We report two elderly women who presented with hypertensive crisis and acute pulmonary oedema, which responded poorly to antihypertensive therapy. The patients were later diagnosed as having hepatitis C virus-related cryoglobulinaemia. Acute pulmonary oedema is a well-known complication of severe hypertension,1 but, to our knowledge, has never been reported in association with mixed cryoglobulinaemia. We report two patients with severe hypertension who presented with pulmonary oedema which was not controlled until cryoglobulinaemia was diagnosed and treated with plasmapheresis and methylprednisolone. Clinical recordsPatient 1Presentation: A 66-year-old woman presented to our emergency department in late February (winter) with severe dyspnoea of 2 hours’ duration. She had a 10-year history of hypertension, and had had a stroke 3 months before, but had recovered. Over the previous month, her blood pressure had been over 210/120 mmHg, and she had intermittent dyspnoea, orthopnoea and leg oedema. On examination, she was orthopnoeic, with blood pressure of 218/124 mmHg, regular pulse of 126 bpm, and respiratory rate of 36 breaths per minute. She had engorged jugular veins, bilateral chest crackles, hyperpigmentation of the legs and marked bipedal pitting oedema. A chest radiograph showed diffuse haziness over both lungs. Electrocardiography (ECG) showed inverted T waves in leads V4 to V6. Oxygen saturation was 77% while breathing 100% O2 (reference range [RR], 95%–100%). Initial management: The patient was intubated and mechanically ventilated. Her central venous pressure was 13 cmH2O (RR, 3–11 cmH2O), and pulmonary wedge pressure was 19 mmHg (RR, 6–12mmHg). She was treated with intravenous glyceryl trinitrate and diuretics, but over the next 48 hours her blood pressure fluctuated between 300/130 mmHg and 200/90 mmHg, and pulmonary oedema persisted. After 2 days, the patient was extubated. Over the next 24 hours, she developed massive bilateral pleural effusions and numerous petechiae over the legs. Echocardiography revealed a normal left ventricular (LV) ejection fraction (72%) and diastolic dysfunction. Radionuclide angiography confirmed these findings. Laboratory tests showed hypoalbuminaemia, proteinuria (daily protein loss, 9.3 g), haematuria with granular casts, impaired renal function, anaemia and thrombocytopenia (Box 1). Nephrotic syndrome was diagnosed. Further tests revealed a decreased serum concentration of complement components C3 and particularly C4, and markedly raised concentration of rheumatoid factor. However, tests were negative for antinuclear (ANA), anti-double-strand-DNA (anti-ds-DNA), antiglomerulo-basement-membrane and antineutrophil-cytoplasmic antibodies. A cryoglobulin test was positive (Box 2). Immunofixation electrophoresis of the cryoprecipitates showed monoclonal IgM/kappa and polyclonal IgG. A test for hepatitis C virus antibodies (anti-HCV) was then performed and was positive. Diagnosis: On Day 27 of admission, the patient was diagnosed with type II mixed cryoglobulinaemia associated with HCV infection. At that time, her blood pressure was still fluctuating between 230/130 mmHg and 180/100 mmHg, and pulmonary oedema and massive pleural effusions persisted, despite vigorous antihypertensive therapy with frusemide, intravenous glyceryl trinitrate, an α-adrenergic blocker and angiotensin-converting enzyme inhibitors. Repeated thoracocentesis was required to release massive effusions (initially transudative, but later haemorrhagic). Renal biopsy revealed diffuse glomerulonephritis with crescent formation. Management: Plasmapheresis was started on Day 27, along with pulse therapy of intravenous methylprednisolone (500 mg daily for 3 days). After five courses of plasmapheresis in 12 days, the hypertension and pulmonary oedema were controlled. The patient was discharged from hospital on Day 57 of admission. At discharge, serum creatinine level was 141 μmol/L (reference range [RR], 53–106 μmol/L), and she was taking prednisolone (25 mg), diltiazem (180 mg), spironolactone (75 mg) and doxazosin (8 mg) per day. Patient 2Presentation: In February, 2 years after Patient 1, a 77-year-old woman presented to our emergency department with a 1-day history of severe dyspnoea and orthopnoea. She had had hypertension for 3 years. On several occasions during the previous month, her blood pressure had risen to 200/120 mmHg. On examination, she was stuporous, with blood pressure of 200/110 mmHg, regular pulse of 112 bpm, and respiratory rate of 36 breaths per minute. She had engorged jugular veins, bilateral chest crackles, hepatomegaly, ascites and bipedal oedema. A chest radiograph showed bilateral diffuse haziness, and ECG showed a generalised low QRS complex. Blood gas analysis showed pH, 7.43 (RR, 7.35–7.45); Paco2, 3.9 kPa (RR, 4.7–5.3 kPa) and Pao2, 11.2 kPa (RR, 12.7–13.3 kPa) while breathing oxygen through a mask. Initial management: The patient was intubated and mechanically ventilated. Central venous pressure was 12 cmH2O. Echocardiography revealed concentric LV hypertrophy, normal LV ejection fraction, but impaired LV diastolic function. Blood pressure fell to 170–200/90–100 mmHg in 2 days, after diuretic and nitroprusside therapy, but pulmonary oedema and respiratory failure did not decrease, even after haemodialysis. She had massive ascites, bilateral pleural effusions, hypoalbuminaemia, proteinuria (daily protein loss, 3.5 g), haematuria, poor renal function, anaemia and thrombocytopenia (Box 1). Nephrotic syndrome was diagnosed. Levels of both C3 and C4 were markedly low. ANA and anti-ds-DNA antibodies were negative, but rheumatoid-factor titre was markedly high. Cryoglobulin tests on Days 14 and 16 of admission were positive. Immunofixation electrophoresis of serum cryoprecipitates showed polyclonal IgG. HCV tests were negative for anti-HCV antibody but positive