Many claims about nutrition and weight loss stem from small, short-term studies, incorrect interpretations or distortions of evidence. Our knowledge of what people eat is poor; difficulties include accurate assessment of consumption, the complex composition of foods and individual variations in nutrient bioavailability. When advice appears to be ineffective, poor compliance is a likely explanation. There is no simple solution to obesity, and no fast way to create the energy deficit required for sustainable loss of fat — weight loss requires long-term commitment to permanently change eating and exercise habits. Valid advice is to reduce overall energy intake, include more vegetables, fruits and wholegrain products and fewer foods high in saturated fat, sugar and salt. While mindful of the need to encourage individuals to make changes, the medical profession needs to lead the charge to advocate for changes to our obesogenic environment.

Rosemary A Stanton OAM, PhD

Ami Schattner,* Noa Ben-Baruch† * Associate Professor of Medicine, † Head, Breast Cancer Unit, Hebrew University Hadassah Medical School, Kaplan Medical Centre, Bilu Junction, Rehovot, 76100, Israel. amiMDATclalit.org.il To the Editor: We describe a patient with malignant ascites and bacterial peritonitis, with no apparent intra-abdominal source of infection. A 56-year-old woman with advanced breast cancer was admitted to hospital with a 10-day history of diffuse abdominal pain, umbilical tenderness, and increasing abdominal girth. Breast cancer had been diagnosed 13 years before admission (T2 N0 M0) and treated with radical mastectomy and adjuvant chemotherapy. Five years before admission, disease had recurred at the chest wall, and 2 years before, liver metastases were found. Chemotherapy had failed, and her only current treatment comprised capecitabine and analgesics. On admission, the patient had tachycardia (110 beats per min), tachypnoea (26 breaths per min), blood pressure of 115/80 mmHg, and no fever or signs of sepsis. Examination showed evidence of local recurrence around the left mastectomy scar, and marked ascites with discoloration, warmth, tenderness and a diffuse infiltration over the umbilicus. There were no signs of peritoneal irritation, nor leg oedema. Blood test results were in the normal range, except for mild leukocytosis (10.6 × 109 cells/L; reference range [RR], 3.8–9.8 × 109 cells/L), with left shift (86% neutrophils, and 6% lymphocytes; RR, up to 67% neutrophils, and at least 32% lymphocytes). X-ray did not show abdominal free air. Abdominal computed tomography revealed ascites, retroperitoneal lymph nodes, omental and umbilical infiltration, and the known liver metastases without signs of portal hypertension. Peritoneal tap removed 2800 mL of fluid. Examination of the fluid revealed a white blood cell count of 2 × 109 cells/L (80% neutrophils), glucose concentration of 790 g/L, and albumin concentration of 22 g/L (serum–ascites albumin gradient, 0.7; a gradient < 1.1 indicates that the patient does not have portal hypertension). Gram stain of the ascitic fluid revealed gram-positive cocci, and culture identified Staphylococcus aureus. Cytological examination showed sheets of atypical enlarged epithelial cells highly suggestive of malignancy. Therapy was begun with parenteral cloxacillin and ciprofloxacin, but the patient died shortly after. This patient’s condition is unlikely to have been spontaneous (“primary”) bacterial peritonitis, which usually occurs in patients with liver cirrhosis, portal hypertension and ascites with high serum–ascites albumin gradient,1 and occasionally in patients with malignant ascites.2 However, in our patient, infection may have originated from the umbilical metastasis. The umbilicus has a direct connection with the intra-abdominal cavity and is also connected to a number of intra-abdominal organs via embryological remnants, such as the umbilical vein and the urachus. Both routes may be involved in the spread of malignant tumour to the umbilicus,3 but spread may also be in the opposite direction, causing peritonitis. This diagnosis may be missed by physicians who may not notice anything new in a patient with longstanding malignant ascites, and may fail to consider bacterial peritonitis, a treatable condition.

