Emergency medicine

Pandemic (H1N1) 2009 influenza has generated many controversies in Australia around case definitions, laboratory diagnosis, case management, medical logistics and travel restrictions. Our experience as clinical advisers in the Victorian Department of Human Services Emergency Operations Centre suggests the following: Case definitions may change frequently, and will tend to become more clinically specific over time. Early in a pandemic, laboratory diagnosis plays a critical role in case finding and pathogen identification. Later in the pandemic, standardised case management applied to well crafted case definitions should reduce reliance on the diagnostic laboratory in clinical management. The diagnostic laboratory will remain critical to monitoring disease surveillance, pathogen virulence, and drug susceptibility. Medical logistics will continue to challenge pandemic managers as the health sector struggles to do the most good for the greatest number of people. Travel restrictions remain scientifically controversial public health recommendations. Issues of scalability (escalation and de-escalation of the response) relating to virus lethality need to be resolved in current pandemic planning.

David A Bradt MD, FACEM, FAFPHM · Joseph Epstein FRACS, BA(Hons), FACEM

Conference delegates workshopped a realistically staged disaster scenario in which they were completely isolated from outside resources If you have to have a disaster, Broome, on the remote Kimberley coast of Western Australia, seems a good place to be; that is, until you take a closer look at what it would be like at the centre of the action. And this is exactly what delegates did during the inaugural conference on Tropical, Emergency and Disaster Medicine (TED-MED), held in Broome on 22–24 May 2009. The conference was attended by 81 delegates, including 28 general practitioners, eight tropical medicine specialists, six emergency medicine specialists and five disaster medicine specialists, plus representatives of government agencies, rural and remote nurse paramedics, clinical laboratory scientists and environmental health and industry participants. In this conference, we used the scenario of a tropical cyclone to move conference attendees outside their comfort zones and draw them into the reality of health crisis management in regional Australia. As it happened, Broome turned out to be an excellent location for the TED-MED conference because of a series of recent events, including the explosion of a refugee boat off the north-west coast of Australia and a tourist vehicle rollover on the Mitchell Plateau to the north-east. To add further realism to the program, there was severe wind damage caused by storms hitting Perth the day before visiting speakers flew into Broome, and the nation was on the verge of moving from the “Delay” phase to the “Contain” phase of the response to pandemic (H1N1) 2009 influenza. There were two triggers for a broad-based conference such as this. One was a renewed emphasis on regional development, particularly in WA’s north-west, where the expansion of the Ord River Irrigation Scheme, mining and petrochemical industries, and tourism are expected to drive a threefold to fourfold expansion of the regional population over the next decade. The second trigger was the Government of WA’s Royalties for Regions policy, under which some of the revenue generated by the mining and resources industry is returned to regional WA in the form of infrastructure funding, and is expected to add impetus to the population growth in the north of the state. In his opening address, WA Director General of Health Peter Flett emphasised the challenges of providing health care to such a thinly spread population in a tropical environment. He said that there was an urgent need to tackle the declining professional population as the baby boomer generation goes into retirement. David Atkinson, from the Kimberley Aboriginal Medical Service Council, compared his extensive experience in remote Aboriginal communities with indigenous communities in remote Canada. The extremes of hot and cold were explored further by retired remote and rural general surgeon Val Lishman AM, who spoke on his work in northern Australia and as an Australasian Antarctic Expedition doctor. Val’s moving snapshot of wilderness medicine in extreme environments was a profound reminder of the importance of resourcefulness and unquenchable optimism in the face of adversity. At the centre of the conference program was a carefully researched disaster scenario (Cyclone TED). Delegates prepared for an extended problem-solving activity through a series of lectures. Major-General Paul Alexander (Australian Defence Force [ADF] Surgeon General) gave the initial plenary session on ADF health capability, reflecting on the role Defence personnel often play in disaster response. He usefully clarified what the Defence Force can do and under what circumstances they would be tasked to assist. Highlights of subsequent parallel sessions were a vivid description by plastic surgeon Fiona Wood of the management of patients with burns who were injured in the Bali bombing, the challenges to medical evacuation from a combat zone by David Werda (former ADF paramedic during United Nations deployment to Somalia), and tag-team presentations on snakebite and emergency resuscitation by George Jelinek and Steve Dunjey (both from the Emergency Department at Sir Charles Gairdner Hospital). Steve’s recent high-profile resuscitation success in outback WA led him to comment that medicine is full of surprises. “You can see unexpected survival in patients under 50 after over 20 minutes’ resuscitation.” The closing straight was led by a relay team of experts. Juliet Hubbard, speaking for Indigenous communities, advocated much wider training of health professionals in cultural safety, particularly in managing major community crises. Alison McMillan (Department of Human Services, Victoria), speaking on the Victorian bushfire disaster, reminded us how quickly local emergency services can be overwhelmed. She gave delegates a sense of the confusion that arises as responding agencies piece together a picture of a disaster. Finally, Brad Santos, a severe-weather expert from the Bureau of Meteorology, left the storm damage in Perth behind him and showed how cyclones behave, with specific reference to their severity and time course. Having given us a taste of what to expect, he introduced the disaster scenario with a scene-setting severe-weather warning. Unlike in many tabletop exercises that aim to advertise the capabilities of host agencies, the details of the scenario were not disclosed to participating agencies. Michael Watson (Clinical Microbiologist, Perth), who led the team of scenario writers, said that he wanted a realistic challenge. As it happened, the date of the conference coincided with peak high tides, enabling Michael and his team to design a realistic scenario in which cyclonic winds caused a storm surge and significant flooding. They envisaged power, telecommunications, the airport, and road links being out of action for 48 hours. To the frustration of health administrators, there was no phone-a-friend-in-Perth option. Police, fire and emergency services, ambulance services, the Royal Flying Doctor Service, the Water Corporation, the Department of Housing and the Department for Child Protection (which is responsible for resettling displaced people) had to rely on what was available locally. There was a lot of tension in the room in the early stages of the disaster scenario as participants grappled with conflicting priorities. In the wrap-up session, table after table recounted tales of resources they discovered when they started to reach out to other groups. Some discovered leadership skills they didn’t know they had. Others showed a natural talent for critical thinking under pressure. One of the conference highlights was a vivid description by Phil Kuhne (Department for Child Protection) of what it would be like in an overcrowded cyclone shelter, and why there wouldn’t be any cyclone parties on his watch. Adding a little realism to the scenario, television crews from two competing channels arrived to interview organisers and speakers just after the scenario started, diverting critical expertise when it was most needed. Cyclone TED was full-on; a draining experience for all those involved. However, there was little rest for the delegates. While the lessons of the disaster scenario were still fresh in their minds, participants split into three parallel skills-development workshops on practical aspects of disaster response, life support with particular emphasis on failed intubation drills, and deployable molecular diagnostic laboratories. Ronan Murray brought the more esoteric aspects of laboratory diagnostic support down to earth by reminding participants of the potential role of the molecular diagnostics laboratory in assisting with front-line clinical decision making in remote or rural regions. The Australasian College of Tropical Medicine took the opportunity to consult on the practical needs of health practitioners in tropical Australia, convening a small group to write up the lessons learned and condense them into a regional development framework — as one delegate put it, the “where we are, where we need to be and how we’re going to get there” of health care in tropical Australia. This process generated the action statement that was presented at the conclusion of the conference. The document, known as the Broome Declaration (Box), captured the spirit of the meeting and provided a sense of direction. In the final discussion of the conference, converting the Declaration into action was debated. There was uncertainty over where resources could be found for infrastructure development, and some scepticism over anything resembling a centrally driven capital project, but there was considerable enthusiasm for local ownership of the process from local delegates. The TED-MED Conference demonstrated that there are people who work at the hot and dusty end of health care who are willing to provide professional leadership. The Broome Declaration represents a benchmark for health development in tropical and regional Australia. It remains to be seen whether there is a substantive political commitment to support front-line health care professionals in developing health capability for regional Australia. The Broome Declaration 1. On this day, 24th May 2009, in Broome, Western Australia, we, the participants in the first consultative tropical medicine summit convened under the auspices of the Australasian College of Tropical Medicine, hereby recognise that the following 10 themes are essential to the development of tropical health: holistic, one health;* collaborative intersectoral partnership; primacy of prevention, early intervention; cultural safety;† subsidiarity;‡ leadership development; proximity of services; immediate availability; effective communication; and strategic urgency. 2. Recognising the current shortfall in health capability in this region as typical of many parts of the tropics, we commit to: establishing tropical health development priorities based on the above themes; informing health authorities of our conclusions; and working toward practical development outcomes within our immediate areas of professional influence. 3. We therefore propose the following specific priorities for north-west Australia: developing a remote access tropical medicine training program; establishing a regional development centre for all stakeholder groups in the Kimberley and the rest of the north-west; and forming a steering group to identify governance and resource support for these outcomes. * A reference to the concept of health as a state of physical, mental and social wellbeing, rather than an absence of disease, first articulated in the Declaration of Alma-Ata.1 † Achieved in a health care setting when carers and providers are attuned to the cultural context of the individuals and communities, and are sensitive to culture-specific vulnerability. ‡ The principle of devolving responsibility for decision making to as close as possible to the level of community at which action is taken.

Timothy J J Inglis DM, FRCPA, FACTM · Ronan J Murray FRCPA, FRACP, FACTM · Michael Watson FRCPA, FRACP, FACTM

To the Editor: The Royal Flying Doctor Service (RFDS) has provided aerial emergency services to patients in the remote Kimberley and Pilbara regions of Western Australia since 1935. Until the 1980s, most evacuations were regional, and only small numbers of patients were transferred to Perth. Demand for long-distance transfers from northern WA has increased as a result of economic growth, improved resuscitation of the seriously ill, advances in treatment only available in major cities, and community expectations of more equitable access to tertiary care. In the Kimberley, a handful of specialists service an area twice the size of Victoria, confronting substantial health problems in the predominantly Indigenous population. The Pilbara, an even larger region (two and a half times the size of Victoria) and the epicentre of massive economic development in mining and energy, is also covered by only limited numbers of specialists and a single regional hospital. During the 12 months to 30 June 2009, the RFDS transferred 1018 patients from the Kimberley and Pilbara regions to Perth, up to 2200 kilometres away, and a similar number were evacuated to facilities within the regions, or to Darwin, up to 1500 kilometres away (Box 1). These patients routinely endure some of the longest medical retrievals anywhere in Australia, if not the world. With turboprop aircraft, retrieval times can be up to 12 hours. Pilot flight-time limitations over such distances mean that 93% of Kimberley patients require multiple aircraft and crews to achieve transfer (Box 2). Patient handovers increase transport time and clinical risk, and require considerable coordination. In October 2009, the RFDS in WA launched a fast long-range medical retrieval jet, available to all of the community, irrespective of their capacity to pay. The aircraft, a Hawker 800XP medium-sized jet, has been funded by corporate sponsorship from the mining company Rio Tinto, as well as by public fundraising and cost recoveries. The aircraft has been exclusively outfitted for its aeromedical role. It has the capacity to retrieve two patients in need of critical care with two medical retrieval teams on board, non-stop from the most distant locations in WA, and can carry a third stretcher patient if necessary. Although they are more expensive to purchase and operate, the use of pure jet aircraft can substantially reduce transport times for patients with complex or time-critical conditions, and thus improve clinical outcomes. This is the first jet in the history of the RFDS, and represents a quantum step forward from the “DH50 machine” referred to in the Journal in 1927,1 or the pressurised turboprop aircraft adopted in the 1980s.2 Flying times for patients will be effectively halved. The aircraft, designated “Rio Tinto Life Flight”, will be integrated into the existing RFDS state-wide retrieval service in WA, which coordinates and operates 14 turboprop aircraft from five centres. This is a significant initiative to improve access and equity to tertiary care for Indigenous and non-Indigenous Western Australians in remote areas. To date, aeromedical jet aircraft have not been government-funded. We hope that by demonstrating the viability and benefits of the service, government support will become available in future years. 1 Trends in Royal Flying Doctor Service long-distance medical retrieval from and within the Kimberley and Pilbara regions of Western Australia Years are financial years to 30 June. 2 Patients requiring more than one aircraft to achieve transfer to Perth Years are financial years to 30 June.