for serum HCV RNA. Diagnosis: The diagnosis of type III mixed cryoglobulinaemia associated with HCV infection was thus established on Day 16 of admission. At that time, the patient was still being mechanically ventilated and needed repeated thoracocentesis (effusions were initially yellow, but later became haemorrhagic). Computed tomography of the head showed multiple ischaemic infarcts. Management: Plasmapheresis and methylprednisolone pulse therapy (1 g intravenously daily for 3 days) were started on Day 17 of admission. The patient was extubated the next day and discharged from hospital 2 weeks later, after two courses of plasmapheresis. Serum creatinine level at discharge was 291.5 μmol/L. DiscussionHypertensive crisis with rapid-onset pulmonary oedema has been associated with coronary artery disease,2 renal artery stenosis3,4 and phaeochromocytoma,5 but a search of English-language articles in PubMed revealed no previous reports of an association with mixed cryoglobulinaemia. The latter is characterised by the presence of cold-precipitable cryoglobulins in serum. Underlying diseases include autoimmune and infectious diseases, especially hepatitis C.6-9 “Mixed” indicates that the cryoglobulins in these patients contain either monoclonal plus polyclonal immunoglobulins (type II cryoglobulinaemia), or polyclonal immunoglobulins (type III cryoglobulinaemia).7 In hepatitis C, cryoglobulins usually contain anti-HCV antibody, HCV RNA and IgM rheumatoid factor (ie, anti-IgG autoantibody).9 Cryoglobulins often trigger the formation of immune complexes, leading to immune-complex-type vasculitis, and produce cutaneous, vasomotor, renal and neurological symptoms.7-9 In our patients, factors precipitating the acute pulmonary oedema included hypertensive crisis, renal insufficiency and probably coronary insufficiency. The hypertensive crisis and pulmonary oedema had abrupt onset, progressed rapidly to respiratory failure, were accompanied by nephrotic syndrome, and responded poorly to antihypertensive and diuretic therapy. Our patients had had moderate hypertension for 3–10 years before their blood pressure suddenly rose markedly 2 to 3 months before the development of pulmonary oedema. Hypertension has been found in 37% of patients with cryoglobulinaemia.6 When the underlying disease of cryoglobulinaemia (eg, hepatitis C) flares up, levels of cryoglobulins (which contain HCV-RNA) increase, resulting in higher levels of circulating immune complexes, acute vasculitis and raised blood viscosity. These factors all precipitate the abrupt rise in blood pressure and pulmonary oedema, and explain the failure of conventional antihypertensive agents. Treating cryoglobulinaemia in our patients decreased renal vasculitis and ischaemia, fluid overload, and ultimately hypertension and pulmonary oedema. Coronary vasculitis, found at autopsy in 22% of patients with mixed cryoglobulinaemia,6 could contribute to pulmonary oedema. However, both our patients had a normal LV ejection fraction, suggesting that neither had significant coronary vasculitis. In both patients, acute pulmonary oedema developed in winter. Whether cold weather worsens hypertension by precipitating more cryoglobulins and increasing viscosity awaits further observation. In our patients, the initial features that led to the suspicion of vasculitis were petechiae, proteinuria and haematuria. Further testing revealed decreased complement levels (especially C4). These and other manifestations, including oedema, ascites, recurrent pleural effusions, cerebral infarction and glomerulonephritis, were caused by circulating cold-precipitable immune complexes and resulting vasculitis.6-9 Chronic HCV infection stimulates B-cell clones to proliferate and produce cryoprecipitable IgM antibody with rheumatoid-factor activity10 — an important laboratory index of HCV-related mixed cryoglobulinaemia. However, Patient 2 was negative for anti-HCV antibody, possibly because the sensitivity of the anti-HCV immunoassay, although high, is still suboptimal,11 or because the anti-HCV antibodies were concentrated in cryoprecipitates, and therefore not detectable by the serum assay.7 In both patients, the refractory hypertension and pulmonary oedema responded to plasmapheresis and methylprednisolone therapy. Conventional treatment of mixed cryoglobulinaemia aims to reduce circulating immune complexes through immunosuppression and plasmapheresis.8 Although immunosuppressive therapy alone could ameliorate vasculitis,12 plasmapheresis has shown hypotensive effect in immune-complex nephritis, including mixed cryoglobulinaemia.13 It also reduces plasma viscosity and improves perfusion of the affected organs,14 thus helping in patients with hypertension, encephalopathy or severe renal impairment. Neither patient had a history of blood transfusion, surgery, intravenous drug use or tattooing. They probably acquired HCV infection through non-sterile injections or acupuncture in local clinics, the most common source of HCV infection in Taiwan.15,16 With the increasing prevalence of hepatitis C,17 knowledge of its extrahepatic manifestations is important. Our two patients illustrate the association with mixed cryoglobulinaemia presenting with hypertensive crisis and acute pulmonary oedema. 1 Blood test results before diagnosis of cryoglobulinaemia Test Patient 1 Patient 2 Reference range Serum albumin (g/L) 24 24 32–45 Serum urea nitrogen (mmol/L) 13.9 36.8 2.9–8.2 Serum creatinine (μmol/L) 230 412 53–106 Haemoglobin (g/L) 59 98 120–160 Platelet count (× 109/L) 105 69 150–450 Complement 3 (g/L) 0.62 0.30 0.79–1.19 Complement 4 (g/L) 0.02 0.07 0.17–0.37 Rheumatoid factor 1:10 240 > 1:20 480 < 1:40 2 Cryoglobulin test Cryoglobulin particles float in the serum and precipitate at the bottom of the test tube at 4°C. The particles dissolve on rewarming of serum to body temperature.