Ami Schattner · Noa Ben-Baruch

To provide physical activity recommendations for people with cardiovascular disease, an Expert Working Group of the National Heart Foundation of Australia in late 2004 reviewed the evidence since the US Surgeon General’s Report: physical activity and health in 1996. The Expert Working Group recommends that: people with established clinically stable cardiovascular disease should aim, over time, to achieve 30 minutes or more of moderate intensity physical activity on most, if not all, days of the week; less intense and even shorter bouts of activity with more rest periods may suffice for those with advanced cardiovascular disease; and regular low-to-moderate level resistance activity, initially under the supervision of an exercise professional, is encouraged. Benefits from regular moderate physical activity for people with cardiovascular disease include augmented physiological functioning, lessening of cardiovascular symptoms, enhanced quality of life, improved coronary risk profile, superior muscle fitness and, for survivors of acute myocardial infarction, lower mortality. The greatest potential for benefit is in those people who were least active before beginning regular physical activity, and this benefit may be achieved even at relatively low levels of physical activity. Medical practitioners should routinely provide brief, appropriate advice on physical activity to people with well-compensated, clinically stable cardiovascular disease.

Tom G Briffa PhD · Andrew Maiorana PhD · Noella J Sheerin RN, BAppSc · Anthony G Stubbs · Brian F Oldenburg PhD · Neville L Sammel DDU, FRACP, FACC · Roger M Allan FRACP, FCSANZ, FACC

John C Bridgman,* William F Heddle† * Cardiology Registrar, † Cardiologist, Flinders Medical Centre, Flinders Drive, Bedford Park, SA 5042. cameronbridgmanAThotmail.com To the Editor: A 50-year-old morbidly obese woman (weight, 183 kg; body mass index, 70 kg/m2) presented after 1 month of worsening dyspnoea. Risk factors for cardiovascular disease included hypertension, smoking and previous heavy alcohol consumption. She had left ventricular failure (thought to be due to diastolic dysfunction) and atrial fibrillation with rapid ventricular response. There was no evidence of infection or pulmonary embolism. A transthoracic echocardiogram showed normal systolic function, although the images were poor. Measurement of arterial blood gases showed a compensated respiratory acidosis (Paco2, 58 mmHg; Pao2, 76 mmHg; pH, 7.39; bicarbonate, 34 mmol/L; base excess, 8 mmol/L). Administration of intravenous digoxin, frusemide and heparin led to some symptomatic improvement. Cardiac monitoring showed atrial fibrillation, with ventricular rates of 120–170 beats/minute despite the digoxin treatment. Overnight, 70 pauses in heartbeat of up to 7 seconds were recorded (Box). The constellation of the nocturnal rhythm disturbance, hypercapnia and obesity suggested sleep disordered breathing as a unifying diagnosis. Further questioning revealed symptoms indicative of obstructive sleep apnoea. Polysomnography, performed that night, showed a respiratory disturbance index (number of apnoeic or hypopnoeic episodes per hour) of 130 (normal value, < 15). The longest apnoeic episode was recorded at 34 seconds. The average minimum oxygen saturation was 84% during non-REM (rapid eye movement) sleep and 64% during REM sleep. The lowest saturations reached during non-REM and REM sleep were 64% and 61%, respectively. These results suggested severe obstructive sleep apnoea.1 The following night, her condition improved with application via mask of continuous positive airway pressure (CPAP) at a level of 12 cm H2O using room air. Cardiac monitoring continued to show atrial fibrillation with high ventricular rates, but no pauses in heartbeat occurred. This allowed treatment with atenolol and digoxin to control the ventricular rate. At 6-week review, the patient was complying with home CPAP therapy and felt well. An electrocardiogram confirmed spontaneous reversion to sinus rhythm at 70 beats/minute. There is increasing evidence to suggest a link between obstructive sleep apnoea and atrial fibrillation.2 Obstructive sleep apnoea is also a risk factor for hypertension, coronary artery disease and heart failure, all of which are known to precipitate atrial fibrillation.3,4 Transient heartblock has been found in 10% of patients with obstructive sleep apnoea. Pauses of up to 2 seconds are a predictable physiological response to inspiratory airflow obstruction and hypoxia. These pauses are exacerbated by negative chronotropes. Studies have shown that bradycardia can be effectively abolished with mask CPAP therapy.5 The dramatic response to CPAP therapy in this patient suggests that sleep apnoea caused the significant nocturnal ventricular pauses and had a role in the aetiology of the atrial fibrillation. Overnight cardiac monitor trace, showing atrial fibrillation and a 7-second pause