Stephen A Langford

With healing hands. The untold story of the Australian civilian surgical teams in Vietnam. Gary McKay, Elizabeth Stewart. Sydney: Allen and Unwin, 2009 (xvii + 286 pp). ISBN 9781741750744. Even after the passage of more than 30 years, Australians retain a collective memory of the war in Vietnam. But the volunteer surgical teams, sent by the government to work in local hospitals and treat the civilian population, have largely been forgotten. From 1964 to 1972, about 450 doctors and nurses served for periods of 3 to 12 months in one of four locations — Long Xuyen, Bien Hoa, Vung Tau and Ba Ria. Some returned for a second or third term. They were exposed to considerable personal danger and, on occasion, were under attack by the Viet Cong. Using diaries, letters and reminiscences of many team members, the authors (McKay, a Vietnam veteran, and Stewart, a historian at the Australian War Memorial) paint a vivid picture of the difficulties and frustrations of medical and surgical practice in primitive conditions with inadequate equipment, in the face of cultural indifference and lukewarm government support. This situation will be familiar to every doctor and nurse who has worked in developing countries in more recent times. More than half the patients treated were the victims of war; many others had been involved in road accidents. The stress under which the team members worked was unrelenting. Many have since suffered physical impairments to their health, with some developing post-traumatic stress disorder. Unlike Vietnam veterans, members of the surgical teams have no entitlement to repatriation benefits. The government has acknowledged their service to Australia by awarding them the same campaign medals given to soldiers, but has withheld the same entitlements. It is not too late, the authors believe, to redress this injustice. They conclude by posing the question, “Was it worth it?” Most of those interviewed seemed to think so, even if little of a permanent nature was achieved. After all, is not the relief of suffering the foremost of a doctor’s duties?

Robert K Likeman

The first rat I met in South Vietnam in 1967 was a hairless pup, jiggled by the tail in front of a bawling infant in a clinic we were holding in a refugee camp in sand dunes on the central coast, south of the city of Tuy Hoa. His mother had produced it from inside her shirt for tranquilising purposes, and it did the trick. As his eyes focused, the infant’s larynx relaxed, and everyone began to feel better until stubby hands groped for the rodent. With a twist of the wrist, however, the mother avoided a spectacle that might have lingered in our minds. I met my second rat later that day. He was a hairy thing, bolting across the sandy road between the barracks, and I wondered what he was doing out in the sun. I was surprised when he came to a sudden stop, and incredulous when he began to move backwards in a limb-whirling shower of sand. I blinked to clear my eyes of perspiration and found the reason for the rat’s reverse: fishing line connecting a rear leg to the hand of a small boy squatting with friends in the shade beside one of the huts. The rat was being reeled in to be released again, and yet again, by serious captors. I met more rats when I went into one of the barracks on a “home visit”. The huts were all the same, erected on the sand from corrugated iron and jammed with 30–40 people and their belongings. The inmates had been relocated from war zones for their own “good” and passed their days in idle misery, eating grain delivered by the government and throwing their refuse into open pits. It was very hot in the barracks — literally like being in an oven because each family cooked its meals over open fires, inside the tin sheds, in the sand dunes, under the blazing sun. The huts were stifling with smoke and humanity. I made my way to one fire to see what was on for lunch and found a frying pan filled with rats. Denuded, disembowelled and beheaded, they sizzled flank by flank under the care of an older woman in black pyjamas. Nearby lay the first of my patients: a man who was sick, febrile and immobilised by a large, painful lump in his groin, which was covered by oedematous, bluish skin. An abscess, I thought, and injected the only antibiotic I had, streptomycin, before moving to the next patient, who also had an abscess. And then, another. This seemed odd, but I remembered the holiday I had once endured as a small boy on a waterless farm in Queensland and the crops of boils that had erupted in the nether regions of several of us children after sharing an inch or two of black bath water. I suspected poor hygiene. It never crossed my mind the abscesses might have had something to do with the rats. But these “boils” were so large, and the people so sick, I aspirated one and sent pus to a nearby United States Air Force laboratory. Returning in a few days for the results, I had barely begun to savour the delicious air conditioning when a door was flung open and the technician announced with great excitement: “It is P. pestis! P. pestis! [Pasteurella pestis; now known as Yersinia pestis]” So what? I wondered, trying to recall any mention of that organism in my recent undergraduate experience at the University of Sydney. The technician informed me that we had discovered an outbreak of plague. Plague in Vietnam did not begin or end in our refugee camp. It was first recorded in 1898 in Nha Trang, south of Tuy Hoa, and the absence of any local name seemed to confirm its novelty.1 It was assumed it had been transported by ship from Hong Kong, where the Chinese epidemic had reached in 1894.1 In 1906, it was reported in Saigon (now Ho Chi Minh City), where it became endemic and caused about 1000 cases a year until the strict French administration managed to restrict it to about 25 cases a year in the 1930s. It increased again in the 1940s, during World War II. From 1962, however, the incidence in South Vietnam soared —5000–10 000 cases were reported annually until 1973,1,2 after which it fell. What caused this apparent outbreak? Where did it come from? Why did it stop? Marshall and colleagues denied an outbreak, stating it had been endemic since importation, and this notable increase merely reflected better identification by the increased numbers of doctors and laboratories associated with the Vietnam War.3 As confirmation of endemicity, they cited outbreaks in refugees and Viet Cong prisoners from regions beyond the reach of allied hospitals.3 Most rejected these denials but, if endemic, where was the fertile reservoir? Rural or town rats? It was argued “if there is no evidence that plague has come from outside sources” it must be based in “local wild rodents”,4 who transmit it either directly to humans, or indirectly, via urban rodents they have infected. Historically, plague has occasionally been associated with rural disruption. In India in 19945,6 and Algeria in 2003,7 outbreaks were preceded by rural earthquakes. Did burrows of rodents in rural areas collapse, forcing their residents to join — and infect — human refugees? Did broken buildings provide access to more food and permit proliferation? In South Vietnam, during the Vietnam War there were two massive disruptions in rural ecology: the bombing campaign and defoliation. Coincident with the outbreak of plague, 7.5 million tons of bombs (plus other ordnance) were dropped on rural South Vietnam: three times the weight dropped in World War II and with 100 times the combined impact of the atomic bombs dropped on Japan.8 Did these artificially made earthquakes drive rural rodents to the towns? Did they rupture grain stores, allowing access to food sources? Was there a limit to how much even a rat could take? Did defoliation alter their eating habits, with the same result? In 1962, Operation Ranch Hand was launched to deprive the Viet Cong of food and cover. It peaked in 1968–1969 and ended in 1971, after the spraying of over 6 million acres of rural land.9 Deforestation increases contact between humans and sylvatic sources,5 and Akiev noted that 86% of cases of plague in South Vietnam between 1966 and 1970 occurred in the most defoliated provinces.10 In many of these provinces, plague appeared for the first time. Although plausible, the theory that rural mammals were the source of plague was contradicted by field studies that found the disease to be surprisingly restricted to town mammals. Although trapping in the countryside was a dangerous pastime in those days, restricting research, Marshall and colleagues found that 99% of infected animals were the town rats, Rattus norvegicus, R. rattus, R. exulans, and the house shrew, Suncus murinus.11 After the war, researchers found that zoonotic foci were restricted to human settlement. Moreover, the flea vector, Xenopsylla cheopis, “exist[ed] only on indoor, commensal rodents”.12 Later, Suntsov and colleagues found only one rare flea to be common to rural and urban rodents, making it unlikely plague would be transferred from one to the other.13 If the rural mammals were not abandoning their homes, humans were. Around 3 million people (10% of the population) were relocated to camps such as ours in Tuy Hoa, and plague has long been recognised as a disease of the poor, crowded in slums where rats proliferate on rubbish.14 Certainly, there was inadequate disposal of rubbish in our camp, but proliferation of the urban rodents may have been even more encouraged by the practice of feeding refugees with grain shipped from central deposits and stored imperfectly in the camps in the provinces.3 This promoted transportation of rats from sites of endemicity and ensured they were well fed for reproduction. Perhaps eating habits further contributed to disease. Human skinners of infected camels15 and marmots have contracted plague through breaks in the skin, and consumers of undercooked meat have become infected.16 The former are likely to present with axillary buboes and the latter cervical, but our cases were predominantly inguinal, suggesting flea bites on the legs. Also, the rats I saw being cooked were more in danger of being over- than underdone. Fleas quickly abandon the cooling bodies of their dead hosts. I suspect the refugees in our camp were infected as they prepared the corpses for dinner. The weather affects the incidence of plague and our outbreak occurred in the drier months, as observed elsewhere. It is argued that eggs and larvae of fleas perish in the wet season.17 However, the onset of the wet can hardly explain the pattern of illness, restricted infectivity and low mortality in the outbreaks in Vietnam compared with historical accounts of other epidemics. In South Vietnam generally, the classic signs of the disease were observed: the bubonic form (after the Greek bubo, for groin), in which lymph nodes draining the infecting bite of the flea are severely affected in association with the usual systemic poisoning by gram-negative bacteria; the septicaemic form, in which the lymph nodes are not prominent; and the pneumonic form, in which bacteria invade the lungs and can be very infectious.3,18 In our outbreak, however, we only recognised the bubonic form, which also seems to have predominated in other regions. Despite the crowding in the barracks, we recognised no pneumonic forms or transference. Less common features of plague were also observed in Vietnam: asymptomatic pharyngeal carriage;19 pharyngitis and cervical adenopathy;20 and meningitis, particularly if undertreated21 — but we recognised none of these forms. Vietnam, however, did not conform to the historical concepts of expanding disaster. Many outbreaks were described, but they remained contained in numbers and sites. For example, we only recognised 15–20 patients with plague, and the disease did not spread to nearby camps or the city of Tuy Hoa; nor, mercifully, did any of our team become infected, despite the lack of any preventive measures. Early diagnosis and treatment was considered “the single most outstanding facet of plague control” in Vietnam, reducing the overall mortality to 1%–5%.3 Our practice of widespread injections of streptomycin, therefore, must have been blindly successful. We did not observe any deaths. Mass vaccination with live attenuated strains of some 10 million South Vietnamese would have contributed to control, but we did not even know this existed. Our public health management bore no responsibility for the containment of plague in our camp. There was none. Did the high ambient temperature inhibit spread? Infectivity in the flea is promoted by a “blockage” in the gut, which allows the bacteria to multiply before being regurgitated into the next host, but Cavanaugh and colleagues showed that blockage was reduced when the temperature of the flea exceeds 27.5°C, and I doubt our camp ever got below that temperature.1 Hinnebusch and colleagues found all fleas fail to block at temperatures greater than 30°C and, moreover, that their lifespan at that temperature is severely reduced, arguably due to dehydration.22 Perhaps the hot, dry environment in the camp, especially in the huts where rats were killed and prepared for food, restricted the passage of the disease by its effect on fleas. The outbreak from 1962 to 1973 was probably due to proliferation of rats and refugees and catalysed by recipes (that involved cooking rodents to prevent starvation), with the bombing and defoliation more a cause of human than rodent displacement. After the war, the reported incidence fell to several hundred cases annually until 1997, and to 22 in 2000.23 No cases have been reported since 2002.24 This progress may reflect better living conditions and patient care in Vietnam, but the natural history of plague has always been episodic, with the disease emerging and disappearing for reasons not understood.7 Pham and colleagues report a reduction in the number of rodents and fleas trapped in central Vietnam from 2000 to 2007, and absence of Y. pestis in both rats and fleas in recent years, and suggest that Vietnam may have entered one of the “silent period[s]” that have historically preceded “sudden explosions of rodent or human plague”.24 Although we did not observe any plague-related deaths in the epidemic in our camp, it might have been close. One night, feeling the need to give a sick child an extra injection (and, it must be confessed, to pursue adventure), three of us set out to visit the camp, which lay on the other side of a wide river, the Song Ba, beyond the security of the town. The road bridge had been destroyed and cars had to traverse the kilometre-long railway bridge on planks of wood that covered the sleepers, about 60 feet above the fast-flowing water. To add to the challenge, no one dared use headlights. We travelled in our old Land Rover whose gears were as disinclined to engage as the brakes, and whose muffler was as loud and steering as loose as the ladies in the “entertainment” area between the camp and the Air Force base. But when we arrived at the camp, and shut down the roaring engine, we were astonished by the silence and emptiness of the streets. It was a moonless night and we had difficulty in finding the right barrack, searching along the road with increasing dismay. The people were slow to open the door, and stood silently while we gave our needle. Firelight flickered on unsmiling faces. Just how “pacified” were these people? Let’s go! We held our breath until the car started and hurried back to the bridge to begin the slow, lurching crossing to safety. Then, about a quarter of the way across, a shape loomed from the darkness in front of us and a huge truck ground to a halt, followed by some others. We had run into an American convoy on its way to war. I was driving and, looking up, against the stars I could see the shape of a machine gunner hunched down upon us. There was a pause, with engines growling like dogs gearing for savagery; then Bruce Hansen, my team leader and good friend, swung open his door, bounded across the sleepers and pounded on the door of the truck, demanding they “back up” because “we were on the bridge first” and we were “Australians”. The driver of the truck did not take long to respond. A head appeared from above me with a simple message delivered with a southern drawl. Stripped of embellishments it was, “You back up right now, or I will push you off”, and it was confirmed by a roar of his engine and a lurch of his mighty truck. There were two practical problems with our gears: finding the right one and holding it in place. Crashing through several, I found reverse and, holding it in place, began the long, backward retreat. My leader maintained criticism of my cowardice — but from the safety of the sleepers. The machine gunner maintained his downward menace. I could have drowned like a rat. Would they have counted me a victim of plague? At least I would have been spared the injections. Boys in South Vietnam play with a lizard and rats, 1967. Reproduced from the Bruce Hansen Collection with permission of his widow, Miranda Hansen. The interior of one of the barracks in the refugee camp near Tuy Hoa, South Vietnam, 1967. Reproduced from the Bruce Hansen Collection with permission of his widow, Miranda Hansen.