Li-Na Lee MD, PhD · Shyh-Chyi Lo MD · Fu-Chi Lin BS · Hon-Ping Lau MD · Jih-Shuin Jerng MD · Pan-Chyr Yang MD, PhD

Drugs, droughts and snouts In the late 1990s, amid a glut of cheap, relatively pure heroin, drug overdose deaths in Australia rose alarmingly. However, for various reasons, the supply later dried up and, by 2001, drug users were reporting a veritable drought. Degenhardt et al watched it all unfold. Did the reduced supply lead to fewer overdoses and deaths, or did users simply overdose on other drugs? Turn to “The effect of a reduction in heroin supply on fatal and non-fatal drug overdoses in New South Wales, Australia” for the answers. Of course, heroin overdose is still a common reason for ambulance callouts. Giving intramuscular naloxone, the usual first-line treatment for suspected drug overdose, exposes ambulance officers to the risk of contracting blood-borne viruses from needlestick injuries. In a randomised controlled trial, Kelly et al tested the theory that intranasal naloxone administration would be just as effective (→ Randomised trial of intranasal versus intramuscular naloxone in prehospital treatment for suspected opioid overdose). Chopper safety We didn’t need films like Black Hawk Down to associate helicopters with danger — watching the news can also do the trick. However, helicopters clearly have a crucial role to play in aeromedical transport, as well as military endeavours. How safe are they? Holland and Cooksley evaluate the accident record over 11 years for Australia’s helicopter emergency services (→ Safety of helicopter aeromedical transport in Australia: a retrospective study). Editorialists Garner and colleagues believe we can further improve helicopter safety — find out how in “Safety of emergency medical service helicopters”. Not to be sneezed at Allergic rhinitis is not a trivial condition when you consider its prevalence and its impact on quality of life, other medical conditions and productivity. Walls and colleagues present a Clinical Update on optimal management of this perennial problem (→ Optimising the management of allergic rhinitis: an Australian perspective). What’s the point? This question — with regard to the medical humanities — is often raised with Gordon, author of one of several articles on this topic. She defines the term "medical humanities" and points out the value of including this subject in the basic medical curriculum, citing "case histories" of doctors and students who've become converts to the cause (→ Medical humanities: to cure sometimes, to relieve often, to comfort always). In fact, Evans, a UK Professor of Humanities in Medicine and a keynote speaker at a conference on the subject in Sydney last year, argues that the reductionism of modern medicine makes engaging with the humanities even more vital (→ Is medicine a “cultural good”?). GP Hellman weighs in for the defence with her compelling tale of the death of a friend. The moral: that story-telling can help doctors cope with tragedy (→ Narrative and illness: the death of a doctor’s friend). Domestic and international relations If you find the latest Australian immunisation schedule (which includes some unfunded vaccines) confusing, you're not alone. The conference report from the 9th National Immunisation/1st Asia-Pacific Vaccine Preventable Diseases Conference held last year politely states that this issue "generated vigorous discussion". You'll be interested to hear, though, that rotavirus and HPV vaccines will not be long in the offing. To put things into global perspective, problems associated with providing vaccines in the Pacific were also highlighted (→ Immunisation at the crossroads: 9th National Immunisation/ 1st Asia-Pacific Vaccine Preventable Diseases Conference). Imagine Imagine there’s no barriers, says Sydney GP Mann, at least not between hospital and community. In this Utopia, the currency is in "bunyas", patient care is seamless, the healthcare world lives as one, and, wait for it, waiting lists fall. You may say she’s a dreamer, but Mann cites evidence that suggests some of this dream is well within reach (→ From "silos" to seamless healthcare: bringing hospitals and GPs back together again). Holiday reading Dip into our Letters to the Editor for our usual varied fare. Did you know about the analgesic tramadol being associated with seizures? How often do hospital doctors prescribe nicotine replacement therapy and how well immunised are our preschoolers against varicella? There were also vigorous responses to previous articles on elective surgery and smokers; using tissue plasminogen activator in stroke; web and telecounselling; playground safety standards; and subsidised access to TNF-α inhibitors (→ Letters). Cold comfort Two years apart, two elderly women presented in extremis to a Taiwanese hospital. Their marked hypertension and pulmonary oedema landed them both in intensive care, where all the usual measures proved ineffective. These women shared a rare complication of a common illness. Lee et al tell the story (→ Hepatitis C-associated cryoglobulinaemia presenting with refractory hypertensive crisis and acute pulmonary oedema)). Another time ... another place If we wish to know about a man, we ask "what is his story — his real, inmost story?" — for each of us is a biography, a story. Each of us is a singular narrative, which is constructed continually, unconsciously, by, through, and in us — through our perceptions, our feelings and thoughts and our actions, not least, our discourse, our spoken narrations. Biologically, physiologically, we are not so different from each other; historically, as narratives, we are each of us unique. Oliver W Sacks, 1985

