnormalities differentially impact across wide domains of visual function. Everyday sight-dependent functions will be affected differently. For example, people with cataracts may experience reduced contrast sensitivity and colour discrimination, while those with advanced glaucoma will lose visual field, but those losses will affect a person’s life independent of visual acuity. Conversely, myopia acquired in old age may reduce visual acuity to less than 6/12 but may also provide spectacle-free near vision adequate for reading and other daily tasks. This may not cause any disability for an elderly person whose life is spent predominantly indoors. Therefore, it seems inappropriate to assume that the 62% of people with visual impairment caused by refractive error suffer visual disability to the extent of those with glaucoma or age-related macular degeneration. A better approach to measuring visual impairment would be to use patient-centred measures, which consider the impact of eye disease on visual performance, rather than the convenient but narrow measure of visual acuity. If visual acuity is to be used, its limitations as an indicator of visual disability should be considered, and inferences about visual impairment should remain constrained by these limitations. The second question which follows from the report that uncorrected refractive error is responsible for 62% of visual loss below 6/12 is: why do people so affected not wear spectacles? Perhaps there are barriers to acquiring spectacles, such as access. However, this seems unlikely as there is an optometrist in every major shopping centre. Certainly, cost may be a barrier, and a study from our Centre has shown that spectacle correction may reduce quality of life in the domains of wellbeing, convenience, and economic concerns.5 Therefore, it seems likely that the cost–benefit balance is such that these people are not sufficiently dis-abled by their vision to go to the inconveni-ence and expense of acquiring spectacles. The authors have raised important issues which require clarification. Is it that visual acuity overestimates the impact of refractive error on visual disability, or is the system for supplying spectacles to Australians failing?

Konrad Pesudovs · Douglas J Coster

Jill E Keeffe,* Hugh R Taylor† * Director, Population Health Division, Department of Ophthalmology, University of Melbourne, and Royal Victorian Eye and Ear Hospital, Locked Bag 8, East Melbourne, VIC 8002; † Professor, Centre for Eye Research, University of Melbourne, VIC. jillekATunimelb.edu.au In reply: Boffa and Pesudovs and Coster all correctly point out that a reduction in visual acuity does not always lead to dis-ability, and that not all people with impaired vision are disabled or report impaired quality of life. Large Australian and American population-based studies have shown that visual acuity below a critical level of 6/12 is associated with disability and affects participation in chosen activities and quality of life.1 When compared with people with normal vision (≥ 6/12), those with impaired vision have an increased risk of falls and hip fractures, depression, difficulties with activities of daily living and social functioning.1 Not all people with reduced visual acuity are affected in the same way at any vision threshold, even if there is a demonstrated statistically significant association between poor vision and visual function and quality of life. For example, not all people with severe visual impairment (visual acuity < 6/60) report an impact on their own visual functioning or quality of life. The impact of poor vision on functional ability is similar for conditions such as cataract or acute macular degeneration as for refractive error. The impact has been shown with both correctable and uncorrectable vision impairment.2 The VF-14 (Visual Function Index) can be used as a measure of visual disability, as suggested by Boffa. It was used in the Melbourne Visual Impairment Project and confirmed the functional implications of vision impairment (visual acuity < 6/12).3 Studies show unequivocally that vision impairment is a social3 and economic4 problem, and suggest the need for health promotion campaigns. Pesudovs and Coster ask why, in a country such as Australia, with optometrists “in every major shopping centre”, do people with refractive error not have the correct spectacles? They suggest some barriers of access to care. The Brotherhood of St Laurence has shown that affordability of glasses and rural disadvantage are barriers to access and equity of use of eye care services.5 Our report highlighted the fact that catar-act is an important cause of vision loss that is highly amenable to surgical intervention.6 We did not discuss the relative risks and outcomes of cataract surgery, which is well documented to be highly successful, with low complication rates (< 2% for most complications),7 and very high cost-effectiveness.