John S Whitehall FRACP, MRCP(UK), DCH

Objective: To determine the relative radio-opacity on plain x-ray of bones of fish species commonly consumed in South East Queensland.Design: A cadaveric sheep model was used to mimic the soft tissues of a human neck. Bones of 10 fish species were placed in the paratracheal tissues and adjacent to the larynx. X-rays were taken and the images (including four control images with no bones) were incorporated into a Microsoft PowerPoint presentation to be interpreted by emergency specialists and registrars. Observers were blinded to which specimens contained fishbones and which did not.Main outcome measures: Sensitivity and specificity of plain x-rays for detecting impacted fishbones.Results: Significant interobserver variability was identified. Despite this, the overall specificity of plain x-rays was 90%. The sensitivity of the technique was 79% overall, but varied significantly between fish species.Conclusion: Lateral soft tissue neck x-ray is an appropriate screening tool in cases of a suspected impacted fishbone. If a fishbone is identified on x-ray, the patient should be referred for endoscopy without further imaging. X-ray may be of limited value in cases of Dory or Spanish mackerel bone ingestion. In such cases, a computed tomography scan should be the first-line investigation.

William R A Davies MB BS · Patricia J Bate PhD, MAppSci, BAppSc(Phty)

We were cruising at 5000 feet, enjoying beautifully clear winter weather, just south of Tennant Creek in the Northern Territory. My friend Don and I were flying in his Cessna 182 and about to turn east and follow the Barkly Highway to a large cattle property known as “Avon Downs”. We were planning to visit an old patient — let’s call her Claire. Originally from England, she was working for the South Australian Government in the NT looking after Aboriginal children in a kindergarten. The story began when a letter arrived from Claire asking if I would make a flying visit to her “back country” village. She heard that I had taken up private flying and had an interest in visiting the bush. My friend Don was a novice private pilot like myself, and we were both very keen to take the opportunity to test our wings on a long flight to the country. Claire lived alone in a large caravan that could accommodate four adults. It was grouped in a large, protected area with three other similar caravans: one served as the ablution block for the children, another was for their changing and rest rooms, and the third was a large classroom where lessons were conducted. Claire was endeavouring to help with training in health and education for young Indigenous children from deprived areas. The excitement was immense as we landed in a cloud of dust on the bush airstrip. We taxied up to Claire, who was surrounded by dancing and shouting children. It was not long before we were chatting about bygone years and about how Claire was coping with the various demands while attempting to introduce Western culture into the Aboriginal community. Claire described her disappointment with the lives of some of her former pupils — for example, girls aged 10 or 12 who, on returning to their Aboriginal communities, were allocated as wives to elders of the tribe. She was anxious to visit some of these older children, who now lived on the coast at Borroloola, about 500 km north of Avon Downs. Why not make a flying visit to Borroloola? It was soon decided that we should. We quickly cleared the aircraft of unwanted gear so that Claire would be able to join us on the flight. We took off early the next morning and arrived at Borroloola after about two and a half hours. Claire was very excited to see her former pupils and learn about their lifestyle and activities in the years since leaving school at Avon Downs. We spent a happy day meeting all the young mothers and their children, and the time passed very quickly. Then we suddenly remembered that the airstrip at Avon Downs did not have landing lights! We realised we had to leave quickly because the calculated flying time would only just allow us to arrive home before last light. When I turned to walk to our aircraft, I met the anxious gaze of the hospital matron: “Could you possibly help with a desperately ill little Aboriginal baby? The Flying Doctor can’t come till tomorrow and this wee child is seriously distressed and unfortunately the hospital sisters can’t help.” I looked across to Don and Claire as I followed the matron running to the sick child’s bedside. He was seriously ill from dehydration after protracted vomiting and diarrhoea and needed an intravenous saline drip. So a small baby with collapsed veins set the challenge for time and urgency. Naturally, my flying companions were a bit anxious about the prospect of delaying our departure. However, the nursing staff were all very grateful for my help. After some effort, the needle entered the vein of this brave little boy, who began to improve with the added fluid. I stood back with relief, which was shared by us all. After a quick farewell we went out to the aircraft. We checked the seatbelts, oil and fuel, then warmed up the engine and leapt into the air on track for Avon Downs. We checked our calculation on the time for last light for Avon Downs with a radio call to Mt Isa traffic control. Our calculations were correct — we would be 25 minutes late for last light on arrival! There were no options at this stage, so we pressed on, hoping the last light of the sunset on the flat landscape would give us sufficient vision. But look! What was that unusual glow ahead on the track near the horizon? That must be close to the Avon Downs airstrip! As we flew nearer to this bright area, while the natural light was failing rapidly, we saw we were being welcomed by numerous cars that had their headlights lighting up the airstrip to guide our return. It seemed the hospital staff from Borroloola had called the folk at Avon Downs and told them about our problem and why we had a delayed departure. Claire was sad to say goodbye to us but, happily, she wrote to say what fun our visit had been and that the little boy had recovered and was doing well. North-eastern region of the Northern Territory

Anthony H T Hodgkinson FRCS, FRACS, FAOrthA

Objective: The belief that the full moon and disturbed behaviour are closely linked is alive and well, despite studies to the contrary. We investigated the possibility that there is an association between only extreme behavioural disturbance and the full moon.Design, setting and participants: We undertook an observational study of patients with violent and acute behavioural disturbance who presented to the emergency department of Calvary Mater Newcastle and patients with less severe behaviour for whom hospital security calls were made.Main outcome measure: Proportion of patients for whom presentation or security call occurred in each lunar phase, modelled as a Poisson process.Results: Of 91 patients with violent and acute behavioural disturbance, 21 (23%) presented during the full moon — double the number for other lunar phases (P = 0.002). Sixty (66%) had either alcohol intoxication or psychostimulant toxicity, and five attacked staff (biting [2], spitting [1], kicking [1] and scratching [1]). In contrast, 512 hospital security calls for patients with less severe behaviour were evenly distributed throughout the lunar cycle.Conclusion: Violent and acute behavioural disturbance manifested more commonly during the full moon.