Allergic rhinitis (AR) is one of the most prevalent medical conditions. It has significant effects on quality of life and can have considerable socioeconomic effects. The traditional classification of perennial and seasonal rhinitis does not distinguish between provoking factors, nor does it indicate the most appropriate treatment. A more useful classification is based on symptoms, which may be intermittent or persistent, and vary widely in severity. The goal of management is to achieve optimal symptom control. Therapeutic options include allergen avoidance, pharmacotherapy and immunotherapy. Antihistamines and intranasal corticosteroids (INCS) have become the cornerstones of therapy. A variety of effective treatments are available for consumers to self-select, without the advice of a doctor or pharmacist. INCS are widely recognised as the most effective pharmacotherapy for AR, in both adults and children. The efficacy of various preparations is similar, but those with low systemic bioavailability are preferred for children and for patients who are also receiving inhaled, topical or systemic corticosteroids.

Ronald S Walls DPhil, FRACP, FRCPA · Robert J Heddle PhD, FRACP, FRCPA · Mimi L K Tang MBBS, PhD, FRACP, FRCPA · Ben J Basger MSc, BPharm, DipHPharm · Graham O Solley MBBS FACP · Guan T Yeo FRACGP, MBBS

Objectives: (1) To assess the number and severity of episodes of Irukandji syndrome in Broome, Western Australia. (2) To correlate demographic, seasonal, geographic and climatic features of Irukandji stings. (3) To assess treatment of Irukandji syndrome at Broome Health Service. (4) To assess the public health impact.Design and setting: (1) A retrospective analysis of jellyfish data forms and charts of 111 patients, identified from Broome Health Service Emergency Department with a discharge diagnosis of marine sting between 1 January 2001 and 1 July 2003. (2) Correlation between climate and Irukandji envenomation data.Main outcome measures: Number of patients with Irukandji syndrome; their demographic and environmental features; the clinical syndrome; treatment requirements.Results: 111 patients were prospectively identified with marine stings; 88 were identified with Irukandji syndrome. Non-Irukandji syndrome data were excluded for analysis. The “jellyfish season” extends from January to May, although stings occur all year round. Only 38% of patients had vinegar applied to the sting site before hospital presentation. Signs and symptoms were variable between individuals, with 20% having no signs of sting at all and welts found in 16%. Fifty per cent of patients were hypertensive at presentation. Distress was found in the majority of patients, with 90% requiring opioid analgesia (morphine equivalent: mean, 20 mg; median, 13 mg) and 17% requiring admission. There was one evacuation to Perth with cardiotoxic marine envenomation resulting in pulmonary oedema, which necessitated 4 days in intensive care. Stings were significantly more common when the ambient median temperature was greater than 28.3°C, after midday, on an incoming high tide and on windy days.Conclusion: The rate of envenomation in northern WA is likely to be the highest currently documented in Australia. There is syndromic variability when compared with the north Queensland experience. This implies different causative jellyfish species that are not yet identified. Stings in Broome can be severe and life threatening; there are significant commercial and public health implications as a result. Management at Broome Hospital is contemporary and effective.

Conrad J Macrokanis MB BS, FRACGP, BSc(Hons) · Nicole L Hall · Jacki K Mein MB BS, FACCHP, MAE

