Emergency medicine

To the Editor: Box jellyfish envenomation, particularly from Chironex fleckeri, is an important cause of morbidity and mortality across coastal areas of northern Australia.1 The distribution of C. fleckeri extends from Broome (18°S) on the Western Australian coast, across the Northern Territory coast and down the east coast of Queensland, at least as far as Gladstone (26°S). Another multitentacled box jellyfish (chirodropid) has been found in north Queensland in the Cairns to Townsville region.2 Smaller than C. fleckeri, this box jellyfish has been called Chiropsalmus quadrigatus. It has not caused documented fatalities in Australia,1 and is likely to be a different species to C. quadrigatus, which has caused many fatalities in the Philippines and Japan.1 The Australian species has therefore more recently been referred to as Chiropsalmus sp. C. fleckeri and Chiropsalmus sp. are both present in tropical waters during the summer months, although C. fleckeri stings have very rarely occurred in each of the months outside the official "stinger season" (October 1 – June 1 for the Northern Territory).3 Over the past 10 years, there have been reports of box jellyfish being present off the beaches of the Gove Peninsula on the northeast tip of Arnhem Land, Northern Territory, during the middle of the year (ie, outside the stinger season). We first obtained samples netted on 2 June 1991 at the Gove mining town of Nhulunbuy (12°S), and in that year the same species was present throughout June and July. Preliminary analysis at the Museum and Art Gallery of the Northern Territory confirmed the jellyfish to be a multitentacled box jellyfish, similar to the Queensland Chiropsalmus sp. The same jellyfish species was netted at Nhulunbuy in June 1992 and September 1993, but not in 1994. Between 5 May and 6 October 2002, hundreds of Gove chirodropids were netted on weekends at the Nhulunbuy town beach by the local surf life-saving club. They were not present every weekend, but on some days hundreds were present in shallow water, precluding swimming and normal club activities. Contact with the tentacles of the jellyfish during netting caused only mild pain, redness and itching, which usually resolved within two hours. There have been no systemic symptoms suggestive of the Irukandji syndrome. The appearance of the Gove chirodropid in large numbers during the cooler mid-year months is unprecedented for Australian chirodropids and has implications for public health warnings. To date the Gove chirodropid has not been found during the summer months, when C. fleckeri is present in the same location. The distribution, ecology and taxonomy of this jellyfish remain to be elucidated. 1: The Gove chirodropid compared with Chironex fleckeri The Gove chirodropid (right) swarms in shallow water and is consistently 5–10 cm in diameter across the bell. This is smaller than Chironex fleckeri (left), which can have a bell diameter of up to 22 cm. The Gove chirodropid is quite fragile and tentacles quickly break off when it is netted, but there are often about five tentacles extending from each pedalium. 2: Comparison of nematocysts Nematocysts (original magnification x 400) from the tentacles of the Gove chirodropid are cigar shaped (right) and therefore similar to those of C. fleckeri (left).