Leonie A Calver · Barrie J Stokes BSc, MSc · Geoffrey K Isbister BSc, FACEM, MD

To the Editor: Two 35 cm long blue-tongue lizards live in the rockery above my home swimming pool (water temperature, 19ºC). While cleaning the pool, I was shocked to see one of them floating motionless on the surface, but with its head held out of the water. Rescue with a net revealed a sluggish but healthy lizard, that slowly crept into the ground cover. Returning to my task, I was devastated to see the other lizard motionless on the bottom of the pool. After rescuing it, I thought it was dead, but a trace of slow muscular movement led me to action. With its head down, I rhythmically squeezed the upper body circumferentially with one hand, expelling an amazing amount of water and then saliva-like fluid. The abdomen, which had been distended to about 7 cm in diameter, reduced in size at least 1 cm. Gradually, there was more sluggish body and limb movement, but no discernible respiration and no opening of the mouth. After about 10 minutes, the eyes opened and I reduced my gentle efforts, but still fluid drained if the head was held down. Eventually, the lizard was placed on the rockery and observed. After a few minutes, it opened its mouth widely, revealing the oral cavity completely full of froth. More head-down draining and rest gradually improved the situation and, some time later, normal respiration seemed to have returned. Later in the day, it had moved about 30 cm and, before nightfall, it had gone. Next morning, both lizards were seen, appearing perfectly healthy and normal. I have no idea how long they were in the pool, or why, but presumably they had had a tussle, a game of chasey or a fight and lost their bearings. After 3 years of retirement from general practice, I felt considerable personal and professional delight! Comment: Lizards generally have simple lung structures compared with those of mammals. Their lungs are basically two membranous sacs, with no bronchial tree that leads to the alveolar sacs in mammals. This means their capacity for oxygen exchange is less than that of mammals. They have, however, many physiological adaptations to compensate for this limitation, including a capability for prolonged anaerobic metabolism and the ability to perform right-to-left cardiac shunting. Consequently, reptiles are much better able to cope with hypoxia than mammals. If hypoxia continues for more than an hour, heart rate may fall 50%, and a right-to-left shunting of up to 80% of cardiac output occurs. Several species of lizards use their capacity to cope with hypoxia to advantage and will submerge themselves for several hours to escape predators. Blue-tongue lizards are a terrestrial species and generally avoid contact with water. If necessary, however, they are very good swimmers. They tend to inflate their lungs, and use their tails to propel themselves across the surface of the water. The lizard described by Darvall probably drowned because of exhaustion and hypothermia. In reptile drowning, it is important to help remove water and respiratory secretions from the lungs using gravity and coupage, particularly as reptiles appear to lack a good mucociliary clearance system. The pool water, being chlorinated, would have had reduced microbial levels, making bacterial pneumonia, seen in accidental drowning in reptiles, less likely. Keeping the reptile warm is also important, to stimulate muscle activity and respiration. Had this lizard failed to respond to drainage and coupage, it may have needed supplementary oxygen, a measure that warrants caution. The respiratory centre of reptiles responds mostly to low partial pressure of oxygen, unlike the respiratory centre of mammals, which normally responds to increased partial pressure of carbon dioxide. Thus, supplying 100% oxygen to reptile patients requiring resuscitation inhibits return to normal respiration. Reptile resuscitation is best provided with normal air, at a rate of six breaths per minute.

William L Darvall · Shelton Smith

The major problem of access block to acute hospital admissions in Australia needs a more radical response than a focus on increasing inpatient beds, as suggested recently. Australia needs to take on board recent changes in United Kingdom hospital systems, which have revolutionised patient flow during acute admissions and dramatically improved efficiency, clinical quality and outcomes. Accident and emergency departments in the UK became recognised as part of acute hospital dysfunction. Now, increasingly, patients needing admission are directed as soon as possible to an acute medical assessment and admission unit (AMAAU), thus freeing accident and emergency staff for re-defined core priorities. AMAAUs require supervision by a new style of acute general physician, who drives timely management of acute medical patients, defines patient needs, estimates the likely date of discharge, and selects the most appropriate inpatient clinical stream. These reforms are staff-intensive and expensive, but cost-effective and patient-focused. They highlight the need for an adequate scale for acute clinical services and defined streams of care within individual hospitals, as well as explicit networking at a regional level to guarantee specialist acute services when needed.

E Haydn Walters DM, FRCP, FRACP · David J Dawson MD, FRCP

To the Editor: A previous report from our institutions identified a steady increase in the prevalence of paediatric treadmill friction burn injuries, from three in 2001 to 17 in 2006.1 We sought to determine whether there was any change in this trend during the past 2 years. Children younger than 16 years with treadmill-related injuries were identified from prospectively collected data from burns and trauma databases maintained by the trauma research nurses at two paediatric tertiary trauma centres in Sydney (the Children’s Hospital at Westmead and Sydney Children’s Hospital) between January 2007 and December 2008. Sixty-five children sustained treadmill-related injuries (17 in 2007 and 48 in 2008); 43 were boys. The mean age at the time of the injury was 3.7 years (range, 9 months to 14 years). Friction burns ranged from less than 1% to 7% of total body surface area, and most patients sustained a total body surface area burn of 1% or less (58 patients). The most common site of injury was fingers and/or hand (49), followed by forearm or upper arm (6), and torso (5). In most cases, a limb or part of a limb was trapped between the rear roller and the treadmill belt. Fourteen patients required surgery, including 13 who underwent a skin grafting procedure. Most injuries occurred while the treadmill was in use by others, with the children approaching unnoticed from behind (46). In nine cases, the injury happened when the patients themselves, at a mean age of 7.8 years (range, 2–12 years), were using the treadmill. The substantial increase in prevalence of treadmill injuries in children during the past 2 years may be related to increased sales of treadmills as the community becomes more conscious of obesity. The data also reflect other Australian studies that show that children younger than 5 years are at greatest risk, accounting for 90% of paediatric treadmill injuries during the period January 2004 to June 2007.2 Despite the risk of injury, particularly for children, there appears to be no current national regulations governing the supply of treadmills or advice that should be given to customers at the point of sale. The New South Wales Government introduced legislation in June 2009 mandating prominent permanent warning labels to be affixed to all new treadmills — the Fair Trading Amendment (Treadmills) Regulation 2008 (NSW). The NSW Office of Fair Trading, with assistance from the NSW Severe Burn Injury Service and Kidsafe NSW, has developed an alert poster (copies of which may be downloaded or ordered from their website) for display at childcare centres, playgroups and places where domestic treadmills are sold.3 The Australian Competition and Consumer Commission recently published a safety alert brochure on domestic treadmills, which contains a safety checklist.4 Although helpful, the brochure does not include previous recommendations such as caution with headset use (ie, decreased awareness of children near the treadmill), and the use of mirrors or alternative positioning to ensure children approaching the treadmill can be seen.1 As most injuries occur within the first 6 months of purchase of the treadmill,5 educating parents seems to be most important around the time of purchase. Design modifications could also reduce the risk of entrapment of a digit or hand.2 It is likely that, without better application of current injury prevention strategies, the prevalence of these injuries will continue to increase.

Lawrence H Kim · Deborah A Maze · Susan Adams · Sarah Guitonich · Siobhan Connolly · Anne Darton · Andrew J A Holland

To the Editor: Contact burns in children caused by hair-straightening devices are increasingly common. Although the dangers of hair dryers and other similar devices are well known,1 there is less awareness of the risks associated with hair straighteners. The relevant Australian Standard does not mention hair straighteners.2 Four recent studies from the United Kingdom have reported on this problem,3-6 but there is no readily identifiable published information from Australia. Hair straighteners consist of two opposing ceramic plates that are held apart when not in use. The plates are reported to reach average temperatures of 169.5°C within 4 minutes 20 seconds of being switched on. They can cause burns (temperature > 66°C) on short-term contact (10 seconds) for a period of up to 9 minutes 20 seconds after being switched off,3 and can take 30 minutes to cool to below 50°C, at which temperature they can cause superficial burns on prolonged contact. Using data collected by the Stuart Pegg Paediatric Burns Centre at the Royal Children’s Hospital, Brisbane, and the Queensland Injury Surveillance Unit, we identified 22 patients treated for hair-straightener injuries between January 2004 and June 2009. Sixteen of these were treated within the past 2 years. The median age of patients was 43.4 months (range, 9 months to 14 years). A mean of 1% of total body surface area was involved. Injuries were to the forearm and hands (16 patients) (Box), foot and lower leg (five patients), and the back (one patient). The burns were significant, with 19 partial-thickness burns, and three full-thickness burns requiring surgery. Nine of the 22 children (41%) required long-term scar management. We observed two typical patterns of injury. In toddlers (16 patients aged 9–48 months), the main mechanism of injury was grasping or pulling down a hair straightener that was either turned on or cooling, with inadequate supervision a common factor. An early-teen group (three patients) had self-inflicted burns from accidental contact or misuse, including one patient who misguidedly used the device in an attempt to remove leg hair, sustaining full-thickness burns requiring skin grafting. Increased awareness of the potential dangers of hair straighteners might help prevent burns. We suggest four precautions: Hair straighteners should be placed out of reach of children during use and storage; Children should be supervised while the device is warming or cooling; Manufacturers should label the device to warn of potential dangers; and Manufacturers should either redesign the device so that plates are not exposed, or provide a cool-touch cover. Burns to a toddler’s hand caused by contact with a hair-straightening device

Zoe M Poiner · Michael D Kerr · Belinda A Wallis · Roy M Kimble

Objective: To determine whether the availability of patients’ own medications (POM) in emergency departments (EDs) results in decreased prescribing errors of patients’ usual medications on admission.Design, participants and setting: Observational study of patients presenting by ambulance to the ED of Austin Hospital, a Melbourne metropolitan teaching hospital, between 13 and 31 March 2006. Patients were enrolled if they were brought to the ED by ambulance, aged 18 years or older, taking four or more regular medications, admitted to hospital, and not referred to a pharmacist before the admission medication chart was written. ED pharmacists determined patients’ regular medications and details of medications brought in by ambulance. Admission medication charts were assessed and discrepancies were recorded as prescribing errors if a change was made after a pharmacist discussed the discrepancy with the prescriber.Main outcome measures: Percentage of medications correctly prescribed when POM were brought in to the ED compared with when they were not; the nature and frequency of prescribing errors on admission.Results: 100 patients were enrolled; they were taking 4–17 regular medications (mean, 8.0; SD, 3.7). Among the 428 POM that were brought to the ED, 56 errors occurred (13.1%); and among the 372 regular medications taken by patients for whom POM were not brought in, 95 errors occurred (25.5%) (difference in percentages, 12.4%; 95% CI, 6.7%–18.0%; P < 0.001). The most prevalent prescribing errors were omissions (40.4%), and most errors (72.8%) were classified as of “moderate” clinical significance.Conclusions: When POM were brought to the ED by paramedics, significantly fewer errors occurred on admission medication charts. An intervention program to encourage paramedics to bring POM to the ED is indicated.