Jill E Keeffe · Hugh R Taylor

The Solomon Islands is a nation of warm people, tropical islands, shipwrecks and malaria. It is also a nation in urgent need of specialised medical care. This is the story of my short time volunteering in the Solomon Islands for the ophthalmic division of the Royal Australasian College of Surgeons, Pacific Islands Project (PIP) in 2004. The PIP, in operation since 1996, is funded by the Australian Agency for International Development (AusAID) and encompasses specialists from 10 surgical specialties who volunteer their time to help address the shortage of local specialists in 11 Pacific Island countries. The ophthalmic team for the Solomon Islands is sponsored to make an annual trip. Eye disease is such a serious problem that they made a second trip in 2004 to the islands of Guadalcanal, Malaita and Gizo, their 11th since the project’s inception The Solomon Islands, formerly known as the British Solomon Islands, gained independence in 1978. They were the scene of some of the bloodiest land, sea and air battles of World War II, and are now emerging from 6 years of ethnic conflict. The predominantly Melanesian people of the Solomon Islands are among the poorest in the South Pacific.1 Honiara is a 3-hour flight from Brisbane, where I first met the PIP team — ophthalmologists Geoff Painter and Jeremy Smith, and ophthalmic nurses Bev Baily and Louise Fowler, all from Sydney — at the Solomon Island Airlines check-in counter. Honiara, GuadalcanalAfter arriving at Honiara-Henderson airstrip, we bounced and weaved along dilapidated roads to make our way to the National Referral Hospital in dusty Honiara. It is the only hospital in the archipelago that has an anaesthetist and the option of performing major surgery. However, it has no intensive care facilities and endures a chronic shortage of medical supplies. The team arrived to the sounds of an animated Christian preacher engaging the crowd of more than 500 patients on the hospital verandah. The patients had been queuing since dawn and many had walked for days on hearing of the impending arrival of an eye team. Essential to ophthalmic care in the Solomon Islands are the specialised eye nurses, headed by Wanta Aluta. Sister Wanta runs the eye clinic at the National Referral Hospital, provides training for the eye nurses at regional eye clinics, and is responsible for the essential triage before each overseas team visits. Dr Qalo, a Solomon Islander, is currently in an ophthalmology training program in Papua New Guinea, sponsored by Foresight Australia. At the clinic, the patients were lined up in rows and the two ophthalmologists moved along the rows using a portable slit lamp to diagnose the ophthalmic condition, most commonly, cataract. Patients had brought their own medical histories, which varied from a small exercise book to a scrap of card. Patients were put on the list for cataract surgery if their visual acuity was measured at less than 6/60. However, many could only discern hand movements and up to 30% were profoundly bilaterally blind. Only a select few with pressing reasons for securing surgery (such as driving a taxi or working as a teacher) were operated on at 6/60. Standard cataract surgery was extracapsular cataract extraction with the insertion of a posterior chamber intraocular lens. In most patients, the density of the cataract made phacoemulsification, and thus, modern small-incision cataract surgery, unsuitable. There were a significant number of young people with cataracts. One unforgettable patient was a 14-year-old boy with bilateral cataract who had lived most of his life being led around by his mother. His left cataract was removed during the team’s last PIP tour, and he now had uncorrected 6/4 vision in his left eye, a big smile, and was ready to have his right cataract removed. The severity of eye conditions is compounded by the delay in presentation. Most patients’ first port of call is a traditional healer for topical application of herbs termed “Kastom medicine”, which, at best, does nothing, and often introduces infection. Auki, MalaitaAfter 2 days in Honiara, Dr Painter and I joined Dr Qalo and Sister Wanta for a 3-hour speedboat trip to Malaita Province. No ophthalmic team had visited Malaita since 2001. We went straight from the port to the eye clinic at Kiluufi Hospital to begin consultations with the 112 patients. We greatly appreciated that Stephen, the Malaitan eye nurse, had measured the visual acuity and divided the group into cataracts and other disorders (mostly pterygium and infections). A disturbing number of children had lime burns on their corneas caused by touching lime hydroxide used by their parents in the preparation of their betel nut mixture. Many elderly patients had decreased visual acuity because of uncorrected refractive errors, for which there were no spectacles available. The general state of patients in Malaita was sobering. They were literally in rags. Worse still, many were hungry. Families generally subsist on vegetable plots with little cash income. Some had made the long journey to the eye clinic by canoe or on foot with scarce provisions over many days. One patient even had a hypoglycaemic attack on arrival at the clinic. Malaita is one of the poorest islands in the country because of its direct involvement in the ethnic conflict. After years of tension, the civil war came to a head on the main island of Guadalcanal in 1998. During the conflict, Malaitan settlers (many second-generation) fled Honiara and went back to Malaita. The impressive organisation at Kiluufi Hospital enabled us to commence surgery on the second day. The team was mostly self-sufficient, bringing two portable microscopes, ophthalmic instruments, an autoclave and disposables with them. Patients were given a peribulbar local anaesthetic by a Solomon Islander resident medical officer, and walked in and out of surgery. Insect repellant was a must to ward off malaria-laden mosquitoes from our exposed legs. The air-conditioned theatre made operating in the humid climate tolerable to us, but the patients needed blankets during the half-hour cataract procedure. After their surgery, the patients were led out to rest until review the next morning. Many slept on vacant benches, under desks or on straw mats on the floor. The pharmacy had no paracetamol for postoperative analgesia. Despite the environmental conditions, the rate of nosocomial infections and endophthalmitis was low. Each morning, I reviewed the postoperative patients and re-measured their visual acuity. Patients, many of whom were seeing for the first time in many years, were intensely grateful and said “Thank you for coming to Malaita”. Patients’ uncorrected visual acuity was tested preoperatively and then one day postoperatively (Box 1). Ideally, visual acuity would be tested again a few months later, but patients’ return to their far-flung homes after treatment makes long-term follow-up unrealistic. While we were working in Auki, Dr Smith and Dr John Szetu (who joined our Team from Vanuatu) worked diligently in Honiara performing a large number of procedures on the Guadalcanal patients we had triaged on arrival. They also introduced more modern technology in the form of phacoemulsification and posterior segment vitrectomy for treating retinal detachment, for the first time to the Solomon Islands. GizoThe third place on the PIP schedule was the beautiful island of Gizo, renowned worldwide as a diving Mecca. The team reunited, which increased surgical efficiency and enabled us to perform a record number of operations overall. ReflectionsWe completed 287 procedures in 2 weeks (Box 2), and provided valuable supplies and teaching. Despite this, time constraints meant that we were not able to extract all of the cataracts of the patients on the surgical list in Honiara or Auki. This left me feeling despondent, as the patients had waited so patiently for up to a week and were so gracefully resigned in their disappointment. Of course, they will be given priority in the future, but the sadness on their faces was obvious. I obtained invaluable experience on neglected ophthalmic disorders and the difficult conditions under which the Solomon Islander nurses and doctors work. It was a privilege to witness the work in the Solomon Islands by the PIP team, but especially the work done by Sister Wanta and her nurses. I now understand and appreciate how Australian development projects are assisting in the development of primary eye care in the Pacific Nations. Sadly, compared with their Pacific neighbours, the Solomon Islands are relatively well resourced. The PIP teams provided ophthalmic surgery, in addition to valuable supplies and teaching; VISION 2020 provided specialised training for eye nurses, who in turn provided a buffer of sustainable eye care during the ethnic conflict; and Foresight Australia provide the opportunity for specialised ophthalmic training. On a broader front, additional assistance is provided by the Regional Assistance Mission to the Solomon Islands (RAMSI), established by Australia and with other Pacific Island Nations at the request of the Solomon Islands government in 2003. RAMSI has authority for peacekeeping and the restoration of basic services, particularly in health. This has been broadly welcomed by most Solomon Islanders.2 The Solomon Islanders have been through difficult times, but their future is looking brighter. 1 Improvement in uncorrected visual acuity for 72 patients after extracapsular cataract surgery at Kiluufi Hospital, Malaita, Solomon Islands* * Vision tested preoperatively and one day postoperatively. Symbols and adjacent numbers indicate the number of patients with preoperative visual acuity as indicated by their position along the horizontal axis that improved postoperatively to the position shown on the vertical axis. The smallest symbols indicate one patient and are not labelled. 2 Presentations and surgery for eye disorders in the Solomon Islands during a 2-week visit by a Pacific Islands Project ophthalmic team in August 2004 Surgery Hospital Patients screened Cataract Pterygium (excision/ graft) Entropion (repair) Diabetic retinopathy (laser) National Referral Hospital 344 151 2 2 4 Kiluufi Hospital 112 72 1 1 na Gizo Hospital 124 38 10 6 na Total 580 261 13 9 4 na = not applicable.