Bart Currie · Melita McKinnon · Bernie Whelan · Philip Alderslade

Puffer fish poisoning has been documented rarely in Australia. It results from ingesting tetrodoxtoxin found in the liver, ovaries, intestines and skin of the fish. Over a recent 16-month period, 11 cases of puffer fish poisoning were reported to the NSW Poisons Information Centre. Symptoms of poisoning may include paralysis, respiratory failure, numbness, paraesthesia, nausea and ataxia. Health professionals should be aware of the condition so as to institute early and appropriate management. (MJA 2002; 177: 650-653) Tetrodotoxin (TTX) is present in high concentrations in the liver, ovaries, intestines and skin of puffer fish (Box 1).1 Although TTX poisoning caused by ingestion of the fish is common in some parts of the world, it occurs only sporadically in Australia, with only 16 published cases reported over the past 200 years.2-7 (This figure does not include the 11 cases described here.) One of the earliest descriptions of puffer fish poisoning in this region can be found in Captain James Cook's journal from his second voyage in 1774 (see Time Capsule, page 653).3 The majority of reported cases have occurred in southeastern Asia,1,8-10 particularly Japan, where puffer fish is considered a delicacy.1,11 Although improved legislation governing marketing and preparation of the fish has reduced the incidence of puffer fish poisoning in Japan, it remains the most common cause of fatal food poisoning, as there are still some unlicensed cooks and untrained workers involved in preparing the fish.1,11 Before 1950, all reported cases in Australia were fatal,5 and in Japan up to 100 deaths a year were reported.11 We describe 11 patients with puffer fish poisoning, four of whom underwent comprehensive neurophysiological testing. Clinical findingsFor the period 1 January 2001 to 13 April 2002, records of 149 453 calls to the NSW Poisons Information Centre were searched for instances of puffer fish poisoning. The Centre covers New South Wales and Tasmania 24 hours a day and the rest of Australia overnight. Of 195 calls coded as food or fish poisoning, there were five calls regarding puffer fish. Two were minor cases involving people who had been squirted with fluid from puffer fish. The three remaining calls were from hospitals: a total of 11 affected people (described here) were involved. Patient 1A 33-year-old woman presented to a semi-rural hospital with nausea and vomiting, perioral paraesthesia, dysarthria, ataxia and hyperventilation after ingesting seven puffer fish several hours earlier (see Box 1). Her vital signs were stable and the FEV1 (forced expiratory volume in one second) was 2.2 litres (normal range, 3.3–4.0 L). However, an hour after presentation she became more dysarthric and developed limb paresis with hyporeflexia. In view of progressive lethargy, dyspnoea and a fall in FEV1 to 1.5 L, she was intubated and ventilated, then transferred to the intensive care unit of a metropolitan teaching hospital. On arrival, the patient was haemodynamically stable but her pupils were dilated and non-reactive to light. Investigations, including a lumbar puncture and cranial computed tomography scan, were normal. With a presumptive diagnosis of tetrodotoxin poisoning, the patient was managed with supportive care. Over the next two days, her condition improved, deep tendon and pupillary reflexes returned, and she was extubated on Day 2. The other symptoms gradually resolved, and she was discharged on Day 5 after full neurological recovery. Patient 2A 40-year-old man presented to a metropolitan teaching hospital (see Box 2). He stated that he had eaten 10 small toadfish eight hours earlier, together with drinking a significant quantity of alcohol. Following ingestion of the toadfish he had collapsed a number of times and felt tingling of his hands and feet and around his mouth. With each collapse, he experienced generalised weakness, but did not lose consciousness. He had no relevant past medical history. On examination he was afebrile, with a pulse rate of 110 beats/minute, blood pressure of 140/80 mmHg, respiratory rate of 16 breaths/minute and oxygen saturation of 96%. A neurological examination was entirely normal. After uneventful overnight observation, he was discharged. Patients 3–11Seven adults and two children ate a soup made from about 30 puffer fish, gutted with heads intact and boiled in fresh water. The cook referred to the fish as puffer fish, and one of us (J U) identified one of the fish as a puffer fish. All nine patients had been previously well, not taking medication, and with no known allergies. The patients' clinical features are shown in Box 2. One child was completely asymptomatic, and the other had mild symptoms of perioral numbness and dysaesthesia of the extremities for five hours. Both were discharged from the emergency department. Most of the seven adults presented to hospital with nausea, perioral and lingual numbness, dysaesthesia of the extremities, dizziness and gait ataxia. Several patients had vomiting and one was experiencing respiratory distress. Neurological examination revealed marked ataxia in all seven patients and limb weakness in two patients (more marked in the upper