John C Bridgman · William F Heddle

Objective: To compare changes in autonomic nervous activity in healthy senior individuals while walking with and without a dog, and during routine activities at home and periods of interacting with the dog at home.Design: Controlled crossover study.Participants and setting: 13 healthy volunteers (3 men, 10 women; mean age, 67.5 years) who walked in a park adjacent to Gunma University, Japan, and 4 volunteers among these who underwent monitoring in their own homes.Interventions: Heart rate variability was monitored continuously by means of a palm-sized electrocardiographic monitor (which facilitated spectral analysis of the RR interval) while participants walked for 30 minutes (first with, then without, the study dog, or vice versa); three participants underwent this intervention on 3 consecutive days. Four participants underwent continuous monitoring for 6 hours in their own homes, including two 30-minute periods of free interaction with the study dog.Main outcome measures: High frequency (HF) power values of heart rate variability, which is a measure of parasympathetic neural activity.Results: During dog-walking, HF power increased significantly (P < 0.01); this increase was sustained throughout each dog walk, and was more pronounced during succeeding dog walks. At home, HF power was 1.87 times greater when the dog was present, and 1.57 times greater (P < 0.01) than in the walking experiment.Conclusions: Walking a dog has potentially greater health benefits as a buffer against stress in senior citizens than walking without a dog; and, independent of actually walking, merely patting and talking to a dog also raises parasympathetic neural activity. Power spectral analysis of heart rate variability shows promise as a non-invasive approach to quantifying clinicophysiological research on human health benefits possibly derived from interaction with companion animals.

Masahiko Motooka MMS · Nell L Kennedy PhD · Hiroto Koike MD, PhD · Tomoyuki Yokoyama MD, PhD

To the Editor: Goldney and Fisher recently reported data on medication use in an Australian community sample and estimated the financial savings that could be made if the number of prescribed medications was reduced.1 However, the assumption that the average number of medications per patient could be reduced ignores the large body of evidence that has accumulated over recent years demonstrating under-use of beneficial medicines. Under-prescribing has been identified in the management of a broad range of chronic conditions, including heart failure, ischaemic heart disease, hypertension, atrial fibrillation, asthma, osteoporosis, pain, and depression.2,3 It has been suggested that under-use of beneficial therapies may be an even bigger problem than over-prescribing, especially in older patients.4,5 As Goldney and Fisher did not collect any clinical information about their study subjects, no conclusions can be drawn about whether medications were more frequently over-prescribed or under-prescribed. Focusing solely on reducing the number of medications prescribed may be misguided and may result in poorer health outcomes. A broader view of prescribing is required, recognising that problems result from both over- and under-prescribing, as well as inappropriate dose selection and monitoring.5

Rohan A Elliott

The last well person. How to stay well despite the health-care system. Nortin M Hadler. Montreal: McGill-Queen’s University Press, 2004 (viii + 313 pp) ISBN 0 7735 2795 8. Somewhat paradoxically, reading this book left me disturbed and critical, despite my wholehearted agreement with most of the imperatives presented in this critical analysis of modern medical practice. The basic message is accurate and important: too many with minor ailments who enter the health care system are convicted of being ill when in fact they are healthy. Well people, Hadler suggests, are those individuals yet to be investigated by a doctor! The health care system is, he argues, poorly evidence-based in far too many areas. Over-diagnosis and the reflexive resort to the prescription pad, rather than reassuring dialogue, is endemic. There is much truth in this of course, but he “doth protest too much, methinks”. For example, Hadler’s views on modern cardiological practices fail to avoid the bias and selective reporting of data he so strongly criticises in others. Individuals with suspected angina are advised to enter into a contract with their doctor that will exclude both angiography and bypass surgery as diagnostic or therapeutic options. In warning patients that much of what a doctor recommends may be of questionable benefit, he fails to educate the lay reader of the possible advantages of early diagnosis and intervention in a person who indeed still feels “well”. Hadler tells us that the book is written for those who are well but nonetheless tempted to stray into a doctor’s office from which they will undoubtedly emerge medicalised. In fact, the contented well are unlikely to pick up this volume while the worried well are unlikely to be persuaded that their concerns are baseless. No, this book is one for students and practitioners of clinical medicine. It is laudably academic in discussing most of the topics covered, with an extensive bibliography and no less than 56 pages of annotated critiques of the studies that, when analysed accurately, support the author’s contentions. Being challenged to re-analyse investigative and therapeutic approaches that are entrenched but by no means evidence-based is, of course, no bad thing, nor hardly revolutionary. Hadler’s challenge to improve statistical analysis to provide outcomes that are undoubtedly clinically relevant is welcomed. Meta-analyses and the Cochrane library have not served our patients well, he argues, wanting us to better define real rather than relative risk. A rheumatologist, Hadler is perhaps at his best when discussing the myriad dubious approaches to the management of musculoskeletal discomfort, turning many patients into invalids entangled in a nightmare of medico-legal wrangling. Such patients, he argues, will receive more help from their therapist than their pharmacist. It is modern medicine’s emphasis on investigations and pharmacy that is driving many patients, who want to ventilate their problems, into the offices of unscientific “alternative” practitioners. Hadler is on shakier ground when he argues that most of us have genes that program us to live for 85 years (plus or minus a few), and will do just that whether or not we treat high cholesterol or moderate hypertension. He doubts the ability of human strategies to have us live longer (a brave assumption given the remarkable increases in longevity achieved even in the post-antibiotic era), and opines that we have made too much of the obesity epidemic in modern societies. He argues that our approach to the diagnosis and management of prostate cancer is often too aggressive, but fails to call for better decision-making that may well save the lives of many who currently die in much discomfort from this malignancy. I’m glad I read this book and have no hesitation in recommending it. We have a long journey ahead of us before we consistently avoid the pitfalls forthrightly identified by Hadler. Doing so will give us our best chance of having many more people remain chronically well because of rather than despite the health care system. John M DwyerEmeritus Professor of Medicine, Sydney, NSW