Michelle L Baker MB BS

Objective: To assess the prevalence and causes of vision loss in Australia and to project these data into the future.Design: Synthesis of data from two cross-sectional population-based cohort studies — the Melbourne Visual Impairment Project and the Blue Mountains Eye Study — and extrapolation to the entire Australian population.Setting and participants: 8376 community and 533 nursing home residents recruited between 1992 and 1996 in urban and rural Victoria and New South Wales.Main outcome measures: Age-standardised prevalence of low vision (visual acuity < 6/12) and blindness (visual acuity < 6/60) (both measured in the best eye, with spectacles if usually worn for distance vision), and their causes for the Australian population for 2000 to 2024, projected from Australian Bureau of Statistics population data.Results: In 2004, 480 300 Australians were estimated to have low vision, including 50 600 with blindness. The most common causes of low vision were undercorrected refractive error (62%), cataract (14%) and age-related macular degeneration (10%). The latter was responsible for almost half of all cases of blindness. The numbers of people with low vision and blindness are projected to almost double by 2024.Conclusions: Vision loss in Australia is a much bigger problem than is usually recognised; 76% of low vision is caused by uncorrected refractive error or cataract, both readily treatable. However, the prevention and treatment of macular degeneration poses a major challenge.

Hugh R Taylor AC, MD · Jill E Keeffe PhD · Hien T V Vu PhD · Jie Jin Wang MMed, PhD · Elena Rochtchina MApplStat · Paul Mitchell MD, PhD · M Lynne Pezzullo BEc

Objective: To describe how a novel program of diabetic retinopathy screening was conceived, refined and sustained in a remote region over 10 years, and to evaluate its activities and outcomes.Design: Program description; analysis of regional screening database; audit of electronic client registers of Aboriginal community controlled health services (ACCHSs).Setting and participants: 1318 Aboriginal and 271 non-Aboriginal individuals who underwent retinal screening in the 5 years to September 2004 in the Kimberley region of north-west Australia; 11 758 regular local Aboriginal clients of Kimberley ACCHSs as at January 2005.Main outcome measures: Characteristics of clients and camera operators, prevalence of retinopathy, photograph quality, screening intervals and coverage.Results: Among Aboriginal clients, 21% had diabetic retinopathy: 19% with non-proliferative retinopathy, 1.2% with proliferative retinopathy, and 2.8% with maculopathy. Corresponding figures for non-Aboriginal clients were 11%, 11%, 0 and 0.4%, respectively. Photograph quality was generally high, and better for non-Aboriginal clients, younger Aboriginal clients and from 2002 (when mydriatic use became universal). Quality was not related to operator qualifications, certification or experience. Of 718 regular Aboriginal clients with diabetes on local ACCHS databases, 48% had a record of retinal screening within the previous 18 months, and 65% within the previous 30 months.Conclusions: Screening for diabetic retinopathy performed locally by Aboriginal health workers and nurses with fundus cameras can be successfully sustained with regional support. Formal certification appears unnecessary. Data sharing across services, client recall and point-of-care prompts generated by electronic information systems, together with policies making primary care providers responsible for care coordination, support appropriate timely screening.