than lower limbs). One patient had decreased sensation in the hands and feet. Most symptoms resolved over 48 hours, but slight weakness and ataxia of the lower limbs remained. These resolved completely over the following week. Neurophysiological investigation was undertaken in four of the adult patients (see Box 3) within 24 hours of ingestion. DiscussionAlthough puffer fish poisoning is rare in Australia, our report highlights the seriousness of TTX poisoning and its potential to be life-threatening.11 However, early recognition of the condition and supportive care in a modern intensive care unit should ensure a safe outcome. The clinical effects of TTX poisoning have been graded by the severity of neurological and cardiovascular involvement (Box 2).11 In this series, one patient had Grade 3 poisoning, and most others Grade 2 poisoning. Most of the patients exhibited typical neurological features, including perioral numbness and/or paraesthesia, distal limb numbness/paraesthesia and ataxia — symptoms similar to those seen in previous case series.1-10 Gastrointestinal features were also typical, with nausea, occasional vomiting, but no diarrhoea. Cardiovascular effects (not present in this series) occur only in the most severe (Grade 4) cases. The onset of symptoms in TTX poisoning is usually rapid, but is dependent on the severity of poisoning. In the moderately severe cases in this series, symptoms had all occurred within 90 minutes. In reported fatal cases and severe poisoning, symptoms have almost always developed within 1–2 hours.10 The majority of moderate to severe cases in this series resolved within five days, consistent with previous reports,3,6 although this also depends on the severity. In minor cases the duration of symptoms may only be a few hours. The relatively mild symptoms experienced by patients 3–11 probably reflect the relatively low dose of TTX ingested. TTX is present in high concentrations in the viscera of puffer fish, particularly the liver and intestines (Box 4). These organs were removed before cooking the fish soup, and the amount of TTX was subsequently diluted by adding fresh water to the soup and possibly by subsequent boiling. With higher levels of TTX, paralysis and respiratory failure are inevitable, although consciousness is not lost except in extreme cases (Box 2). Of interest, such a process has been implicated in the phenomenon of "zombification" in Haiti.22,23 Nerve conduction studies revealed clear abnormalities. Nerves in the patients tested were of high threshold, and exhibited slow conduction and reduced-amplitude compound potentials, indicating that some axons were unable to conduct at all. This effect was greater in sensory than motor axons, correlating well with the greater prominence of sensory symptoms (dysaesthesiae and numbness) relative to motor symptoms (weakness) in these patients. Voltage-dependent Na+ channels underlie action potential generation and are the chief determinants of membrane excitability in human nerves.24,25 Tetrodotoxin blocks Na+ channels at very low concentrations, affecting action potential generation and impulse conduction. It is important that health professionals are aware of TTX poisoning because of the potential for severe and life-threatening effects. All but the mildest cases (Grade 1) should be admitted to hospital for observation until the peak of the clinical effects has passed. After 24 hours it is extremely unlikely that life-threatening effects will occur in patients who have not already developed severe effects. Early diagnosis by recognition of the combination of clinical effects in people ingesting puffer fish is essential to management. 1: The common toadfish (Tetractenos hamiltoni) The fish pictured here is approximately 10 cm in length. Photo courtesy of Erik Schlogl. 2: Description of 11 patients presenting with puffer fish poisoning Patient Sex, age Onset (minutes) Gastrointestinal features Neurological features Duration of symptoms Severity grade* 1 F, 33 NR Nausea, vomiting Perioral paraesthesia, dysarthria, ataxia, limb weakness, hyporeflexia and ophthalmoplegia. Decreased FEV1, with respiratory failure. 5 days 3 2 M, 40 60 Nil Perioral and extremity paraesthesia, dizziness. 18 hours 2 3 F, 5 NA Nil Nil. NA NA 4 F, 12 NR Nil Perioral and extremity paraesthesia. < 6 hours 2 5† M, 33 30 Nausea, vomiting Perioral and lingual numbness, dysaesthesia of extremities, dizziness and gait ataxia. 5 days 2 6† F, 47 NR Nausea, vomiting Perioral and extremity paraesthesia, dizziness and gait ataxia. 5 days 2 7 M, 39 60 Vomiting Perioral and lingual numbness, dysaesthesia of extremities, dizziness and gait ataxia. Mildly reduced power in upper and lower limbs. 5 days 2 8† M, 41 60 Nil Perioral numbness, dysaesthesia of extremities, dizziness and gait ataxia. Decreased sensation in hands and feet ("glove-and-stocking" distribution). 5 days 2 9 F, 35 60 Vomiting; simultaneous incomplete miscarriage Perioral and lingual numbness, dysaesthesia of extremities, slight dizziness and gait ataxia. Normal power and sensation. Respiratory distress. 5 days 2 10† M, 47 30 Nausea Perioral and lingual numbness, dysaesthesia of extremities, dizziness and gait ataxia. Mildly reduced power in upper and lower limbs. 