John M Dwyer

The presumption that fictional characters may have real diseases is nothing new. The description of mental illness is a constant feature in literary criticism, and with increasing frequency, descriptions of physical afflictions suffered by literary characters have been showing up in the medical literature. Various characters have even lent their names to medical syndromes — who doesn’t know that Pickwickian Syndrome derives its name from a character in Charles Dickens’ Pickwick Papers or that the Lilliputian Syndrome derives its name from the land of little people in Jonathon Swift’s Gulliver’s Travels?1 However, characters in children’s literature have been less well examined for physical maladies. Save for a recent article on head trauma in nursery rhymes,2 this area seems largely unexplored. We propose that children’s literature provides a wealth of descriptions of disease states; one only has to look. Consider the following as examples. Winnie the Pooh The tale of Winnie the Pooh, A A Milne’s good-natured but bumbling bear, seems on the surface to be a simple children’s story. However, examining Mr. Milne’s hero in a medical light casts a different shadow — that of a short, heavy-set, polyphagic bear. It is not difficult to appreciate the relative corpulence of Winnie the Pooh. In fact, it is well described. In Chapter 2 of Winnie the Pooh, Pooh becomes lodged firmly in the doorway of his friend Rabbit’s house as a direct result of his generous girth.3 Does he, however, have true truncal obesity? To test this theory, we measured the classic Pooh doll belonging to one of our daughters. The waistline measurement was found to be 37 cm; the hip circumference was 38.5 cm. This gives a waist to hip ratio of 0.96, well over the 0.9 necessary to define abdominal obesity. This got us thinking . . . Could Pooh be an early example of the metabolic syndrome? By World Health Organization criteria, he would also need to have hyperinsulinaemia and hypertension or dyslipidaemia.4 While it is difficult (if not impossible) to measure the fasting plasma glucose level and blood pressure of a fictional character, we do believe that Milne left clues for us to follow. The first is that Pooh is always hungry — the polyphagia of impaired glucose tolerance. The second is the very nature of his food — as everyone knows, honey-coated translated to Latin is mellitus. We think that Winnie the Pooh may be a very appropriate spokesperson for metformin. Humpty DumptyHumpty Dumpty sat on a wall, Humpty Dumpty had a great fall, All the king’s horses and all the king’s men Couldn’t put Humpty together again. So, what caused the massive trauma that apparently befell Humpty Dumpty? The classic image of this character is that of a large egg, which has fallen from a wall. However, the origin of this image is exceedingly unclear. Might it, in fact, be that Humpty Dumpty was actually not an egg, but rather a human with eggshell-like bones? We propose that Mr Dumpty actually suffered from osteopetrosis, a rare disorder characterised by impaired resorption of bone by osteoclasts.5 The resulting bone is exceedingly dense and can, in severe cases, crowd out haematopoietic cells. This results in exceedingly brittle bones, and affected individuals have frequent fractures, not infrequently from “great falls”. Also, with the displacement of the marrow, extramedullary haematopoiesis is common and frequently causes hepatosplenomegaly.5 Is it possible that Mr Dumpty acquired a distended abdomen as a result of organomegaly, producing a torso that was egg-shaped? Furthermore, the resultant anaemia may lead to pallor, causing the skin to assume a colour reminiscent of an eggshell. The possibility that Mr Dumpty represents the first described case of osteopetrosis is high, and should be investigated further. Goldilocks and the three bearsIn this classic tale, Goldilocks happens upon the three bears’ house. She samples all of their food, angrily rejecting their porridge as either too hot or too cold. Then, after finding the perfect bed, she falls into a deep sleep. These are all horribly inappropriate things to do in a stranger’s house. In this story, we appear to have hypersomnia, polyphagia, social disinhibition, and irritability — all strongly characteristic of the Kleine–Levin syndrome.6 This syndrome typically (though not always) occurs in adolescent males, and involves periods of hypersomnia followed by megaphagia. While Goldilocks does not exhibit the hypersexuality frequently associated with this disorder, she