Esther W Chan BPharm(Hons), MClinPharm · Simone E Taylor PharmD, GCCRM · Jennifer L Marriott BPharm, PhD, GCHE · Bill Barger AssDipHthSci, MICACert

A 49-year-old man presented with verapamil toxicity complicated by hypotension and a junctional rhythm, in the context of deliberate self-poisoning with multiple drugs. The patient’s hypotension normalised following the early use of high-dose insulin euglycaemic therapy (HIET), without the need for additional vasopressors; it recurred when HIET was prematurely stopped, and again stabilised when HIET was recommenced. Consideration should be given to the early use of HIET in treating severe calcium channel blocker toxicity, rather than as a last resort after other therapies have failed. (MJA 2009; 191: 350-352) Clinical recordA 49-year-old man presented to a peripheral hospital emergency department 1–1.5 h after deliberately ingesting multiple medications: verapamil (unknown amount), controlled-release morphine sulfate (20 × 30 mg), diazepam (50 × 5 mg) and tramadol (15 × 200 mg). He was a smoker with a history of depression, ethanol misuse, chronic back pain, hypertension and a previous instance of deliberate self-poisoning with multiple drugs. At initial assessment, the patient’s vital signs were: temperature, 36.8°C; pulse, 84 beats/min; respiratory rate, 19 breaths/min; blood pressure (BP), 115/80 mmHg; oxygen saturation, 95% on room air; and Glasgow Coma Scale score, 14/15. He was drowsy, disorientated to time, and had 2 mm pupils that were equal and reactive. He had ataxia, dysarthria and was generally weak. His breath ethanol concentration was 0.172 mg%. Thirty minutes later, the patient was hypotensive (BP, 85/45 mmHg; pulse, 72 beats/min). He was treated with oxygen, 2 L intravenous (IV) 0.9% saline, a naloxone IV infusion (400 μg/h), and 10 mL IV 10% calcium gluconate. He was transferred to a tertiary referral centre and, on arrival (at 2.25 h after initial presentation), his BP was 85/45 mmHg, pulse was 64 beats/min, and an electrocardiogram (ECG) showed a junctional rhythm. Rapid sequence intubation (with propofol 40 mg + 20 mg IV and suxamethonium 100 mg IV) was performed for airway protection and ongoing management of haemodynamic instability, while metaraminol IV boluses (total, 0.7 mg) were administered. Activated charcoal (50 g) was given, and sedation was maintained with a propofol infusion. The patient remained hypotensive (BP, 75/45 mmHg; pulse, 56 beats/min) after intubation, so high-dose insulin euglycaemic therapy (HIET) was commenced at 3.5 hours after presentation. He was given dextrose (50 mL 50% glucose) and a 30 IU short-acting insulin IV bolus (~ 0.5 IU/kg), followed by a further bolus of 50 mL 50% glucose and a short-acting insulin IV infusion (30 IU/h) (Box 1). His BP improved to 110/70 mmHg at 4 hours, with a pulse of 82 beats/min and sinus rhythm on ECG, and he remained stable during transfer to the intensive care unit (ICU). The insulin infusion was abruptly stopped 5.5 hours after presentation, on arrival in the ICU. The patient’s hypotension subsequently recurred (systolic BP, 70 mmHg; pulse, 75 beats/min), prompting administration of 500 mL IV Gelofusine (a colloidal plasma volume substitute; B. Braun, Sydney, NSW) and commencement of an adrenaline IV infusion (20 μg/min). The insulin infusion (30 IU/h) was restarted at 8.5 hours, and his BP again stabilised (Box 1). The propofol IV infusion was gradually increased from 50 mg/h to 150 mg/h between 5.5 hours and 11.5 hours after presentation, and a noradrenaline IV infusion was commenced at 9.5 hours to maintain normotension. At 15.5 hours, pulmonary artery catheter measurements showed a high cardiac index (5.1 L/min/m2; reference range [RR], 2.5–4.0 L/min/m2) and a low systemic vascular resistance index (1047 dynes·s/cm5/m2; RR, 1900–2400 dynes·s/cm5/m2); the patient’s pulse was 85 beats/min and BP was 140/60 mmHg. HIET was continued and the patient remained haemodynamically stable. Adrenaline and noradrenaline were weaned off (at 17.5 hours and 23.5 hours, respectively), despite the propofol infusion rate being increased to 500 mg/h at 18.5 hours. Once sedation was withdrawn, the patient was extubated at 26.5 hours. Insulin was weaned over 5 h and discontinued at 30.5 hours; dextrose was stopped 1 h later. The patient was transferred to the observation ward and discharged well later that day, after psychiatric clearance. During treatment with HIET, the patient’s blood glucose levels were checked hourly and ranged from 6.6 mmol/L to 13.2 mmol/L (RR, 3.5–5.5 mmol/L). He received about 25 g/h of dextrose (mostly as 50% dextrose infusions). Potassium and magnesium levels were also serially monitored; the minimum potassium level was 2.7 mmol/L (RR, 3.5–5.0 mmol/L) at 8.75 hours, and the magnesium level troughed at 0.5 mmol/L (RR, 0.75–1.05 mmol/L) at 15 hours. These were corrected with a total of 200 mmol of potassium chloride and 20 mmol magnesium chloride. DiscussionHIET is an increasingly accepted therapy for calcium channel blocker (CCB) toxicity, but reports of its use are limited and it remains controversial. Indeed, the scarcity of severe CCB poisoning cases means that a randomised controlled trial of HIET may not be feasible.1 Treating clinicians who seek advice from clinical toxicologists are often hesitant about the high doses required and the potential for adverse effects. Such hesitancy is potentially harmful, as a hypotensive patient with a CCB overdose who otherwise appears well is at risk of abrupt lethal cardiovascular collapse.1 HIET is traditionally recommended after other therapies have failed.2,3 This case report aims to raise awareness of HIET for the treatment of CCB toxicity and supports its early use, rather than as a last resort.4 Verapamil binds the alpha-1 subunit of L-type calcium channels, preventing the intracellular influx of calcium.5 These channels are functionally important in cardiac myocytes, vascular smooth muscle cells, and islet beta cells.5 Verapamil’s cardiac toxicity results from excessive negative inotropy, negative chronotropy and negative dromotropy, characterised by myocardial depression, sinus bradycardia, and atrioventricular node blockade.4 Vascular smooth muscle tone is impaired, resulting in decreased afterload, systemic hypotension, and coronary vasodilation.5 Less well known are the metabolic effects of CCBs such as verapamil. Under the stress of the drug-induced shock state, the cardiac myocytes shift from using free fatty acids, their favoured “resting state” energy substrate, to carbohydrates.3,4 CCB toxicity also impairs the uptake of glucose and free fatty acids by cardiac myocytes3,4 and inhibits calcium-dependent mitochondrial activity required for glucose catabolism.3,4 Furthermore, insulin release is dependent on calcium influx into islet beta cells through L-type calcium channels.3,4 Thus, CCB toxicity can cause hypoinsulinaemia,3,4 which, in conjunction with CCB-induced insulin resistance, may lead to hyperglycaemia and a ketoacidotic state.6 Atropine, calcium boluses and infusions, glucagon, inotropes, vasopressors, and cardiac pacing have all been advocated for managing CCB toxicity, despite questionable efficacy.3,4,7-9 For instance, the evidence for glucagon is limited to small, non-blinded animal studies where no survival benefit or improvement in mean arterial pressure was shown, although heart rate improved in some cases.7 Rarely, heroic measures such as extracorporeal circulatory support and intra-aortic balloon counterpulsation have been successfully employed.5,10 HIET was first used to treat verapamil toxicity in humans in 1993, with a favourable outcome.6 Since then, in addition to animal studies, there have been nearly 70 cases reporting the beneficial use of HIET in humans, with an overall survival rate of 85%.8 However, to our knowledge, use of HIET in humans before the administration of glucagon or vasopressors has only been reported once.6 There have been some reports of HIET failure in treating CCB toxicity, although the dosing of insulin was low or uncertain, or it was used late.6,8 Early use of HIET may be more effective than HIET rescue therapy, as CCB-induced insulin resistance is greatest in the first 24 hours2 and the maximal haemodynamic benefit of HIET may not occur immediately.6 HIET may allow the heart to overcome metabolic starvation in CCB toxicity, which compounds the direct CCB impairment of myocardial contractility.3,4 Insulin increases glucose and lactate uptake by myocardial cells and improves function without increased oxygen demand.11,12 It also induces pyruvate dehydrogenase, hastening myocardial lactate oxidation, and helps clear the cytosol of glycolytic byproducts that impair calcium handling and cause diastolic dysfunction.3 Insulin promotes excitation–contraction coupling and contractility because enhanced glycolysis promotes increased sarcoplasmic reticulum-associated calcium ATPase activity and increased cytoplasmic calcium concentrations, and promotes calcium entrance into mitochondria and sarcolemma.3 HIET may be best used adjunctively with other measures such as catecholamines, for two reasons. First, insulin-mediated inotropy is not catecholamine-mediated, and is not affected by β blockers.3 Second, although insulin appears to improve myocardial contractility, it has no chronotropic effect and may cause vasodilation.3,8 HIET is safe, and adverse events are predictable, uncommon, and easily managed.2,8 The maximum safe dose of insulin is unknown, but loading doses of 0.5–1.0 IU/kg followed by infusions of 0.1–2.5 IU/kg/h are typically used.8 Interestingly, neither the inadvertent administration of a 1000 IU insulin loading dose for verapamil toxicity13 nor treatment of toxic cardiogenic shock for 2 days with a 6 IU/kg/h insulin infusion had any adverse effects.14 Adverse effects of HIET include hypoglycaemia, hypokalaemia, hypomagnesaemia, and hypophosphataemia.2,6,8 Although these are rarely clinically significant, they necessitate careful monitoring. Hypoglycaemia (blood glucose < 3.3 mmol/L) occurred in 16% of 55 published cases,8 and no cases of hypoglycaemia within 24 hours of CCB overdose were noted in Greene and colleagues’ series of seven cases.2 Greene et al also reported a mean dextrose requirement of 0.05 g/kg/h (range, 0–0.17 g/kg/h), although the mean blood glucose level exceeded the euglycaemic range.2 Some cases of severe CCB toxicity in patients presenting with hyperglycaemia do not require any additional glucose administration despite high-dose insulin therapy,15 and hypoglycaemia may be more likely in milder cases without marked hypotension.8 In addition, hypokalaemia (potassium < 3.5 mmol/L) was noted in only two patients in Greene et al’s small series, with a minimum potassium level of 2.8 mmol/L.2 Excessive correction of hypokalaemia should be avoided, because it reflects the intracellular shift of potassium from the extracellular compartment due to the action of insulin, rather than a potassium-depleted state.4 Interestingly, hypokalaemia in HIET may augment myocardial contractility by enhancing calcium entry during systole, and increased intracellular potassium may have a membrane-stabilising effect in excitable cells.4,6 In conclusion, we advocate consideration of the early use of HIET (as detailed in Box 2) for the prevention and treatment of life-threatening complications from potentially lethal CCB overdoses. HIET is safe, inexpensive and freely available, and suitable for use even in remote settings before transfer to a referral centre. 1 Early changes in the patient’s systolic blood pressure (SBP) and heart rate, relative to treatment with high-dose insulin and adrenaline infusions Following administration of a 0.5 IU/kg short-acting insulin bolus 3.5 hours after presentation, a short-acting insulin intravenous infusion (0.5 IU/kg/h) was commenced (black line), and the patient’s blood pressure improved. The infusion was abruptly discontinued 2 hours later and the patient again became hypotensive. This resolved following commencement of an adrenaline infusion (20 μg/min) (grey arrow), and the insulin infusion (0.5 IU/kg/h) was restarted 8.5 hours after presentation (black arrow). 2 Recommended high-dose insulin euglycaemic therapy protocol,3,4,9 based on the clinical experience of the Western Australian Toxicology Service, published case reports, reviews and animal studies Commence therapy with: Glucose 25 g (50 mL of 50% solution) IV bolus, unless marked hyperglycaemia (blood glucose > 22 mmol/L) is present Short-acting insulin 1 IU/kg bolus to maximally saturate insulin receptors Continue therapy with: Short-acting insulin infusion starting at 0.5 IU/kg/h and titrated every 30 min to a maximum of 5 IU/kg/h* Dextrose 25 g/h IV infusion titrated to maintain euglycaemia (blood glucose, 5.5–14 mmol/L); central venous access may be required to allow use of concentrated solutions (eg, 50% dextrose) and limit excess volume administration Monitor: Glucose — every 20 min for first hour, then every 1 h Potassium — replace only if < 2.5 mmol/L and there is a source of potassium loss Therapeutic end points: Improvement in myocardial ejection fraction (> 50%); increased BP (systolic BP > 90 mmHg in adults) Adequate heart rate (> 60 beats/min) Resolution of acidaemia; euglycaemia; adequate urine output (1–2 mL/kg/h) Reversal of cardiac conduction abnormalities (QRS interval < 120 ms) Improved mentation Therapy is weaned after the withdrawal of other vasopressors, as cardiotoxicity resolves. Dextrose may be required after cessation of insulin. IV = intravenous. BP = blood pressure. * The maximum safe and effective rate of infusion is unknown but may be even higher than 5 IU/kg/h. In animal studies, insulin infusions as high as 10 IU/kg/h have been safely used.11