How did I come to be in East Timor? That is the exact question I asked myself upon arriving in Dili, the national capital, with my husband Ben, our 2-year-old son Oscar and 6-month-old daughter Chloe in tow. It was very hot and humid and there was a real threat of a looming dengue epidemic from Indonesia. My anxiety for the health of our children was in no way eased when, a few days after our arrival, an Australian expatriate asked, “What sort of a place is this to bring kids?”. Main entrance to the Dili National Hospital I had been aware of a program coordinated by Eugene Athan, an infectious diseases physician, whereby Australian physicians could work at the Dili National Hospital. As an infectious diseases physician with an interest in medicine in developing countries, and having been assured of the political stability of the country, I put up my hand to go. Ben was able to take time off work to care for our children. After many months of planning, multiple vaccinations, and reassuring family and friends of our safety and wellbeing, we arrived in Dili in late January 2004. The Dili National Hospital is run by the East Timor Ministry of Health. The hospital medical staff consists of overseas visiting specialists, Indonesian emergency department doctors, and Timorese resident doctors working on the wards and in the outpatient department. There are no locally trained specialists — a major limitation to the long-term goal of having an autonomous Timorese hospital. I worked on the women’s medical ward for 2 months. While not arduous, the work was emotionally draining. In my first week, there were three postpartum deaths due to presumed sepsis. Like anyone, I found this difficult to deal with, but being there with my family, and still breastfeeding Chloe, made it even harder. My emotions were fuelled by the thought that one family now consisted of a husband without a wife, and four kids without a mum. The harsh reality of the estimated maternal mortality in Timor (around 800 per 100 000 live births) is that this family circumstance is not uncommon. Despite Portuguese being the official language, the majority of Timorese people speak either Tetum, Indonesian, or one of 16 indigenous languages. As my Tetum capabilities were limited to pleasantries, I relied heavily on certain hospital staff to interpret for me. Needless to say, taking an adequate history and communicating with the patients and hospital staff proved to be a challenge — like a combination of charades and Pictionary. The language barrier became even more difficult towards the end of my stint, when a Chinese medical team arrived that included doctors, a nurse and a translator. They had spent 6 months learning Portuguese, which, despite the best of intentions, was of no practical use to the majority of people at the hospital. One of the beaches within an hour’s drive of Dili. These were a favourite place for expatriates and United Nations staff to gather on Sunday afternoons. The hospital was serviced by hospital and national laboratories that performed basic testing, which was intermittently available and of variable standard. Malaria films were regularly performed, with frequent positive results. Biochemical tests, including tests for urea and creatinine, were not available during my stay. Minimal microbiological investigations (including tuberculosis smears, and serology for HIV, hepatitis B, hepatitis C and syphilis) were available. Pathology specimens were sent to Australia, with a 6–8-week turnaround time. The major medical problems I encountered at the hospital included tuberculosis, malaria, renal failure, heart failure, thyroid disease and hypertension. As all patients had varying degrees of malnutrition, I kept them in hospital for as long as possible, knowing that the hospital would provide nutritious meals. Of concern was the lack of a single positive sputum smear test for acid-fast bacilli during my stay. For whatever reason (be it deficiencies in collection, transport, processing, laboratory technique or reporting), all sputum smears were negative. Aware that this could not be accurate, I introduced antituberculosis therapies in patients for whom there was a high suspicion of tuberculosis based on clinical features and x-ray results. Of greater public health concern was the lack of mycobacterial culture and sensitivity testing facilities. A national tuberculosis control program has been established to monitor patients during treatment, but some patients did not complete their therapy and it is unclear whether drug resistance is a problem. It was hard to believe we were only a 1-hour flight away from Australia. Drug therapy options were limited to an essential drug list; however, even these, at times, were unavailable. Although we had previously worked in Africa, we found it difficult to comprehend that the national hospital of one of Australia’s close neighbours could have such limited resources. Despite their many hardships and difficulties, I was touched by the loving nature and strong sense of family among the Timorese people. They were very receptive to us as a family, but we certainly raised some eyebrows. For starters, I was working while Ben stayed at home with the kids, which many locals found amusing! Ben spent most of the time fighting off malaria and dengue-carrying mosquitoes and keeping the kids and himself cool by whatever means, including a staple diet of ice-cream for the kids and beer for himself. During weekends off, we were able to hire a car and explore many beautiful parts of the country. Having spent only a short period of time at the Dili hospital, I was grateful for the welcome I received and the warmth of the hospital staff. Upon leaving, I felt I had contributed to the health of my patients, and yet had a deep sense of sadness because it seemed that the healthcare system may worsen before it improves. So, were we foolish to take our kids to Timor? On the contrary — we believe that we took them to a place full of caring, loving and welcoming people who deserve the chance to live a better life.