does display its characteristic irritability, confusion, and impulsive behaviour. As for the apparent reversal of the sleep–eat phase in this story, it is highly likely that Goldilocks had awoken from sleep immediately before the initiation of the tale. Little Boy BlueLittle Boy Blue, come blow your horn The sheep’s in the meadow, the cow’s in the corn, Where’s the little boy who looks after the sheep? Under the haystack, fast asleep. To conventional thinkers and many a child, this rhyme conjures up an image of a lazy little boy, dressed all in blue catching an ill-timed nap while his chores go unfinished. We suggest an alternative hypothesis. As individuals can change their clothing quite easily, it would be folly to record for posterity a rhyme based upon colour of the the garments of a small child. On the other hand, what if the “blue” represents some intrinsic property of the individual? We propose that Little Boy Blue was actually cyanotic, causing a bluish hue in his skin. Examining the rest of the data available in the rhyme, it would seem likely that Little Boy Blue was born with the rare Taussig–Bing syndrome (a ventricular septal defect located immediately below the pulmonary valve).7 This causes transposition of the great vessels and subsequent pulmonary hypertension. Severe pulmonary hypertension doubtlessly led to shortness of breath and fatigue, necessitating frequent sleep. The act of blowing a horn would undoubtedly decrease venous return by increasing intrathoracic pressure and causing a relative decrement in the forward flow of blood. It is not difficult to imagine that this would be unsettling to anyone with already compromised respiratory function, let alone a small child. Little Boy Blue was not lazy; he merely needed a cardiothoracic surgeon. Modern examplesRaggedy Ann is a well known red-haired character (as is her male counterpart, Raggedy Andy, who must be mentioned for the sake of political correctness). To even the most casual observer, Ms Ann does not appear to be the picture of health. Immediately noticeable is the straight, coarse, red hair surrounding a plump, round face. Further investigation and more careful physical examination reveal in Ms Ann more subtle signs of disease. Vital signs show Ms Ann to be hypothermic (in fact dangerously close to poikilothermic) and underweight. Further dermatological inspection shows her to have extremely dry skin. Neurological evaluation shows some degree of muscle flaccidity and perhaps even atrophy. Given these findings, it seems entirely likely that Ms Ann suffers from protein malnutrition, or more specifically, Kwashiorkor.8 Ms Ann is apathetic about this probable diagnosis (and everything else for that matter), which is also a symptom of the disease. The trend continues. Modern day characters exhibit modern day afflictions. A certain olive-colored, swine-loving amphibian host of a children’s television show appears to be suffering from a variety of maladies. His most striking feature is his greenish hue; but we should not overlook his obvious exophthalmos, absence of a visible nose, hyperkineticism, and loss of coordination. A MEDLINE search gives a possible unifying answer for this constellation of symptoms: exposure to nitromethane. As this chemical is a common synthesis intermediate in agricultural fumigants and biocides, it is likely that this unfort-unate’s pond was exposed. National Toxicology Program studies of toxicology and carcinogenesis related to nitromethane in F344/N rats and B6C3F1 mice show that this chemical can cause hyperactivity and loss of coordination; hepatomegaly; anaemia; increased methaemoglobin concentration; and exophthalmos along with olfactory degeneration.9 This character’s protuberant eyes and lack of nasal structures are self-evident. We postulate that his greenish hue is in fact a combination of anaemia and increased bilirubin level from methaemoglobinaemia, worsened by hepatic dysfunction. His anaemia may be severe enough to cause a peripheral cyanosis, with his jaundice and cyanosis combining to cause a greenish colouration. ConclusionWe believe we have made nothing short of tenuous arguments that nursery rhymes and other popular children’s literature are often thinly veiled references to chronic disease states. We advise physicians to become observant of the literary works that their children and grandchildren enjoy, and, if possible, to subject them to the rigour of evidenced-based medical analysis. This might be an activity that brings the whole family together.