5 days 2 11 M, 50 90 Nausea Perioral numbness, dizziness and gait ataxia. Normal power and sensation. 5 days 2 NA = not applicable. NR = not recorded. * Clinical grading system for tetrodotoxin poisoning based on symptoms and signs present (after Fukuda and Tani12): Grade 1: perioral numbness and paraesthesia, with or without gastrointestinal symptoms (mainly nausea). Grade 2: numbness of tongue, face and other areas (distal); early motor paralysis and incoordination; slurred speech; normal reflexes. Grade 3: generalised flaccid paralysis, respiratory failure (dyspnoea), aphonia and fixed/dilated pupils; patient still conscious. Grade 4: severe respiratory failure and hypoxia; hypotension, bradycardia and cardiac dysrhythmias; unconsciousness may occur. † Neurophysiological testing was done on these patients (see Box 3). 3: Neurophysiological investigation of patients with puffer fish poisoning Neurophysiological investigation* was performed in four adult patients (numbered 5, 6, 8 and 10 in Box 2) within 24 hours of puffer fish ingestion. None of the patients studied had a history of medical conditions known to affect nerve function, and none were taking any regular prescribed medication. Results of motor (Figures A1–A3) and sensory (Figures B1–B3) nerve conduction studies of the median nerve in patients with puffer fish poisoning and control subjects are compared. (Results are expressed as mean ± standard error of the mean and compared using an unpaired two-tailed t-test.) Stimulus–response curves showed that the stimulus current (threshold) required to generate compound muscle action potentials (CMAPs) and sensory nerve action potentials (SNAPs) was significantly higher in patients with puffer fish poisoning than control subjects, suggesting an overall reduction in axonal membrane excitability (Figures A1, B1).13 Compound potentials were smaller in amplitude (Figures A2, B2) and of longer latency (Figures A3, B3) in affected patients compared with controls. These parameters are dependent on Na+ channel function and suggest reduction both in the number of conducting axons and in the conduction velocity of those axons still available for impulse transmission. Overall, these findings indicate a reduction in Na+ conductance in the nerves of affected patients, consistent with direct blockade of axonal Na+ channels by tetrodotoxin. *Method: Motor and sensory nerve conduction studies of the median nerve were performed using surface electrodes. Results were compared with established normative data using previously described standard techniques.14,15 The median nerve was stimulated at the wrist, with the evoked orthodromic compound muscle action potential (CMAP) recorded from thenar muscles and antidromic sensory nerve action potential (SNAP) recorded using ring electrodes around the index finger. Latency was measured to peak response. Skin temperature was recorded at the site of stimulation in each patient throughout the study, and individual measurements were compensated for temperature using the relationship found in normal subjects.16,17 4: Puffer fish poisoning Tetrodotoxin (TTX) is present in high concentrations in the liver of puffer fish, with progressively decreasing amounts in the ovaries, intestines and skin.1 TTX poisoning can occur from ingestion of a wide range of bony fish from families in the order Tetraodontiformes, most importantly the family Tetraodontidae (puffer fish).11 While none of our cases were confirmed by expert identification of the fish, the description by the patients suggested puffer fish (sometimes called "toadfish" in Australia), and the clinical features were consistent with TTX poisoning. Although ciguatera is also caused by ingestion of fish, the clinical effects differ, and tropical reef fish are mainly implicated.18 The fish ingested by patients 2–11 were from the Georges River, in southern Sydney. While 35 species from the family Tetraodontidae occur in New South Wales, the species in the cases described here were most likely Tetractenos hamiltoni (common toadfish), T. glaber (smooth toadfish), or Torquigener pleurogramma (weeping or banded toadfish), all of which are common and have been recorded in the Georges River and Botany Bay (Doug Hoese and Mark McGrouther, Fish Section, Australian Museum, personal communication). The common toadfish is a sandy to whitish colour, with small brown spots over most of the back and upper sides. The lower sides often have brown bars and blotches (Box 1). It occurs from southern New South Wales to northern Queensland in shallow coastal waters and estuaries. The smooth toadfish looks similar to the common toadfish, but has larger spots and distinct body spines. With other species of puffer fish found in tropical waters, the potential for TTX poisoning exists in many coastal regions of Australia. The in-vitro effects of TTX are well characterised. It is a selective blocker of voltage-sensitive sodium channels and prevents conduction in motor and sensory nerves by blocking sodium channels at the nodes of Ranvier.11,19 Less is known about the in-vivo effects in humans. Nerve conduction studies have been limited,20,21 and demonstrate effects on muscle and sensory action potential amplitudes.20