Richard B Murray MB BS, MPH · Sue M Metcalf MPH · Philomena M Lewis AHW · Jacqueline K Mein MB BS, FACShM, MAE · Ian L McAllister FRANZCO

Craig A Aboltins,* John R Daffy,† Penny Allen‡ * Infectious Diseases Registrar, † Infectious Diseases Physician, St Vincent’s Hospital, Victoria Parade, Fitzroy, VIC 3065; ‡ Ophthalmologist, Royal Victorian Eye and Ear Hospital, East Melbourne, VIC. craigaboltinsATnetspace.net.au To the Editor: Within the last 12 months, four injecting drug users (IDUs) who had been injecting buprenorphine presented to the Royal Victorian Eye and Ear Hospital with endogenous fungal endophthalmitis (EFE) involving Candida species. All four patients admitted that they had diverted or obtained diverted sublingual buprenorphine from the oral cavity after it was dispensed. They had dissolved the remaining drug in water and injected it intravenously. We present an illustrative case. A 28-year-old woman presented with a 4-week history of left eye pain and erythema. She had a 10-year history of intravenous drug use. Over the previous 6 months, she had been regularly injecting buprenorphine that was prescribed to a friend. The friend had been removing the partially dissolved buprenorphine from his mouth before giving it to our patient. On examination, the patient could only detect hand movement with her left eye. Fundoscopy showed vitritis with a “snow ball appearance” consistent with EFE. Treatment involved vitrectomy, intravitreal amphotericin and oral fluconazole. Candida albicans was cultured from vitreal specimens. Her visual acuity had improved to 1/60 at the time of discharge. Intravenous drug use is known to be a risk factor for EFE. Candida species are the usual causative organisms, but Aspergillus species have also been reported.1 In the 1980s, there were many reports of candida endophthalmitis in injecting drug users associated with the use of “brown” (or Iranian) heroin. The “brown” heroin required an acidic substance, often lemon juice, as a solvent. Lemon juice was shown to be the source of the candida.2 However, over the past 10 years, the heroin available in Australia has been water soluble, and sterile or tap water is usually used to dissolve the heroin before injection. None of the cases we report in this letter involved lemon juice to dissolve heroin or buprenorphine before injection. Buprenorphine has been available in Australia since 2001 for the treatment of opiate addiction. It is usually dispensed daily by pharmacies in a crushed tablet form. Pharmacists are required to watch patients place and dissolve the medication under the tongue before they leave the pharmacy. Contamination of injected buprenorphine with orally derived Candida species presents a recently recognised cause of fungal endophthalmitis in injecting drug users.3 Doctors, pharmacists and drug users need to be aware of the risk of this sight-threatening complication.