Brown J McCallum MD · Stuart M Smith MD

An urgent alternative watershed management strategy is needed The world has vast natural reservoirs of geological arsenic. The ubiquitous nature of this element means that in some countries arsenic contaminates drinking water, enters the food chain and imposes significant human health risks. Globally, up to 100 million people are at risk of exposure to excessive levels of naturally occurring arsenic in well water or groundwater.1 The countries where arsenic levels in drinking water supplies exceed acceptable levels include Argentina, Bangladesh, Bolivia, Chile, China, Hungary, India, Mexico, Nepal, Peru, Romania, Taiwan, the United States and Vietnam.1,2 A young girl drinking water from a tube-well. (Reproduced with permission: PE-12G-003/Shehzad Noorani/UNICEF Bangladesh.) In Bangladesh, the problem is particularly widespread. Many of the tube-wells in Bangladesh, which supply 95% of the water to 138 million people,3 are contaminated with arsenic at concentrations much higher than the current recommended levels.4,5 If no action is taken now, it is likely that within 20 years a substantial proportion of the Bangladeshi population will develop arsenic-related disease, including cancer. Here, we describe the magnitude and the consequences of the problem, and consider what actions are being pursued and what more needs to be done to prevent this potential public health catastrophe from becoming a reality. Arsenic is a human carcinogen.6 Chronic arsenicosis is characterised by hyperpigmentation and hyperkeratosis of the skin and cancers of the skin, lungs and bladder. Other adverse health effects include hypertension, cardiovascular disease (ischaemic heart disease), cerebrovascular disease, diabetes and reproductive effects including low birthweight, higher occurrence of spontaneous abortions and stillbirths, and congenital malformations in the offspring.7 The World Health Organization’s Guidelines for drinking-water quality8 set a provisional level for arsenic in drinking water of 10 μg/L (or 10 ppb [parts per billion]). In Australia, the guideline value set by the National Health and Medical Research Council and the Agricultural and Resource Management Council of Australia and New Zealand is 7 μg/L.9 However, in many developing countries, including Bangladesh, 50 μ g/L is commonly adopted as the guideline value, often for economic reasons, thus exposing the population to long-term risks.10 In Bangladesh, since the 1970s, in an effort to curb water-borne diseases from pathogen-contaminated surface water sources, over 10 million tube-wells have been installed by aid agencies and non-government organisations as sources of clean drinking water. Unfortunately, arsenic was not measured in tube-well water until the 1990s, and it is now known that 30%–90% of the wells in many of the villages tested contain levels in excess of the national standard of 50 μg/L — placing tens of millions of Bangladeshis at even higher risk.4,11 Arsenic-related skin lesions and the other non-cancerous conditions caused by arsenic contamination have a latency period of about 5–10 years, whereas the latency period for arsenic-related cancers is about 20–30 years. A full survey of contaminated wells in Bangladesh has yet to be completed, but initial estimates predict the cancer burden on the health system will be substantial. Lifetime excess mortality risks (per 100 000 persons) from liver, bladder and lung cancer attributable to arsenic in drinking water have been reported as 0.9, 21.5, and 175.9 in males, and 3.4, 2.1, and 48.3 in females, respectively.12 In countries such as Bangladesh whose gross domestic product or gross national income is dwarfed by those of developed nations (Bangladesh is rated 54th of 60 countries),13 the burden of arsenicosis will have a significant impact on the economy, health system and social structure. Construction of a dug-well in Bangladesh which uses a shallower aquifer to provide “arsenic free” water. An urgent alternative watershed management strategy is needed to prevent further arsenic poisoning, and several options are currently being investigated. Bangladesh’s high annual rainfall means that a key option is large catchments and dams with proper disinfection facilities to treat pathogens from surface water supply. But this is considered a long-term solution, requiring large capital investments beyond the resources of Bangladesh. For an immediate solution, relatively inexpensive interventions are being trialled at the family or village levels. These include the use of alternative water sources with low arsenic concentrations, such as dug-wells, deep tube-wells and rainwater storage. Other strategies have included the use of slow sand-filtration systems with or without chlorination and low-cost domestic filtration and/or precipitation systems using iron compounds, alum, or coal fly ash. Ultimately, it is likely there will be more than one solution. The advantages and disadvantages of these strategies have been discussed.5 Cost and compliance will be the governing factors — but we can be certain that action must be taken now. Since the problem was discovered, international aid agencies have been working with the government of Bangladesh and non-government organisations in an attempt to test every tube-well in Bangladesh to identify which wells have arsenic-free drinking water. They are also implementing many small to medium sized water treatment technologies to reduce arsenic contamination, as discussed above. However, future priorities should focus on large-scale nationally managed watershed programs and better utilisation of the vast surface water source that exists in Bangladesh. In addition, international effort is needed to find effective therapies for the people who have developed arsenicosis. Some view this as a problem that only concerns the developing world. However, continuing pressures on water resources in many developed countries, coupled with the presence of geological arsenic and acid sulfate soils, indicate that the events now occurring in Bangladesh could be repeated elsewhere. For example, in mineral-rich countries, where acid sulfate soil is prevalent in many areas, the acid-generating potential of the soil will mobilise arsenic present in ore bodies resulting in arsenic contamination in the groundwater. Recently, we have focused on the effect of the catastrophic tsunami in Asia, hurricanes in the United States, and the earthquake in Pakistan and Kashmir — natural disasters that have claimed many lives. Generally, acute disasters get a lot more media and political attention and international aid. But we also need to look to the horizon to reduce the arsenic-induced casualty that is happening in Bangladesh where tens of millions of people’s lives are potentially at risk.