Carolyn L Beckett MB BS(Hons), FRACP

I wanted to work somewhere exotic, experience a different lifestyle and contribute to health advancement in a developing country. So I was delighted when Australian Volunteers International offered both me and my partner, also a doctor, a 2-year placement (February 2002 to February 2004) in Makira Province, previously the Eastern Solomon Islands. The village of Gupuna, Ugi Island, farewells our touring team. Life in the Solomon IslandsThe Solomon Islands have a subsistence agricultural economy. Of a population of 450 000, 85% live self-sufficient lifestyles involving small-scale farming, fishing, fetching water, cooking on wood fires, building and weaving. Outside events, even major ones like terrorist attacks, seem far away. Life on fertile volcanic soil surrounded by the Pacific Ocean maintains Solomon Islanders in good health. They work hard physically and enjoy a diet rich in fruit, vegetables and fish. However, they increasingly seek to supplement their traditional diet with rice, flour, canned meats and instant noodles. Healthcare in Makira ProvinceThe major causes of death in the Solomon Islands are infectious diseases and perinatal conditions.1,2 HIV/AIDS has not yet had a significant impact there.1 Makira Province, with 33 000 people, had no doctor working either when we arrived or when we left. Kirakira, the provincial capital, has a small hospital with 86 beds — plenty for patients, with spare beds for relatives. Coping with the hospital’s unreliable medication supply was a challenge — sometimes it was well resourced, while at other times we struggled to manage, using the most suitable medication available at the time. People suffered for want of paracetamol, and died for want of oxygen. Nurses helped us manage patients with malaria, tuberculosis and congenital syphilis, as they knew more about managing these conditions than we did. The most common diagnoses of the 2322 patients admitted during our stay are shown in the Box. There is a national referral hospital in the capital, Honiara, where we could refer patients we were unable to manage in Kirakira. Together with specialist eye, reproductive health and tuberculosis/leprosy nurses, I established a program of touring the 34 clinics in the province to provide support to clinic staff and treat patients. Most clinics are in coastal villages, accessible by aluminium dinghy and outboard motor. As the villages may see no shipping for months, people must be totally self-sufficient. Clinic nurses manage most cases of malaria, pneumonia and gastroenteritis that are not managed at home. Under national policy, every village should be within 3 hours’ walk of a clinic, but the country’s economic situation has not enabled this policy to be fully implemented. Nevertheless, the patients I saw while touring were in remarkably good health. Common referrals to me were for back pain, hip pain, and dysmenorrhoea. It was difficult to advise the staff in the clinics that had no supplies and no means to transport patients. Australia is currently funding the purchase of solar-powered two-way radios for each clinic (radios must be solar-powered because supplies of consumables are unreliable). Trauma and related infectionsSkin and soft tissue infections, abscesses, joint and bone infections, and pyomyositis were common in Makira. These infections may be occupational hazards of subsistence farming, but young children and even neonates were affected. We drained copious amounts of pus under ketamine anaesthesia, but, unfortunately, we often had no suitable antibiotic treatment. We treated many cases, including osteomyelitis and septic arthritis, with oral doxycycline, erythromycin or chloramphenicol. There were about 12 motor vehicles in Kirakira, and the first-ever motor vehicle accident happened during our stay. A passenger in a utility tray was crushed against another vehicle. He fractured seven ribs on one side and nine on the other. We had no intercostal catheters to manage the haemopneumothorax, no intubation facilities, and no resources to evacuate him. Yet, amazingly, he survived with analgesia, oxygen, intravenous fluids and basic physiotherapy (“Hold your chest and blow hard!”). His high level of physical fitness, as a subsistence farmer, most likely saved his life. Non-communicable diseasesNon-communicable diet- and lifestyle-related diseases that are major causes of morbidity and mortality in Australia are only beginning to reach rural Solomon Islanders. We saw mouth cancers among betel-nut chewers, and liver and cervical cancers. Diabetes manifests with peripheral vascular disease, and hypertension with stroke. No myocardial ischaemia was diagnosed during our stay. Challenges and rewardsThe general standard of health and health services, despite the country’s economic difficulties, highlights the fine personal qualities of the people. Nurses continued working during periods when they were not paid. I recall one nurse who visited the hospital on a day when she was off duty. Noting that no nurses were working, she went home, put on her uniform, and returned to cover the day’s shift. As there was no stationery provided for health services, people carried exercise books for their health records. Patient-held records provide continuity of care from village health workers to visiting overseas specialists, and also give patients ready access to the information.3 We spent a memorable 2 years in the Solomon Islands, proving to me that overseas volunteer work is enriching and rewarding. It provides an opportunity to support colleagues in countries where healthcare staff are difficult to recruit and retain. Common diagnoses of patients admitted to Kirakira Hospital (excluding admissions for childbirth), Jan 2002–Dec 2003 Discharge diagnosis* Infants Children 1–5 years Children 5–15 years Adults Total Malaria 45 77 81 336 539 Skin infections, abscesses, cellulitis, carbuncles, impetigo 12 37 32 129 210 Trauma 0 9 37 82 128 Pneumonia 48 29 9 27 113 Gastroenteritis 11 17 0 13 41 Osteomyelitis, pyomyositis, septic arthritis 0 3 13 21 37 Tuberculosis 2 1 3 17 23 Cancer 1 0 0 19 20 * Not mutually exclusive.