Craig A Aboltins · John R Daffy · Penny Allen

Clinical record A 6-year-old girl presented to her general practitioner with a red left eye. She reported no pain or irritation, but did have difficulty seeing into the distance with blurring of vision in the affected eye. Associated with this symptom was the onset of neck stiffness with limitation in neck flexion and rotation. This had increased gradually over the preceding month and was most problematic in the morning. There were no associated fevers, rashes, gastrointestinal or genitourinary symptoms. She had been well in the past, was not taking any medications, and her vaccinations were up to date. Her elder sister had been diagnosed with juvenile idiopathic arthritis (JIA) at the age of 18 months, her mother had type 1 diabetes mellitus. A maternal aunt had been diagnosed with rheumatoid arthritis 4 years earlier. Examination revealed inflamed palpebral conjunctivae in the left eye, and mild restriction in the range of neck rotation and flexion. There were no other findings. The patient was diagnosed with conjunctivitis and intermittently prescribed chloramphenicol eye drops over 3 months. The neck discomfort continued over this period, despite physiotherapy. Ultrasonography of the neck showed no abnormalities apart from “unusual lymphadenopathy”. This finding prompted a referral to a paediatric oncologist who believed uveitis should be considered in light of the child’s family history of JIA. She was referred for an ophthalmologist’s opinion. At ophthalmological review, her vision was 6/7.5 in the right eye and 6/12 in the left eye. There was band keratopathy (see Box 1) present in the region of the visual axis and the pupil was adherent to the lens by posterior synechiae. The child’s vision continued to deteriorate to 6/24 in the left eye despite treatment with topical dexamethasone 0.1% and atropine 1%. She was referred to the rheumatology service. The rheumatologist found that the child had an elevated erythrocyte sedimentation rate of 43 mm/hour (normal range, 0–20 mm/hour), but the C-reactive protein concentration was within normal limits at 4 mg/L (normal range, 0–10 mg/L). The antinuclear antibody (ANA) titre was strongly positive at over 1:2560, and showed a homogenous pattern. The double-stranded DNA titre (Farr assay) was within normal limits at < 5 U/mL (normal range, < 11 U/mL). The extractable nuclear antigen screen was negative. Treatment with non-steroidal anti-inflammatory drugs resulted in little improvement, so therapy with oral prednisolone and pulse methylprednisolone was commenced. We saw her when she was admitted for the first of 3 methylprednisolone pulses (625 mg intravenously). Vision in the right eye was 6/9 and in the left it was 6/36. Topical medication was continued and the vision in the left eye improved modestly to 6/24. She was then discharged on topical treatment, and systemic treatment with 2.5 mg methotrexate weekly was commenced. This increased to 7.5 mg weekly over one month. At the most recent review, conducted at the time of the final dose of intravenous methylprednisolone, the vision was stable at 6/6, the intraocular pressure was within normal limits and the anterior chamber appeared quiet, the band keratopathy had partially resolved, but the posterior synechiae remained. The neck symptoms had resolved. Uveitis associated with JIA can have an insidious onset, and is often asymptomatic before sight-threatening complications develop. It is an inflammatory condition of the eye, involving the uveal tract,1 and is frequently not seen until a thorough slit lamp examination is performed. Without a slit lamp one may see an inflamed eye with ciliary injection, and the iris may appear adherent to the lens (Box 2). Anterior uveitis is the most common form of childhood uveitis.2 Anatomically, the inflammation involves the iris and the anterior part of the ciliary body. This form of uveitis is the type most commonly associated with JIA. Less common causes of anterior uveitis include herpetic uveitis, Behçet’s disease and Fuch’s heterochromic iridocyclitis.2 The insidious course and difficulty of diagnosis in preverbal children paves the way for the development of sight-threatening complications. Over time, even low-grade inflammation can lead to cataract, glaucoma, maculopathy and the band keratopathy which was demonstrated in this child. Over 75% of eyes affected by JIA-associated uveitis can develop one or more complications.2 Lessons from practice Uveitis is associated with sight-threatening complications. These complications may have an insidious onset and may initially be asymptomatic. Children with juvenile idiopathic arthritis often have active inflammation without any symptoms and should therefore have ophthalmic screening, as early treatment can be sight-saving. Any person presenting with a persistent red eye and blurred vision should trigger suspicion of a sinister disorder, such as uveitis or acute glaucoma. Early referral to an ophthalmologist for these conditions is imperative. The risk of these complications developing heralds the need to be acutely aware of the signs, and to institute and maintain screening programs for children with JIA. Children with JIA who are at a high risk of developing uveitis, that is, those who have pauciarticular arthritis and a positive titre for antinuclear antibody (ANA) at a young age, need slit lamp examination by an ophthalmologist at 3–4 month intervals. Children with JIA who are assessed to be at a low risk of developing uveitis (ie, those who have a negative ANA titre with systemic disease of more than 4 years duration) should be seen at 12-month intervals.3 The development of uveitis in children with JIA is not uncommon, and a child presenting with unilateral red eye must raise the suspicion of uveitis. However, even in the absence of a red eye, children with JIA may develop ocular inflammation, which, if not detected, can proceed to permanent visual loss. Ophthalmic advice should therefore be sought sooner rather than later. The left eye of our patient with arrows indicating the band keratopathy found at initial review. 2 The eye of another patient with arrows (large) showing the ciliary injection typical of acute anterior uveitis Smaller arrows show areas of the iris adherent to the lens (posterior synechiae).

Shane R Durkin MB BS(Hons) · Theresa M Casey MB BS, GDPH, FRANZCO

Marc M Cohen Professor of Complementary Medicine, School of Health Sciences, RMIT University, PO Box 71, Bundoora, VIC 3083; and President, Australasian Integrative Medicine Association. marc.cohenATrmit.edu.au To the Editor: I read Constable’s article1 on age-related macular degeneration with interest, but was surprised at its somewhat guarded advice on nutritional supplementation and the fact that it gave only passing reference to uncontrolled studies of the carotenoids lutein and zeaxanthin and failed to mention a number of controlled studies that have recently shed light on the potential for these nutrients to influence the progression of age-related macular degeneration (ARMD). Lutein and its isomer, zeaxanthin, are deposited in the macula, where they make up the macular pigments and act as a blue-light filter to protect the underlying tissues from phototoxic damage, as well as providing antioxidant activity. Lutein was not available in supplement form at the time of conducting the Age-Related Eye Disease Study (AREDS).2 However, the more recent Lutein Antioxidant Supplementation Trial (LAST), a double-masked, placebo-controlled, randomised trial of lutein and antioxidant supplementation in people with ARMD, demonstrated that taking 10 mg lutein daily, with or without additional nutrients, improved visual function.3 Interestingly, lutein supplementation was also found to improve vision in a small, randomised, placebo-controlled study of people with cataracts. It was suggested that these improvements were due to improved macular function and increased macular pigment density.4 Furthermore, a recent study showed that lutein supplementation results in increased macular pigment density in both normal and ARMD patients.5 Lutein occurs naturally in foods such as eggs, spinach, romaine (cos) lettuce, broccoli, zucchini, corn, peas and Brussels sprouts. Although lutein is readily absorbed from foods and dietary supplements, surveys indicate that average lutein intake may be below levels that are associated with disease prevention.6 Toxicology studies have established that lutein is generally safe, with potential for use as a supplement in foods and beverages.6 While advice on smoking cessation and increasing fruit and vegetable intake is useful for a wide range of conditions, including ARMD, Constable’s statement that “antioxidant supplements should be recommended if a fresh diet is impractical and if retinal signs of progression are present”1 appears overly cautious. In light of recent findings on the potential benefits of antioxidants such as lutein, and the low cost and minimal risks associated with supplementation compared with the potentially devastating consequences of blindness from ARMD, it may be prudent to make more general recommendations on nutritional supplements, rather than waiting until signs of retinal progression are evident.