Geoffrey K Isbister BSc, MB BS, FACEM · Julie Son MB BS · Josef Ujma MB BS · Brendon Smith DipRACOG, DA, FACEM · D G Milder MB BS, MD, FRACP · Frank Wang BSc(Med), MB BS · Catriona J Maclean MB BS · Cindy S-Y Lin MEngSc, PhD · Matthew C Kiernan PhD, FRACP · Corrine R Balit BPharm

Objective: To determine the effect of temperature on lethality of venom from Chironex fleckeri (the potentially fatal box jellyfish).Design: Venom extracted from nematocysts of mature Chironex fleckeri specimens was exposed to temperatures between 4°C and 58°C for periods of two, five or 20 minutes, and then injected into freshwater crayfish (Cherax quadricarinatus) to assess lethality.Main outcome measure: Venom lethality, assessed as time to cardiac standstill in crayfish after intramuscular injection.Results: Venom lethality was significantly affected by both temperature (F7,34 = 21915; P < 0.0001) and time of exposure (F2,34 = 9907; P < 0.0001). No significant loss of lethality was seen after exposure to temperatures ≤ 39°C, even after 20 minutes' exposure. At temperatures ≥ 43°C, venom lost its lethality more rapidly the longer the exposure time. Venom was non-lethal after exposure to 48°C for 20 minutes, 53°C for five minutes, and 58°C for two minutes.Conclusion: Exposure to heat dramatically reduces the lethality of extracted C. fleckeri venom. Although heat application may be of limited use in treating C. fleckeri envenoming because of the speed of symptom onset, its use in other box-jellyfish envenomings, such as Irukandji syndrome, requires investigation.

Teresa J Carrette MSc · Jamie E Seymour PhD · Paul Cullen FACEM · Peter L Peiera FACEM · Mark Little FACEM, MPHTM

A healthy young man, upon placing the palm of his hand on a wooden floor, experienced an immediate severe burning sensation. A small black shiny beetle was found lying partially crushed. The initial burning pain in the palm subsided, but a dull discomfort persisted for several hours. Examination revealed two areas of dark yellow-brown discoloration, resembling the colour of iodine, on the palm (Box 1). These measured about 1 × 2 cm, with a surrounding halo of mild erythema. The affected skin had normal texture, markings, and sensation, and no blistering or vesication was seen. The patient remained systemically well throughout the episode. No evidence of external biting, stinging or defensive apparatus was found on inspection. The skin changes lasted 3–4 days, and resolved completely. The beetle was identified as a species of bombardier beetle by Daniel Bickel of the Australian Museum, Sydney. Bombardier beetles belong to the large Carabidae family of active predatory ground beetles, and comprise the subfamily Brachininae, with some 500 species. One species, Pherosophus verticalis, is widespread in Australia (Box 2). Chemicals are used defensively by many ground beetles, usually discharged as a fine spray when threatened. At least nine diverse groups of noxious chemicals have been found in these insects, including acids, phenols, hydrocarbons and quinones.1 When threatened, bombardier beetles emit a defensive spray of heated benzoquinones from the tip of the abdomen.2 The quinones are produced explosively at the moment of ejection. This involves a two-chamber system — an inner reservoir chamber stores a solution of hydroquinones and hydrogen peroxide, and a separate reaction chamber contains oxidative enzymes (catalase and peroxidase).3 Mixing of the reaction components leads to catalytic events, with a rapid build-up of pressure from liberated oxygen, and explosive discharge of oxidised benzoquinones (Box 2). This can be accompanied by an audible "pop". The temperature of the emitted reaction mixture has been measured at 100°C.3 This boiling spray can be directed in all directions by a revolvable turret arrangement on the abdominal tip, and effectively deters both vertebrate and invertebrate predators.4 Australia is rich in beetles, with about 20 000 native species recorded.5 Despite this diversity of forms, beetles are rarely directly harmful to humans.6 1: The affected areas of the patient's hand 2: The bombardier beetle and its chemical weapon 1: Pherosophus verticalis, the Australian bombardier beetle. 2: A schematic diagram of the internal defensive gland. The secretory apparatus (A) produces an aqueous solution of hydroquinones and hydrogen peroxide, which is stored in the reservoir (B). When threatened, the beetle releases fluid from the reservoir into the reaction chamber (C), which contains a mixture of catalases and peroxidases. These enzymes catalyse an explosive reaction. The boiling mixture discharges in a spray through the abdominal tip. Reproduced with permission from NSW Agriculture.