Rosalie Schultz MB BS, MPH

We have a fabulous country out there, with lots of people who will benefit from our skills I was tired of seeing myself in my patients — white, middle-aged, middle-class, menopausal women — the “worried well”. It was time for a change. Time to leave my renovated terrace in inner Sydney. Time to put down the glass of champagne, cancel the subscription to the opera, put in storage my five pairs of boots from the Manhattan winter sales, and head off to “the bush” for a seachange. The bush was not an unknown entity for me. Although I’ve lived most of my life in cities, mainly Sydney, I was born in rural Wagga Wagga, the daughter of the first university-trained vet to practise west of the Blue Mountains. I spent my preschool days with my father, flying in a Tiger Moth to attend cows in obstructed labour, and delighting in watching his whole arm disappearing inside the birthing cow. So, my idea of what it would be like working in rural and remote Australia was partly based on these early experiences. Nonetheless, some of my friends were a little sceptical, viewing this decision as a whim, a blip in my middle-class, ABC Classic FM-saturated life. How wrong they were! I have ended up embracing wholeheartedly this wonderful life, committed to spending the rest of my working days facing the challenges of being a doctor in remote Aboriginal communities. It’s not all fun and games, of course. For a multitude of reasons, the health of Aboriginal people, as we all know from media reports and journal articles, is much worse that that of other Australians. In remote areas, the people often do not seek help until the advanced stages of an illness. A person with a toothache may first present with a huge dental abscess and a fever; another, with an unchecked ear infection, may be first diagnosed with a cerebral abscess; a pregnant woman may wander in for her initial check-up at 38 weeks’ gestation; painful joints are more likely to be lupus or rheumatic fever than osteoarthritis; and chest pain in a 26-year-old man must be treated as a myocardial infarction until proved otherwise. Flying over Arnhem Land. Photo courtesy Dan Armstrong. But medicine in the Northern Territory has grown up with an infrastructure geared to remote communities and to Aboriginal health. Having always believed in a public health system in which treatment priority is determined by illness severity (as in emergency departments in public hospitals), I was thrilled to find that the Northern Territory delivers the type of healthcare I believe in. Requests for outpatient appointments are faxed to the specialist in charge of that department and “triaged”. A woman with cervical intraepithelial neoplasia (CIN) grade III will be seen before one with grade I, and a woman with a history of breast cancer with recent weight loss and low back pain will be seen within a week. No preferential treatment linked to income or social standing. Just the sickest are seen first. Exactly how public medicine should be. Working in Aboriginal health in the Northern Territory is like working in a big cooperative family. I have never known such a sense of collegiality, and a lack of competition between healthcare providers. Help is always at the end of a phone. An emergency evacuation is organised via the district medical officer on duty for that day or night. There may be some input from a registrar or specialist to fine tune the patient’s treatment before air evacuation, and, if the patient’s condition is unstable, a registrar may accompany the nurse on the flight and perform the necessary resuscitation procedures before evacuation. Each time I have accompanied a patient to the airstrip for a medivac, I have watched the plane take off with tears in my eyes and an embarrassingly “proud to be Australian” lump in my throat. Not just the feeling that at last the patient is in safe(r) hands, but the feeling that not many countries provide such a fabulous service. But what of the communities I have worked in, the life I now lead, and the medicine I now practise. My favourite community is in western Arnhem Land, and I will return to this community in January 2005 to take up a 12-month contract. My first job there was in the “Wet”, that time of year when the skies become more ominously black as the day progresses, and the thunderstorms and lightning displays make the 1812 Overture and the Sydney Harbour New Year’s Eve fireworks display seem like child’s play. When the heavens open, the rain buckets down and the temperature drops a welcome 10°C. And, in the “Top End”, this is the time when tropical diseases blossom, and any person with symptoms of pneumonia or explosive fevers with skin lesions is diagnosed as having melioidosis until proved otherwise. This disease has a reasonably high fatality rate (the books say 17%), and the causative organism lives in the soil in the rainy season, so anyone with a cough and high fever is pumped with intravenous ceftriaxone and immediately evacuated. On a single day in this community during the Wet, our patients included a man with suspected melioidosis (which turned out to be septicaemia from a staphylococcus pustule on his leg); a 9-year-old with a huge, hard tonsillar lymph node and a massive cavity in a nearby tooth (I suspected osteomyelitis); and a 21-year-old girl who, as a child, had miraculously survived a gigantic brain abscess that developed from mastoiditis (which in turn developed from an untreated ear infection). She presented with headaches and vomiting, probably associated with a blockage in the shunt extending from her brain to her belly. And to top it off, there was a 17-year-old girl with active (treated) tuberculosis that appeared to have spread to her kidneys. All these people had to be either evacuated (with limited places on the Aerial Medical Service plane) or flown on a charter plane to Jabiru and then taken by bus to Darwin. A nightmare to organise, but somehow it gets done. One of my most memorable experiences involved visiting an outstation that, in the Wet, could only be reached by a small twin-engine plane. I had asked the outstation nurse what supplies to bring — lunch? water? stethoscope? “Just water and stethoscope”, she said. “Keep it light. Forget about the lunch. Rebecca and Samuel [at the outstation] have a pack of about 60 dogs, and they’ve become unmanageable. In fact, Rebecca and Samuel have moved out into the humpy outside, as the dogs have taken over the house. If you bring your lunch, they’ll smell it and eat you and your lunch for starters.” “Righto”, I said, always casual in the face of impending disaster. And she wasn’t far wrong. We flew over the Arnhem Land escarpment, some of the most beautiful wilderness country I have ever seen, and as the plane skidded to a halt on the very short airstrip we were prevented from getting out by a mob of about 20 ferocious dogs, who obviously thought the pilot, nurse and doctor were their breakfast, lunch and dinner by air express. Rebecca finally managed to call them off and we set up the clinic on the veranda, tending to the needs of eight people with a variety of disorders — chronic obstructive airway disease, rheumatic heart disease (requiring monthly penicillin injections and regular echocardiography and cardiology review), newly diagnosed hepatitis B, a child with anaemia, hypertension, as well as the usual smattering of hypercholesterolaemia, worms and diabetes. For all those urban GPs out there who are feeling sluggish and jaded, I thoroughly recommend considering a seachange to rural and remote Australia. If your emergency medicine skills are somewhat rusty (mine were totally obsolete), head off to your local ED and spend a few months eating humble pie while interns and residents show you the latest ropes. Book into a few courses, such as emergency life support (ELS) and early management of surgical trauma (EMST). If you’ve decided that remote Aboriginal communities might be your cup of tea, practise communicating with your neighbours from non-English-speaking backgrounds. Or, better still, travel to a country whose language and culture is totally different from your own, get ill (but not too seriously), and experience at first hand how difficult it is to describe your symptoms to a doctor or nurse who doesn’t speak your language. We have a fabulous country out there, with lots of people who will benefit from our skills. My best advice to anyone who wants to see Australia, and is ready to experience new challenges and work with some of the most disadvantaged people in the world, is to pick up the ball, run with it, and, in the words of a famous running shoe company, JUST DO IT!