Marc M Cohen

Ian J Constable Director, Lions Eye Institute, Centre for Ophthalmology and Visual Science, University of Western Australia, 2 Verdun Street, Nedlands, WA 6009. ijcATcyllene.uwa.edu.au In reply: While the published literature on dietary supplementation with the antioxidants lutein and zeaxanthin is highly encouraging, it does not yet pass the requisite standards for public endorsement provided by large-scale, independent, evidence-based medical trials. The controlled (“LAST”) trial of lutein1 cited by Cohen consisted of just 91 patients divided into three subgroups including the placebo group, who were followed for only 1 year. The measurement of visual improvement on a Snellen chart would not be accepted as “gold standard” evidence by major granting agencies and regulatory affairs bodies, who demand the higher discrimination of a logarithmic visual acuity chart. Moreover, the data were not derived from multicentre trials and independently assessed. It is instructive to compare the methodology of the LAST trial with that of the ARED Study,2 which involved 11 centres, 3640 patients and an average follow-up of 6.3 years. For these reasons, although I mentioned lutein in an encouraging fashion, I did not endorse it to the same extent as vitamin C, vitamin E and zinc supplements. The other reasons for giving limited recommendation of antioxidant supplements at this stage relate to the fact that it is not yet clear to what extent supplements would be beneficial over and above a diet targeted to provide these antioxidants in plentiful supply. It may yet be shown that a nutritious diet — with emphasis on brightly coloured and leafy vegetables, fresh fruits, nuts and fish, coupled with reduced processed vegetable oils (except olive oil) — can, alone, provide substantial protection. While the supplements are generally deemed to be safe, they are not without occasional serious side-effects and have not been followed long term. Richer, one of the authors of the lutein study, 1 acknowledges commercial relationships with the supplement suppliers, and states that the study requires greater numbers and long-term follow-up to be confirmed. Cohen cited a second article3 that refers to a 2-year study of cataract, in which a mere 17 patients were allocated to three subgroups including the placebo group. It is not usual practice to quote conclusions from such a small, and therefore potentially unreliable, trial design. Cohen is right to point to lutein and possibly zeaxanthin supplements as an encouraging possibility for preventing blindness from macular degeneration, and I hope the evident enthusiasm and rapid marketing of lutein proves justified in the long run by forthcoming major trials.

Ian J Constable

CorrectionRe: “Bilateral acute angle closure caused by supraciliary effusions associated with venlafaxine intake” by de Guzman M H P, Thiagalingam S, Ong P Y and Goldberg I in the 7 February 2005 issue of the Journal (Med J Aust 2005; 182: 121-123). In the second paragraph of the “Clinical record”, the number “3” appears, instead of a multiplication symbol, in two places. The second sentence should read “Spectacle correction revealed compound hypermetropic astigmatism (right eye, +1.00 + 1.50 × 75°; left eye, +1.75 + 2.25 × 110°).” In the same article, the initial capital letter (“V”) of the first paragraph after the clinical record box is missing: the first word should be “Venlafaxine”. Similarly, in the article by Ng C V T [page 120] in the same issue, the initial capital letter (“M”) is missing: the first word of the first paragraph should be “Myasthenia”. The html and pdf versions of these articles were correct when published online.

Maria Hannah Pia de Guzman MD, DPBO · Sureka Thiagalingam MPH, MB ChB · Poh Yan Ong MD, MS · Ivan Goldberg MB BS, FRANZCO, FRACS