Jack C Ng PhD, DABT · Michael R Moore PhD, DSc

Objective: To describe the epidemiology and clinical features of box jellyfish envenoming in the Top End of the Northern Territory and, in particular, confirmed stings from the major Australian box jellyfish, Chironex fleckeri. Design: Prospective collection of clinical data and skin scrapings or sticky-tape tests for nematocyst identification from patients presenting to Royal Darwin Hospital and remote coastal community health clinics in the Northern Territory, spanning 10 950 km of coastline; analysis of tidal, weather and seasonal data. Patients: All patients with jellyfish sting details recorded between 1 April 1991 and 30 May 2004. Main outcome measures: Demographic and clinical features, use of C. fleckeri antivenom, and associations between weather, seasonal and tidal factors and confirmed C. fleckeri stings. Results: Of 606 jellyfish stings documented, 225 were confirmed to have been caused by C. fleckeri. 37% of C. fleckeri stings were in children, 92% occurred during the “stinger season” (1 October to 1 June), 83% occurred in water 1 m or less deep, and 17% occured while victims were entering the water. Stings were least common on outgoing tides (P < 0.001) and commonest between 15:00 and 18:00 (P < 0.001) and on days with wind speed less than that month’s average (P < 0.001). Nearly all victims experienced immediate pain, but this could often be controlled with ice; only 30% required parenteral narcotics and 8% required hospital admission. Cardiorespiratory arrest occurred within several minutes of the sting in the one fatal case, involving a 3-year-old girl with only 1.2 m of visible tentacle contact. C. fleckeri antivenom was given to another 21 patients, none of whom had life-threatening features at the time they were given antivenom. Conclusions: Most C. fleckeri stings are not life-threatening; patients who die usually have cardiopulmonary arrest within minutes of the sting. The potential benefit of antivenom and magnesium under these circumstances remains to be shown, but a protocol with their rapid use is recommended if cardiopulmonary arrest has occurred. Unfortunately, this is unrealistic for many rural coastal locations, and the priority remains prevention of stings by keeping people, especially children, out of the sea during the stinger season.

Bart J Currie FRACP, DTM+H · Susan P Jacups BN, MPH