Glynis A Johns MB BS, DPH, MPhil

To the Editor: Pseudoephedrine is no longer a banned substance in sport.1 It was originally banned to protect athletes from overuse and its dangers. Has it become harmless or are athletes more intelligent? This highlights much of the confusion in drug testing. Athletes with diabetes are permitted to use insulin for therapy, but those with hypertension are not allowed to take β-blockers. Both drugs are popularly believed in athletic circles to improve performance. What is to stop an athlete with diabetes from taking extra insulin for performance enhancement? Why do we discriminate against those with hypertension? There is a ban on oxygen-transport drugs and on physical environment enhancers such as hypobaric chambers. Both are alleged to produce the same result, but only use of the drug can be tested. The penalty for the drug user is disqualification, but for the hypobaric enthusiast a rousing cheer for a drug-free effort. The crime is the same, so why vary the penalty? There is never likely to be a level playing field under the present system, in which one reads of positive test results being swept under the table. How will drug testing eliminate the genetic inequalities between athletes? How will testing improve the availability of top-level coaches and training facilities to all? How can it eliminate the inequality in financial incentives, allowing some athletes to train for 6 hours daily while others have to work to enable them to train for even 2 hours daily? We have swimming costumes that decrease drag in the water,1 resulting in faster times. These are not universally available, giving their owners an advantage. A level playing field will never exist in our present system. It is incongruous that in all this mess, only drugs are available to all. The current frenzy to test blood has ethical problems which have not been addressed.2 What is to happen to an athlete who develops an infection from a dirty needle? Who is responsible for the tester who has a needlestick injury from an HIV-positive athlete? It is worth remembering that this diagnosis will only be made 3 months after the Games, when everyone has dispersed. The whole area needs to be reviewed by an outside body with no vested interest in the outcome.

Anthony P Millar

Psychotic illness and its treatment are associated with an increased rate of diabetes and worsening blood sugar control. The newer, second-generation antipsychotic agents are more likely to produce this effect than the first-generation agents, but both contribute to the problem. The effect is usually related to insulin resistance through weight gain, but other mechanisms may exist. Diabetic ketoacidosis is rare. Management of psychosis takes priority over concerns about the potential metabolic sequelae of treatment, but the prevalence of the latter requires that all patients taking antipsychotic agents be actively screened and treated. Patients treated with antipsychotic agents need baseline and regular checks, including weight, blood glucose and lipid levels and blood pressure. Management of psychosis with its attendant medical problems requires a multidisciplinary approach, with primary health practitioners playing a central role. Mortality and medical morbidity is higher in those with psychosis than expected; preventive measures, combined with early detection and treatment of hyperglycaemia and other metabolic problems, is a key public health issue.

Tim J R Lambert BSc, FRANZCP · Leon H Chapman FRACP

An 80-year-old woman with a history of hypertension presented to the emergency department with a 3-hour history of dyspnoea and precordial discomfort. Serum concentrations of troponin T, creatine kinase and creatine kinase MB isoenzyme were normal. An electrocardiogram (Box 1) showed changes consistent with myocardial ischaemia. When the patient developed haemodynamic instability, cardiac catheterisation was performed (Box 2). The patient’s condition improved after an intra-aortic balloon pump (a catheter-mounted balloon positioned in the descending aorta and timed to inflate during diastole) was placed for the management of cardiogenic shock. An echocardiogram 3 weeks later showed normal left ventricular size and function. The patient had acute transient apical ballooning with normal coronary arteries (“Takotsubo” cardiomyopathy). First described in 1990,1 the presentation is similar to that of acute transmural myocardial ischaemia, with chest symptoms and electrocardiographic changes ranging from ST-segment elevation to T-wave inversion without ST shifts.2,3 Postulated triggering factors for transient apical ballooning have included onset or exacerbation of systemic disorders (eg, cerebrovascular accident, asthma, acute abdomen) and extreme emotional distress.2 Women are 6–12 times more likely to be affected than men.2-4 The in-hospital mortality rate is less than 1%,2 and there is usually complete functional recovery of the left ventricle within 2 weeks.3,4 The 2-year recurrence rate is less than 3%.2 The optimal therapy for this condition is unknown. 1 Electrocardiogram, showing delayed R-wave progression and inverted T waves in the anterolateral leads 2 Images from cardiac catheterisation A. End-diastolic left ventriculogram. B. End-systolic left ventriculogram, showing akinesia/dyskinesia of the apical and mid portions of the left ventricle and hyperdynamic motion at the base. The left ventricular ejection fraction was 30%, with elevated left ventricular end-diastolic pressure of 35 mmHg. C. Normal end-systolic left ventriculogram (from a different patient). D. Left coronary angiogram, showing a normal left anterior descending artery.

Constantin B Marcu MD · Kristen M Andresen MD · Thomas J Donohue MD, FACC