Christopher P Nickson MB ChB, DTMH, GCertClinTox · Mark Little FACEM, DTMH, MPHTM

To the Editor: Francis and colleagues revealed a significant 29-minute decrease in the median emergency department (ED) length of stay and reductions in mean turnaround times for full blood count requests following the redesign of pathology processes.1 Laboratory performance and clinician satisfaction are intrinsically bound up with the timeliness of test results, not least because of their effects on patient diagnosis and treatment. The association between test turnaround times and ED length of stay is difficult to decipher. The reasons for this, as pointed out by Francis et al, include the many potential variables that contribute to patient length of stay in EDs. Turnaround times can also vary dramatically according to laboratory operating procedures and work processes. Nevertheless, there is a strong imperative to monitor these indicators as contributors to designing effective interventions to improve the quality and outcomes of patient care. Our research has also revealed that pathology test turnaround times are a significant contributor to ED length of stay at a major teaching hospital in Sydney. Using regression analysis to account for a number of contributing length-of-stay variables (eg, triage category, patient age, number of tests ordered), we produced a model that accounted for 25.4% of the variance in ED length of stay, of which pathology test turnaround time was a significant contributor.2 Further, studies of the effects of electronic test-ordering systems on test turnaround times in five Australian hospitals have shown that introduction of these systems in each instance was associated with significant declines in test turnaround times.2-4 Thus, there appears to be converging evidence of a relationship between efficient test ordering and processing and reduced ED length of stay.5 In addition to the types of interventions described by Francis et al, electronic test ordering should be considered as a system-wide intervention that may contribute to improved efficiency and patient outcomes. Decision support within such systems provides an added ability to provide alerts and guidance in the test-ordering process.

Andrew Georgiou · Johanna I Westbrook

In reply: A recent report on the state of Australian public hospitals highlights figures of 320.6 emergency presentations per 1000 weighted population, with 88% of presentations being triage categories 1–4, and 66% of patients not admitted.1 In our experience, pathology tests are performed on more than 50% of patients in these triage categories who present to emergency departments, and decisions regarding patient care are delayed pending availability of test results. In addition to the initiatives that we described,2 Georgiou and Westbrook describe other initiatives that deliver significant, sustained improvements in health care efficiency. Many have emphasised the need to improve efficiency in the health care system by utilising evidence-based best practice. However, a recently published discussion paper highlights the challenges associated with ensuring that health care workers have access to, and actually use, evidence-based processes and protocols that have been shown to benefit patients.3 Similarly, delays in care may contribute to patient harm, and decisions about resource allocation and organisational systems do not always explicitly take this risk into consideration.3 These challenges may be partly related to the different funding arrangements in the Australian health care system. Apart from the obvious federal–state dichotomy, diagnostics, such as pathology services, and the associated information technology are often funded separately to the hospitals and health care professionals relying on these services. As a result, one of the challenges of implementing initiatives that improve efficiency relates to current and historical allocative funding arrangements, where costs may be borne by one cost centre, and benefits are delivered to patients and other elements of the health care system (ie, other health care providers and departments). It is essential that the Productivity Commission4 considers all of these elements in its review to identify significant efficiency improvements within the hospital system. Effectiveness, allocative efficiency and dynamic efficiency are just as important as simple economic efficiency. Unnecessary delays in the health care system are not only associated with capital costs — they are also associated with an array of direct and indirect costs related to caring for patients who endure an unnecessarily protracted journey through the health care system. It will take courage and commitment to implement and achieve appropriate use of evidence-based care (perhaps via mandates3) and appropriately fund all elements of patient care, so that improvements in care and overall cost savings are not hindered by historical funding constraints.

Andrew J Francis · Michael J Ray · Mary C Marshall

To the Editor: Cameron and colleagues are to be congratulated on their article outlining strategies that do and do not help improve the access of emergency medical patients to public hospital ward beds.1 The authors fail to mention one strategy that is particularly relevant to rural hospitals, namely, referring privately insured medical patients who present to emergency departments directly to tertiary medical services at private hospitals. This strategy has the dual benefit of providing a hospital bed for a patient in a rural emergency department who requires hospital admission, and relieving some of the external pressures on metropolitan tertiary referral public hospitals to provide beds. Traditionally, private health insurance has been thought of as providing patients with the ability to obtain treatment from the doctor and hospital of their choice. Increasingly, private health insurance is giving patients the ability to choose between staying on an emergency department trolley and being able to access a hospital bed in a timely manner. It is worth noting that privately insured patients who require services that are not provided at our hospital (such as interventional cardiology, neurosurgery, cardiothoracic surgery and faciomaxillary surgery) can sometimes access a bed in a private hospital about 500 km away sooner than we can find them a bed in our hospital prior to transfer to a tertiary public hospital. A significant impediment to this process for some privately insured patients is the inability of private hospitals to perform insurance fund checks out-of-hours. While most private health insurance funds provide internet authorisations and confirmations of a patient’s insurance status to private hospitals, some do not. In one case, this meant the wife of a patient with unstable angina pectoris had to provide a cash guarantee of $28 000 on a Sunday so that her husband could have an angiogram the next day. Even though they had “top-level” private health insurance cover, the private hospital could not confirm their insurance status and obtain an authorisation from their health insurance fund on a weekend. Patients with private health insurance should be able to use the benefits of their insurance 24 hours a day, 7 days a week. Private health insurance funds that do not provide 24-hour authorisations to private hospitals for hospital admission should state this limitation clearly in their insurance product as a part of their statutory product disclosure statements. Such disclosure would provide relevant information to consumers to enable them to make an informed choice about their private health insurer.

Antony Nocera

To the Editor: Since colonial times, alcohol has been central to Australia’s political, cultural and social fabric.1 In the past year, concern about alcohol misuse has re-emerged as a dominant feature in the political landscape. We analysed the New South Wales emergency department (ED) data collection, on the NSW Department of Health’s HOIST (Health Outcomes and Information Statistical Toolkit) database, to describe the epidemiology of ED attendances due to acute alcohol problems. Data from 43 hospitals that contributed reasonably complete diagnosis information since 2000 were used. Attendances were selected using codes for alcohol intoxication, alcohol dependence/withdrawal, or drug or alcohol blood test from the ninth and 10th revisions of the International classification of diseases (ICD-9 and ICD-10) or from the Systematized Nomenclature of Medicine — Clinical Terms (SNOMED-CT). Population rates by age, sex and year were calculated. To assess the association between alcohol-related ED presentations and large public social events, time series of 24-hour counts ending at midday were used (because most presentations for acute alcohol problems occur at night).2 Between 2005 and 2008, the rate of ED presentations for acute alcohol problems rose sharply from around 110 to almost 150 per 100 000 population (Box 1). Between 2000 and 2008, the highest rates of ED attendance involved 18–24-year-olds of both sexes, and 25–64-year-old men. The largest increase was among 18–24-year-olds. Notably, in that age group, the rate in women converged with that of men at 228 per 100 000 in 2004 and was then higher until it re-converged in 2008 at around 390 per 100 000. In all years, the rate of presentation in 10–17-year-olds was slightly higher for females than for males (Box 2). Among children aged less than 10 years, the rate was under four per 100 000 in all years. Many peaks in ED attendance coincided with large public gatherings, including New Year’s Eve celebrations and the closing of the 2000 Sydney Olympic Games. In 2007 and 2008 especially, the Sydney Gay and Lesbian Mardi Gras was associated with marked increases (Box 3), which may reflect underlying increases in alcohol use in the younger age groups that might be attracted to this now mainstream event. Because the coverage of the ED data collection was limited, these figures underestimate the true incidence. Nevertheless, most urban and larger rural hospitals were included. We were unable to include the far greater number of ED presentations in which alcohol use was a factor, but not the primary reason for presentation.3 The trends and rates we observed were similar to those found in a recent Victorian study of young people.4 The small decline in overall rate from 2000 to 2002 (Box 1) is consistent with declining per-capita consumption of beer and spirits, while the subsequent increase in young people, which flattened out in 2008, is similar to the trend in consumption of ready-to-drink alcoholic beverages over the same period.5 Studies of the types of beverages used before ED presentation are urgently required to assess whether this is a causal association. Analysis of routine ED databases can provide a timely insight into the social and epidemiological context of high-risk drinking. The rise in alcohol-related presentation among teenagers and young adults bodes poorly for subsequent long-term alcohol use disorders and other risk behaviours and their consequences.6 The correlation between peaks in ED presentations and large-scale social events suggests that the development of cultural norms may have a strong influence on individuals’ behavioural choices. 1 Number and rate of presentations to 43 emergency departments for acute alcohol problems, New South Wales, 2000–2008 Year 2000 2001 2002 2003 2004 2005 2006 2007 2008 Number 6400 6215 6203 6762 6826 7652 9112 10119 10382 Rate per 100 000 population* 98.7 94.5 93.6 101.3 101.7 113.2 133.7 147.1 149.4 * Rates are an underestimate because not all NSW emergency departments are included. 2 Population rate of presentations to 43 emergency departments for acute alcohol problems,* by year, sex and age,† New South Wales, 2000–2008 * Rates are an underestimate because not all NSW emergency departments are included. † Values not shown for people aged < 10 years because all values were below 4/100 000 population. 3 Daily counts* of presentations to 43 emergency departments for acute alcohol problems, New South Wales, 2000–2008 * Counts are aggregated over 24-hour periods, ending at midday.