Clinical record A 35-year-old man presented to the emergency department complaining of right visual blurring and discomfort overnight. Over the previous 2 years, similar episodes had occurred, mostly at night or in dim lighting, affecting one eye at a time and resolving spontaneously each time. The patient was not using any type of medication at the time when the episodes began to occur. Although infrequent initially, these episodes had increased to two or three times a week after mirtazapine, a tetracyclic antidepressant, had been prescribed for depression and anxiety 5 months previously. Symptoms persisted despite treatment being changed to sertraline, a selective serotonin reuptake inhibitor (SSRI). Ten days before presentation, the sertraline was replaced by venlafaxine 75 mg once a day. Symptoms were occurring about every other day. There was no other significant ocular or family history. Spectacle correction revealed compound hypermetropic astigmatism (right eye, +1.00 + 1.50 × 75° left eye, +1.75 + 2.25 × 110°). On presentation, the patient’s visual acuity was 6/24, improving, with a pinhole before the eye, to 6/9 (right eye) and 6/6 (left eye). The right pupil was fixed and mid-dilated and the cornea was mildly oedematous. Both anterior chambers were axially shallow, with forward displacement of the iris–lens diaphragm (ie, the plane formed by the iris and the anterior surface of the lens at the pupil). Intraocular pressures were 69 mmHg (right eye) and 62 mmHg (left eye) (intraocular pressure > 21 mmHg is generally considered as being elevated). Gonioscopy revealed bilateral completely closed angles. The patient was given intravenous mannitol 100 g over 40 minutes, oral acetazolamide 500 mg, topical timolol 0.5%, apraclonidine 1% and pilocarpine 2%. Intraocular pressures fell to 13 mmHg and 5 mmHg in the right and left eyes, respectively. Gonioscopically, the angles could now be opened with indentation of the cornea; however, the anterior chambers remained shallow. Bilateral laser peripheral iridotomies were performed on the day of presentation (left eye) and on the next day (right eye) to eliminate pupil block. Post-iridotomy gonioscopy showed no change in the angle configuration or anterior chamber depth. The patient was sent home with instructions to take oral acetazolamide 250 mg three times a day, topical timolol 0.5% once a day, pilocarpine 2% four times a day, and brimonidine 2% twice a day. Venlafaxine was discontinued. The patient refused alternative antidepressant medication and requested referral to a psychiatrist or psychologist for counselling. On Day 4 after the patient presented with acute angle closure, ultrasound biomicroscopy showed bilateral supraciliary effusions and anterior chamber shallowing (Box 1). Manifest refraction (ie, manual subjective measurement of refractive error) at this time revealed a myopic shift of about 3 dioptres in each eye. Over several weeks, medications to lower intraocular pressure were withdrawn one by one. Follow-up ultrasound biomicroscopy showed gradual resolution of the supraciliary effusion, which was complete some 5 weeks after the acute attack. The anterior chambers deepened slightly and the patient’s usual hypermetropic refraction returned. Gonioscopy at this time still showed easily occludable angles. Bilateral laser peripheral iridoplasties were performed to reduce the risk of future angle closure. Venlafaxine is described as a safe and effective antidepressant that is chemically distinct from other antidepressants.1 It is a non-selective inhibitor of the reuptake of serotonin, norepinephrine and dopamine and has no anticholinergic activity in vitro. Because of their relative lack of anticholinergic effects, venlafaxine and similarly acting selective serotonin reuptake inhibitors (SSRIs) are preferred over tri- and tetracyclic antidepressants for patients who are at risk of angle closure. We report the case of a young patient taking venlafaxine who developed simultaneous bilateral acute angle closure secondary to supraciliary effusions. Angle closure and/or acute transient myopia possibly caused by supraciliary effusion has been reported for many drugs, including sulfonamides, tetracycline and some diuretics.2 Supraciliary effusions causing secondary angle closure in patients taking topiramate3-5 and sulfonamides6 have been documented by ultrasound biomicroscopy by various authors. The postulated mechanisms by which supraciliary effusions produce angle-closure glaucoma and transient myopia are illustrated in Box 2. There have been reports in the literature of angle closure or increased intraocular pressure in patients taking venlafaxine8,9 or SSRIs.5,10-15 We found one previous report of bilateral acute angle-closure glaucoma in a patient taking venlafaxine8 and one report of raised intraocular pressure in two known glaucoma patients with narrow angles taking venlafaxine.9 Eleven cases of raised intraocular pressure in patients taking SSRIs have been reported to the Australian Adverse Drug Reactions Advisory Committee.10 However, the mechanisms for the raised intraocular pressure in these cases are not mentioned. To our knowledge, ours is the first reported case of acute angle closure in a patient taking venlafaxine in which the presence of a supraciliary effusion precipitating the secondary angle closure has been identified by ultrasonography. Furthermore, our patient was taking only venlafaxine at the time of presentation. The patient in the abovementioned case of acute angle closure8 had taken four other medications immediately before starting or during treatment with venlafaxine. There is a case report of secondary angle closure due to supraciliary effusions in a patient taking topiramate who was also taking venlafaxine, but the authors attributed the effusions to the topiramate.4 It is possible that the mirtazapine and sertraline taken previously by our patient contributed to his condition, as did his underlying hypermetropic status. It may be that the weak anticholinergic or mydriatic effects of serotonergic drugs are sufficient to precipitate angle closure by a mechanism similar to that of the cyclic antidepressants.6,8 The serotonergic effects of these drugs may also have a role in angle closure.11,14,16 Serotonin and serotonin receptors have been found in the human ciliary body, and serotonin, its agonists and antagonists do affect intraocular pressure.17 The supraciliary effusions documented here are evidence of the serotonergic effects of venlafaxine causing angle closure, although the precise cause for the effusions is unknown. Lessons from practice Use venlafaxine (and antidepressants in general) with caution in patients who are at risk of angle-closure glaucoma. Patients at risk are those with hypermetropic refraction (ie, whose distance spectacles magnify objects) and those with symptoms of angle closure (intermittent blurring of vision associated with seeing coloured rings around lights, eye redness, or eye pain). Such symptoms should not be dismissed as “migrainous”. Patients at risk of angle closure should undergo ophthalmological screening, particularly gonioscopy, before starting antidepressant drugs. Because any patient could develop a supraciliary effusion in response to various drugs (especially antidepressants), it is prudent to include symptoms of angle closure when educating patients about possible side effects of these drugs. They should seek ophthalmological care if they experience symptoms of angle closure or a myopic shift in their vision. 1 Ultrasound biomicroscopy images, Day 4 after the patient presented with acute angle closure A: Supraciliary effusion, right eye (arrow). (C = cornea; CB = ciliary body; I = iris; S = sclera.) B: Shallow anterior chamber, left eye. The large area of iris–lens apposition indicates forward displacement of the lens. Pupil block has already been relieved by peripheral iridotomy (not shown). (AC = anterior chamber; C = cornea; I = iris; L = lens.) 2 Postulated mechanisms by which supraciliary effusions produce angle-closure glaucoma and transient myopia * Based on information from Craig et al.7