Paul G Chee BMed(Hons), BMedSc · Scott M Dunkley FRACP, FRCPA

Objectives: To investigate the relationship between access block in the emergency department (ED) (defined as total time from arrival to transfer from the ED over eight hours) and inpatient length of stay (LOS).Design and setting: Retrospective cohort study of all admissions through the ED to a tertiary hospital in Canberra, Australian Capital Territory, during 1999.Main outcome measures: Total time in the ED and LOS, calculated in days from ED departure to hospital discharge (non-overnight admissions were assigned LOS of one day, and all LOS were truncated at 10 days).Results: 11 906 admissions were included, and 919 experienced access block (7.7%). Mean LOS was 4.9 days in those who experienced access block (95% CI, 4.7–5.1), compared with 4.1 days in the no-block group (95% CI, 4.0–4.2; P < 0.0001). Subgroup analysis showed that this "access block effect" occurred across different severities of illness and diagnoses. A strong relationship was found between longer LOS and arrival of access-block patients on the inpatient ward outside office hours (0800–1600 weekdays).Conclusions: This is the first study to show an association between access block and a measure of outcome outside the ED. If the effect of access block on LOS is reproduced in other settings, there are major implications for hospital management.

Drew B Richardson FACEM

To the Editor: It was most enlightening to read the articles on cosmetic surgery in the 17 June 2002 issue of the Journal. In particular, the Clinical Update by Castle et al on psychosocial wellbeing and cosmetic surgery1 is pertinent to everyday practice. The warning given that cosmetic specialists should be concerned about patients who have had numerous procedures, in particular patients who have previously sued physicians, is a poignant one. Psychological testing of patients who wish to have plastic and cosmetic surgery is not routine, and plastic or cosmetic surgeons cannot be expected to carry out such testing. Liaison with psychologists and psychiatrists can be conducted on a case-specific basis, but not routinely. The aim is to screen for body dysmorphic disorder, but this can be quite difficult, as the presentation is often obscure.2 In reality we live in a world where appearance is very important, and self-esteem is related to appearance. Age discrimination is a reality, and cosmetic surgery has been shown to improve a patient's psychosocial wellbeing.3 The issue of advertising of cosmetic surgery services is a vexed one, as is the issue of where cosmetic surgery should be performed. As it is usually not performed in public hospitals, it has been relegated to the private sector in Australia, and private hospital appointments that might include cosmetic surgery have been vigorously protected by special-interest craft groups in Australia. Misconceptions by the general medical community are rife, due to both the lack of exposure to cosmetic surgical procedures and the lack of information on the subject. The assistance of the general practitioner, together with a thorough patient history, is very valuable in determining whether cosmetic surgery is likely to have a positive psychosocial outcome. Unfortunately, the generally poor attitude of the Australian medical community towards cosmetic surgery has led to patients being afraid of a negative response when asking their GPs about cosmetic surgery. Often referrals are either not made or are made by an anonymous practitioner, which is not an ideal situation. Liaison with surgeons who have previously treated a patient is ideal, but cooperation in this area is not always forthcoming, as some surgeons fear litigation from former patients. With most cosmetic surgeons being shut out of the medical mainstream, access to potential patients comes through normal commercial means, such as advertising in the Yellow Pages and in magazines. It is to be hoped that in future there will be more contact between cosmetic surgeons and other medical practitioners so that the true benefits and risks of the procedures can be understood by the general medical community, who, in turn, can counsel their patients in a sympathetic manner as to whether cosmetic surgery is advisable.