David J Muscatello · Sarah V Thackway · Daniel A Belshaw · David McGrath

Objective: To describe demographic, geographical and clinical features of envenoming by the rough-scaled snake (RSS) (Tropidechis carinatus).Design, setting and participants: Prospective cohort study of RSS snakebite victims, recruited between January 2004 and December 2008, as part of the Australian Snakebite Project. RSS envenoming cases were confirmed by snake identification and/or venom-specific enzyme immunoassay.Main outcome measures: Clinical and laboratory features of envenoming.Results: There were 24 confirmed cases of RSS envenoming, nearly all occurring in coastal areas between northern New South Wales and south-eastern Queensland. Twenty-three patients had local bite-site effects and 17 had at least three non-specific systemic effects (eg, nausea, headache). All 24 had venom-induced consumption coagulopathy (VICC), and 19 had an international normalised ratio > 3.0. Six had bleeding from the bite site or intravenous cannula site, 10 had blood detected on urinalysis, and one had a major intra-abdominal haemorrhage. Mild neurotoxicity developed in two patients, and one patient developed myotoxicity with generalised myalgia, myoglobinuria and a peak creatine kinase level of 59 700 IU/L. Twenty-three patients were treated with antivenom (21 with tiger snake antivenom, two with polyvalent antivenom). Free venom was undetectable in 19 of 20 blood samples taken after antivenom administration.Conclusion: RSS envenoming occurs predominantly in coastal areas of northern NSW and southern Queensland, and within this range, most envenoming is due to the RSS rather than tiger snakes. Clinically it is characterised by VICC, with mild neurotoxicity and myotoxicity in some cases. Tiger snake antivenom appears to be effective against RSS envenoming.

Melissa Gan MB BS · Margaret A O’Leary PhD · Simon G A Brown MB BS, FACEM, PhD · Tamara Jacoby BSc · David Spain MB BS, FACEM · Alan Tankel FACEM · Chris Gavaghan MB BS, FACEM · Peter Garrett MB BS, FACEM · Geoffrey K Isbister BSc, FACEM, MD

Acute medical units can help fast-track medical patient assessment and admission to hospital Hospitals in Australia are experiencing increasing numbers of medical presentations (ie, patients requiring admission under the care of a physician rather than a surgeon) in a context of ongoing restriction of inpatient beds. The resulting pressure on emergency departments (EDs) causes frustration for health care workers and administrators alike, as they struggle to meet key performance indicators that are designed to minimise the time that patients spend on trolleys in the corridors of EDs. Many hospitals have responded to this challenge by developing acute medical units (AMUs) that are equipped to fast-track patients with medical problems to the care of inpatient physicians (ie, staff physicians and visiting medical officers) and multidisciplinary teams who can best plan the management, care and disposition (destination after leaving the AMU) of these patients. On 24 April 2009, a seminar titled “Acute medical assessment units: improving care and flow for medical patients” was held at the Royal Children’s Hospital, Melbourne. The meeting was called by The Alfred Hospital, Melbourne, to assess the current state of evolution and performance of AMUs in Australia and New Zealand, and was supported by the Victorian Government Department of Human Services (DHS), Monash University National Health and Medical Research Council (NHMRC) Centre of Research Excellence in Patient Safety (CRE-PS) and the Internal Medicine Society of Australia and New Zealand (IMSANZ). Speakers from Australia and NZ addressed 210 attendees, including 78 doctors, 45 nurses, 17 DHS staff, 14 business analysts, 18 allied health professionals and pharmacists, 20 research educators and 10 representatives of relevant medical colleges. Here, we present the major themes presented for discussion and debate; speaker slides are available at http://www.crepatientsafety.org.au/seminars/. In the keynote presentation, Associate Professor John Henley (Visiting Professor, The Alfred Hospital) drew on years of experience running the AMU at Auckland City Hospital, NZ, and consulting on AMUs throughout Australasia. He emphasised the value of AMU staff working closely with ED staff, collocating the AMU and ED, and sharing administration across both units. At Auckland City Hospital, the AMU provides infrastructure, administration, and nursing and allied health support, but patients are seen by inpatient physician teams, with no default service provided in the AMU. This arrangement places the onus on the inpatient physician teams to attend to their patients promptly, and encourages continuity of care. This continuity is more difficult to achieve in AMUs that have their own medical staff, as distinct from inpatient physician teams. Henley also emphasised the importance of monitored beds, imaging equipment that is in close proximity to the AMU, and consulting rooms that permit urgent review of patients who are likely to require admission at the request of local general practitioners (thus bypassing the need for their assessment in the ED). In 2006, Henley co-authored a position statement on AMUs on behalf of IMSANZ.1 An international and historical perspective on AMUs was provided by one of us (P F J), drawing on extensive involvement in the establishment of AMUs in the United Kingdom. When the UK National Health Service applied severe penalties for hospitals that failed to move most patients from the ED within 4 hours, AMUs were developed throughout the country, supported by a new subspecialty — acute medicine. Introduction of a 4-hour rule is now pending in Western Australia, further focusing attention on AMUs. The importance of designing units according to the functionality required by individual hospitals was also emphasised — some units are designed to manage only patients with acute medical emergencies; some are designed to manage all medical admissions other than intensive care and critical care unit admissions; and some are primarily aimed at managing hospital bed issues, without a particular medical focus. Some units also accept surgical patients. This point was later reinforced by Associate Professor David Russell (Director, General Medicine, Royal Melbourne Hospital), who noted that the AMU should be regarded as a “philosophy of care”, not simply as a geographical entity. The value of effective change-management strategies in successful introduction of the AMU, particularly from the nursing perspective, was illustrated by one of us (L T O). Ms Glynis Jenkins (Project Coordinator, Acute Assessment Unit, Royal Perth Hospital, Perth) highlighted the importance of effective engagement with allied health staff, who play a crucial role in the AMU in both the UK and WA. Access block that results from delayed discharge and poor “back-door” availability of subacute and community care (paucity of options for discharging current inpatients who no longer require acute care but are not well enough to go directly home) is a major barrier to patient care, patient flow and ED key performance indicators. Dr Pieter De Villiers Smit (Acting Director, Emergency Department, The Alfred Hospital) described examples of how access block can impede patient management and safety. Professor Peter Cameron (Physician, Emergency Department, The Alfred Hospital, and Director, NHMRC CRE-PS), who chaired the session on identifying and addressing barriers, recently expanded on this topic in this Journal.2 Access block increases patient length of stay and incidence of adverse events, and decreases quality of care. In Australia, the excess mortality in hospitals attributable to access block matches that of the national road toll. Access block is a hospital-wide responsibility, rather than a problem within and for the ED itself, but is rarely acknowledged as such. Lugubrious specialty referral processes (whereby a patient can be referred, in turn, to several different subspecialties before being accepted for management) and significant delays in allocation of hospital beds contribute to access block. Associate Professor Ian Scott (General Physician and Director, Department of Internal Medicine and Clinical Epidemiology, Princess Alexandra Hospital, Brisbane) reviewed the limited evidence base for efficacy of AMUs. In uncontrolled and often poor-quality studies, AMUs reduced estimated bed costs, and probably contributed to decreases in mortality, patient length of stay in hospital, ED admission waiting times and numbers of outlier patients (ie, patients whose allocated hospital bed is in a ward other than the ward that is usually managed by their admitting team). AMUs can also increase the allocation of patients to appropriate subspecialties, increase staff and patient satisfaction, and facilitate the direct discharge of patients from hospital without an increase in the readmission rate. Professor Don Campbell (Head, General Medicine Department, Clayton Campus, Monash Medical Centre, Melbourne) illustrated how simulation modelling and clinical audit data can be used to optimise the use of resources in AMUs. In the UK, acute medicine is practised as an independent subspecialty that has its own Society of Acute Medicine, whereas in Australia and NZ it is part of the training of a general physician. An ageing general physician workforce with a paucity of young trainees and consultants threatens the development of AMUs in Australia. One of us (H H N) presented alarming data from the 11th annual report of the Medical Training and Review Panel (MTRP),3 the Medical Labour Force Survey4 and the Specialist Advisory Committee in General Medicine of the Royal Australasian College of Physicians (RACP) (Surinder Ahluwalia, Education Officer, Education Deanery, RACP, personal communication). In 2006, general medicine was the third most populated physician specialty in Australia, after cardiology and gastroenterology, but had the highest proportion of ageing physicians and the smallest number of new graduates — only four general physicians received their RACP Fellowship in 2006, in contrast with 42 cardiologists and 19 gastroenterologists. At least 200 additional general physicians are required in Australia, although a structured workforce analysis in this area has not been undertaken recently. The numbers of trainees entering cardiology and gastroenterology exceeded the MTRP recommendations, but no recommendation is provided for general medicine. There appears to be little regulation of trainee numbers in each subspecialty by the RACP or health departments, and a relative oversupply of cardiology and gastroenterology trainees. Numbers of general medicine trainees in 2009 are higher than for 2007, but fewer than 40% of those who do some advanced training in general medicine actually practise in this specialty. A major workforce strategy to replenish the ranks of general physicians is required. Cross-training of subspecialty trainees (who are encouraged to maintain their general medicine skills) could provide an interim solution until numbers of dedicated general medicine trainees and dual specialty trainees increase. Additional appointments of full-time general physicians and affirmative action in remuneration could also help — this has been successful in the training of geriatricians. The meeting concluded with Professor Paddy Phillips (Chief Medical Officer, South Australia) summarising what administrators want from those designing and running their AMUs. He focused on four themes: clarity, reliability, accountability and working together, a useful checklist for any initiative. This was a timely presentation, as it was part of the session on implementation that was chaired by Ms Margaret Grigg, Assistant Director of the Access and Metropolitan Performance Branch within the Victorian Government DHS. This department will no doubt receive requests for additional funding of Victoria’s AMUs from the inspired attendees of the seminar.