Maria Hannah Pia de Guzman MD, DPBO · Sureka Thiagalingam MPH, MB ChB · Poh Yan Ong MD, MS · Ivan Goldberg MB BS, FRANZCO, FRACS

Much has been written about false memories — memories that are a distortion of an actual experience, or a confabulation of an imagined one. Memory and its reliability or otherwise have profound implications for us all, not only in our daily lives, but clinically and medicolegally. How often does a medical negligence or misconduct allegation boil down to “he said, she said” evidence? And we have all experienced the mismatch of memories of events shared in the distant past by more than one person. This personal anecdote records the same event as recalled by two people. Quite fortuitously in this instance, objective contemporaneous evidence settled the disagreement. Being a borderline student in Chemistry I, my poor performance in the practical examination was enough to secure a fail mark and a repeat of first-year medicine. During my rerun of Chemistry, I consistently failed to identify the colours of certain metals when held in the Bunsen flame. The Ishihara chart confirmed partial red–green colour blindness. Four years later, in 1959, I bumped into a medical school colleague in Paris, and we visited an art gallery together. Throughout the ensuing 45 years, my memory has been that the gallery was the Louvre. I have a clear memory of our standing before an impressionist painting by Manet, with mainly blue to purple hues, of Paris in the rain. My companion commented how wonderfully the red roofs contrasted with the overall bluish colours. I asked, “What red roofs?”. I could not see them until she pointed them out, and was intensely disappointed by this aesthetic consequence of my red–green handicap. That night I recorded the unhappy event in my diary. I have since visited perhaps no more than two or three art galleries, and then only as a reluctant companion to my wife. Van Gogh’s bedroom in Arles Van Gogh’s bedroom in Arles (oil on canvas — Musée d’Orsay, Paris; photo RMN © Gérard Blot) — one of three versions of the same painting, and most likely the one I saw. This one, painted while Van Gogh was voluntarily confined to a mental asylum in Saint-Rémy, includes a self-portrait as one of the paintings above the bed. In a letter to his brother, Théo, Vincent wrote “. . . it’s just simply my bedroom, only here colour is to do everything . . .” Fast forward to 2002. By chance, I re-established communication with my student colleague, now a psychiatrist in England. I commented how she had been someone I had always remembered, in large measure because of our joint experience at the Louvre. She replied that our gallery visit had made its mark on her, too. In subsequent decades of lecturing, she had taken care, when preparing slides, overheads and PowerPoint presentations, to avoid colours that might be confusing to men like me. However, the painting had not been in the Louvre, she said, but at a museum of impressionist art near the Place de la Concorde. Furthermore, the red I had not been able to see in the painting was not Parisian roofs in the rain, but the red heads of birds! Quite fortuitously, at the time of this correspondence, I was transcribing my 1959 European travel diary into typescript. I quickly checked my entry for the day at the art gallery. Yes, my colleague was right: it was a museum at the Place de la Concorde, not the Louvre. (The museum was, in fact, the Musée du Jeu de Paume at the Place de la Concorde, which housed the collection of impressionist paintings of the Louvre before they were relocated to the Musée d’Orsay in 1986.) But the painting in question? No red roofs in a rainy Paris. No birds with red heads. It was the famous Van Gogh painting of his bedroom in Arles, with the large, red coverlet on his bed! I had been familiar with Van Gogh’s bedroom painting for many years before going to Europe. But my memory, over nearly five decades, remains of rainy red roofs. No matter that I have searched the catalogues of the Impressionists and have not found such a painting. No matter that I now know that the painting with the invisible reds was the Van Gogh pictured here, my memory remains undiminished — red roofs in the rain! I still “see” them clearly. As for my colleague, despite my presenting her with the contemporaneous evidence of my diary, she, in turn, “knows” that the picture was of birds with red heads!

Peter C Arnold BSc, MB BCh, BA