Darryl J Hodgkinson

Major incident medical management and support. The practical approach. Advanced life support. 2nd edition. Hodgetts TJ, Mackway-Jones K, editors. London: BMJ Books, 2002 (xv + 222 pp). ISBN 0 7279 1391 3. Bushfires, bus and train crashes, and multiple shootings happen in Australia and this is why the Major Incident Medical Management and Support (MIMMS) course was started in about 1995. The course has flourished since then, and now, with terrorism and biological threats very real after September 11 and recent events in Bali, this concise and comprehensive second edition is timely. This volume aims to teach all doctors (from GPs to emergency care specialists) a practical approach to a situation where they are at the scene of a disaster where the number of injured exceed the available resources. It sets out a structured approach and outlines the roles of the various services involved. The clinician will find that this approach is clearly explained. Aided by tables and diagrams, the reader is shown how to assess the scene, communicate appropriately with the services, use an accepted quick triage sieve (in the field using respiratory rate and capillary return), deal with the dead, and do practical procedures from airway management to femoral nerve blocks. Various topics, from media interaction to chemical and radiological incidents, are covered, although biological agents seem to have been forgotten. The great strength of this work is that it is relevant and very practical. It is supplied in a loose-leaf folder so that it can be updated, and there are spaces to record specific local details. In spite of a respected Australian contributor it does have a British flavour, but the principles are universal. In our fast-moving and troubled society, no doctor, whether a rural GP or a city doctor, can be sure he or she will escape being caught up in a major incident. Having medically responded to several of Australia’s major disasters I have done the MIMMS course, and I always take this excellent manual with me. Both are to be recommended most highly. Gordian W O FuldeDirector, Emergency Medicine St Vincent’s Hospital, Sydney, NSW