Harvey H Newnham MB BS, FRACP, PhD · Campbell H Thompson DPhil, FRACP, MD · Paul F Jenkins MB BChir, FRCP, FRACP · Lauri T O’Brien RN, RM, BN

Objective: To examine the response of the Victorian State Trauma System to the February 2009 bushfires.Design and setting: A retrospective review of the strategic response required to treat patients with bushfire-related injury in the first 72 hours of the Victorian bushfires that began on 7 February 2009. Emergency department (ED) presentations and initial management of patients presenting to the state’s adult burns centre (The Alfred Hospital [The Alfred]) were analysed, as well as injuries and deaths associated with the fires.Results: There were 414 patients who presented to hospital EDs as a result of the bushfires. Patients were triaged at the emergency scene, at treatment centres and in hospital. National and statewide burns disaster plans were activated. Twenty-two patients with burns presented to the state’s burns referral centres, of whom 18 were adults. Adult burns patients at The Alfred spent 48.7 hours in theatre in the first 72 hours. There were a further 390 bushfire-related ED presentations across the state in the first 72 hours. Most patients with serious burns were triaged to and managed at burns referral centres. Throughout the disaster, burns referral centres continued to have substantial surge capacity.Conclusions: Most bushfire victims either died, or survived with minor injuries. As a result of good prehospital triage and planning, the small number of patients with serious burns did not overload the acute health care system.

Peter A Cameron MB BS, MD, FACEM · Biswadev Mitra MB BS, MHSM, FACEM · Mark Fitzgerald MB BS, FACEM · Carlos D Scheinkestel FRACP, FJFICM, DipDHM · Andrew Stripp BBSc(Hons), MSc · Chris Batey CCRN · Louise Niggemeyer RN, ICCert, MEd · Melinda Truesdale MB BS, FACEM, GradDipHSM · Paul Holman ASM, GradDipHealthAdmin, MACAP · Rishi Mehra MB BS, PGDipEcho, FANZCA · Jason Wasiak MPH, BN, GradDipCritCareNurs · Heather Cleland MB BS, FRACS

Objective: To understand the current organisation of services for people with transient ischaemic attack (TIA) and the processes of assessment and management across Australian hospitals.Design and setting: Cross-sectional survey in 2008 of 134 Australian hospitals, mostly urban centres that treat large numbers of stroke patients.Main outcome measures: Survey questions covered assessment, early management and follow-up practices, as well as organisation of services for TIA.Results: Seventy-four hospitals (55%) responded: 47 (64%) reported access to a stroke unit, and 19 (26%) to a specialist clinic for TIA. Initial assessment included blood tests, electrocardiogram and brain computed tomography at most sites (92%–94%), and carotid imaging at more than half (65%), but magnetic resonance imaging at only 3% of sites. A tool to stratify the risk of subsequent stroke was used at 38 sites (51%), more commonly in hospitals with a stroke unit than in those without such a unit (64% v 30%; P = 0.005). Treatment was initiated at the initial assessment at 42 sites (58%), more commonly at stroke unit than non-stroke unit sites (68% v 37%; P = 0.007). Formalised policies for management of TIA patients were used at 38 sites (54%), with clear differences between sites with a stroke unit and those without (70% v 25%; P < 0.001).Conclusion: Access to rapid assessment and management services for TIA varies considerably between Australian hospitals. The presence of organised stroke care at a hospital leads to improved processes of care for patients presenting with TIA.

Christopher J Price BSc, BSW · David J Blacker MB BS, FRACP · Rohan S Grimley MB BS, BScMed, FRACP · Helen M Dewey PhD, FRACP, FAFRM(RACP) · Richard P Gerraty MD, FRACP · Simon A Koblar BM BS, FRACP, PhD · Sonia M Denisenko BPhys, MPH · Catherine E Storey MB BS, MSc, FRACP · Christopher F Bladin MB BS, MD, FRACP · Kelvin M Hill BApplSci(Physiotherapy), GradDipBusComm

Objectives: To determine whether redesign of pathology processes, including indicators of sample priority, could reduce patient length of stay (LOS) in an emergency department (ED), and assess the long-term impact of two indicators of sample priority on pathology clinical performance indicators for ED samples.Design, setting and participants: Two observational studies of de-identified data from standard databases were conducted — a single-site pilot trial of patients attending the ED of one hospital compared with historical controls, and a multisite study of 132 521 full blood count (FBC) requests for patients attending seven EDs that utilised either of two pathology process changes (coloured specimen transport bags alone, or coloured specimen bags plus blood tubes with a priority indicator).Main outcome measures: LOS in the ED was measured for the pilot trial, and collected-to-validated times for FBCs that fulfilled computer algorithm validation rules were measured for the multisite study.Results: In the pilot trial, the redesigned pathology process resulted in a 29-minute reduction (15.6%) in the median ED LOS for all patients (P < 0.001) compared with historical controls. In the multisite study, use of coloured specimen bags plus blood tubes with a priority indicator resulted in an 8-minute reduction (20.1%) in mean collected-to-validated times for FBC requests compared with FBC requests that used coloured specimen bags alone (P < 0.001).Conclusions: Our pilot trial revealed a direct relationship between pathology process design and LOS in the ED, suggesting that redesigned pathology processes can significantly reduce LOS in the ED. Our multisite study showed that collecting samples directly into blood tubes with an incorporated priority indicator reduces pathology test turnaround times. These data suggest that LOS in the ED can be significantly reduced by simple changes to pathology processes, such as collecting samples directly into specimen containers with an incorporated priority indicator.

Andrew J Francis MB BS(Hons), FRCPA · Michael J Ray PhD, BAppSc(Medical Technology) · Mary C Marshall BAppSc(Biology), GradDip Professional Communications

To the Editor: A 70-year-old woman presented to the emergency department with intense pain, erythema, oedema and haemorrhagic bullae of the right lower leg. Twenty-four hours earlier, she had fallen into warm seawater on the south coast of New South Wales, sustaining a penetrating wound by an unknown object. She reported developing excruciating pain and the noted leg changes within hours of the injury. She had a history of systemic lupus erythematosus (SLE), managed long-term with 7.5 mg oral prednisone daily. Soon after presentation, she rapidly developed septic shock, becoming hypotensive, tachycardic, hypoxic and confused. She was experiencing rigors and required inotropic support. On examination, there was marked cellulitis of the right lower leg with purpura and bullae. No crepitus was detectable in the tissues. There was no clinical or laboratory evidence of disseminated intravascular coagulation. Broad-spectrum empirical antibiotic treatment with intravenous gentamicin, cephazolin and metronidazole was commenced, and urgent, extensive surgical debridement of the lower limb was performed (Box). Wound culture swabs and tissue samples were sent for microbiological and histopathological examination. On Day 2, blood cultures taken at initial presentation were positive for Vibrio vulnificus, as were tissue swabs. Based on susceptibility testing, antibiotic therapy was reduced to a single agent, intravenous ciprofloxacin 400 mg twice daily. The patient’s postoperative clinical recovery was slow, but her SLE did not flare up, and on Day 23 she was transferred to a tertiary referral centre for lower-limb skin grafting. Cellulitis is a common presentation to emergency departments, and common organisms are usually implicated. However, in some cases, the presence of more unusual pathogens, such as V. vulnificus, should be considered. V. vulnificus is a virulent halophilic (salt-loving) gram-negative bacterium associated with seawater temperatures (usual range, 18°–24°C). It has two distinct clinical presentations.1,2 The first, well recognised, is septicaemia after ingestion of raw or undercooked seafood, such as oysters, causing acute gastrointestinal disease. The second, not always considered, is necrotising wound infections, as in this case. Open wounds can be directly inoculated with V. vulnificus from seawater containing the organism. “Vulnificus” is a Latin term meaning “inflicting wounds”. Hippocrates described perhaps the first recorded case of a fisherman with pain in the foot, fever, delirium and blistering skin.3 Patients with primary wound infections caused by V. vulnificus develop painful, rapidly progressing cellulitis. More unusually, our patient developed fulminant sepsis from an open wound infection. Patients who are immunocompromised, especially those with alcoholic liver disease, hepatitis B or hepatitis C, have a higher risk of infection with V. vulnificus, as well as patients, like ours, who take long-term steroid therapy.2 Management requires timely recognition, antibiotic therapy and prompt surgical review. Cellulitis of right lower leg caused by infection with Vibrio vulnificus

Tamara C Preda · Veronica A Preda · Allan P Mekisic

Textbook of disaster psychiatry. Robert J Ursano, Carol S Fullerton, Lars Weisaeth, Beverley Raphael, editors. Cambridge: Cambridge University Press, 2007 (xii + 346 pp). ISBN 978 0 521 85235 7. Disasters, by their nature, are unexpected and often occur when services are least able to respond, such as the tsunami on Boxing Day in 2004. Therefore, the ready availability of resource material is particularly important in disaster management. Due to recognition of the importance of well coordinated and planned recovery programs, there is also growing interest in providing structured academic courses in the disaster field. For these activities, the Textbook of disaster psychiatry is a high-quality, welcomed edition to an already competitive stable. The editors are doyens of the field and bring together a richness of experience, knowledge, and anecdote that combine to provide a text of unusual depth. They focus not only on the challenges facing clinicians, but also on the obstacles the broader systems confront in the face of disasters. A text providing an integrative methodology for a broader public health approach is a valuable tool to ensure optimal long-term outcomes. This is not simply a disguised textbook on post-traumatic stress disorder; it has relevance beyond mental health practitioners. Despite the fact that individuals’ adaptive behaviour determines the success or otherwise of physical disaster relief programs, mental health programs are often seen as a low priority in disaster management. As a consequence, this text will be valuable to coordinators of medical services and those involved in community and social reconstruction. While the editors are truly an international group, the authors of the text are all, bar one, from the United States. Nevertheless, this does not detract from the international applicability of the content and approaches that it espouses. This is a book to have on the shelf for the day when the sky falls in.

Alexander C McFarlane