Gordian W O Fulde

The Irukandji syndrome was named in 1952.1 It is the set of severe systemic symptoms that occur some 30 minutes after some jellyfish stings.2,3 The only species so far identified as causing the syndrome is Carukia barnesi, a small carybdeid box jellyfish occurring in the Cairns area (latitude, 16o44'S; longitude, 145o40'E), north Queensland.3 The bell of this tiny jellyfish is just 12 mm in diameter in mature specimens. The original description of the Irukandji syndrome is (paraphrased): the severe systemic symptoms developing 30 minutes or so after a mild skin sting from Carukia barnesi. Severe low back pain; excruciating muscle cramps in all four limbs, the abdomen and chest; sweating, anxiety, restlessness, nausea, vomiting, headache and palpitations occur.2,3 Since this original description, based on stings occurring around Cairns in north Queensland, life-threatening hypertension,3 pulmonary oedema and toxic global heart dilatation4 have been added as further complications of the syndrome. These symptoms were described after Irukandji syndrome resulted from stings occurring in the Whitsunday Islands, and later in the tropical Great Barrier Reef region.5 Recent research now suggests this syndrome is caused by at least five or six small carybdeids similar to C. barnesi and two larger carybdeid jellyfish species (bell diameter about 60–70 mm at maturity; L-A Gershwin, PhD student, University of California, Berkeley, 1999; and J Seymour, Senior Lecturer, James Cook University 2000–2002; personal communications), with the difference in severity of symptoms probably varying with the species. We describe the first recorded death from Irukandji syndrome in an overseas tourist on Hamilton Island in the Whitsunday Islands, Queensland (20o20'S, 148o56'E), in January 2002. This case was followed by another death of a 44-year-old tourist from the US in April 2002 from Irukandji syndrome on the outer Great Barrier Reef, off Port Douglas, about 1300 kilometres north of the first fatality.6 Both deaths occurred from intracerebral haemorrhage after severe hypertension caused by envenomation by a jellyfish. Clinical recordOn 30 January 2002, at about 1115 hours, a 58-year-old tourist from the UK was stung on the face and chest soon after entering shallow water at a beach on Hamilton Island. He did not see the creature, but said to his wife "something has got me", and they left the water. Over about 20 minutes he became distressed, with generalised muscular cramping pains, sweating, anxiety and nausea. He presented to the resort doctor, who noted he had hypertension (260/160 mmHg) and tachycardia (pulse, 142 beats per minute) and he was given 100 mg pethidine, 15 mg morphine, 10 mg metoclopramide, 25 mg promethazine and 5 mg diazepam, all intramuscularly, at 1150 hours. At 1200 hours his condition suddenly deteriorated and he became unresponsive, with stertorous breathing. A provisional diagnosis of cerebrovascular accident (CVA) was made. His past medical history included an aortic valve replacement in 1995 for aortic stenosis (he was taking 8 mg warfarin daily, and had had an international normalised ratio [INR] of 5.0 a week earlier). Intravenous access was obtained, an airway inserted with oxygen supplementation, electrocardiographic monitoring begun, and urgent transfer to a mainland hospital requested. A doctor and nurse flight team arrived at 1400 hours to find the patient unconscious with fixed dilated pupils and a blood pressure of 180/64 mmHg. The patient was sweating, salivating profusely, had a mild epistaxis, stertorous breathing and erythematous flushing of the face, neck and anterior chest. He was given 2.5 mg midazolam and 100 mg suxamethonium intravenously, and intubated; sedation was maintained with midazolam, morphine and vecuronium, and he was given 1 mg aliquots of phentolamine in an attempt to control his blood pressure, although this remained between 210/134 mmHg and 170/110 mmHg during the flight. He arrived at Mackay Base Hospital at 1620 hours. No attempt was made to sample nematocysts, as no sting site was clearly delineated, although skin flushing and intermittent diaphoresis (of the face and upper body; noted in helicopter, but not specified in notes) were noted and remained throughout the night. A chest radiograph showed cardiomegaly and unfolding of the aorta. Initial electrocardiography showed atrial fibrillation and right bundle branch block. Computed tomography scan, showing extensive intracerebral haemorrhage Computed tomography of the brain showed an 8 × 5 × 7 cm haemorrhage centred on the basal ganglia, 1 cm midline shift and right lateral ventricle effacement with subarachnoid extension filling the third and fourth ventricles, a small haemorrhage in the cerebral peduncles and the left caudate nucleus, with blood surrounding the brainstem at the foramen magnum (Box). The haemorrhage was not considered surgically salvageable by the neurosurgeon. On admission, his INR was 4.9 (recommended range, 2.0–3.5), and he was given 5 mg vitamin K and four units of fresh frozen plasma. Glyceryltrinitrate infusion was started at 1 μg per minute and increased to 20 μg per minute to maintain diastolic BP at < 90 mmHg. His troponin-T level was 0.27 μg/L (normal range, < 0.005 μg/L) and white blood cell count was 17.6 × 109/L (normal range, 4.5–10.5 × 109/L). Results of liver function tests were normal, although the aspartate aminotransferase level increased to 51 U/L (normal range, < 40 U/L) by 0630 hours the next morning. Bilateral lung crepitations were noted at 0250 hours. A chest x-ray showed peribronchial cuffing consistent with early pulmonary oedema: 40 mg frusemide was given intravenously. The patient's pupils remained fixed and dilated, and brain death was confirmed at 1710 hours on 31 January. A postmortem examination was not performed. DiscussionStings causing the delayed effects of the Irukandji syndrome are well known in the Whitsunday area, with almost every patient developing hypertension and a rise in cardiac troponin levels,7 as seen in our patient. Some develop delayed toxic cardiac dilatation and heart failure; a few develop painful neurasthenic burning pain in both lower limbs or in the jaw, priapism or acute angioneurotic oedema within minutes of the initial sting, often accompanied by an audible wheeze.7 Stings from the outer Great Barrier Reef in the Cairns region have also caused severe hypertension and heart failure.5 The second death from intracranial haemorrhage after jellyfish envenomation occurred in this northern reef area and was attributed to hypertension of an Irukandji syndrome.6 Hypertension can be life-threatening, with the highest readings being some 280/180 mmHg.7 Our patient's high INR probably placed him at much higher risk of a cerebrovascular accident. Similar deaths may have occurred in the past, with the relationship to Irukandji syndrome not being recognised. There is currently no first aid treatment for carybdeid jellyfish stings, although immediate vinegar dousing is advised to prevent further envenomation from inactivated stinging cells present on the skin.7,8 Blood pressure must be monitored after envenomation and hypertension treated with 5 mg phentolamine given intravenously (although in this case the aliquots were smaller because high ambient temperature and humidity with profuse sweating caused clinical dehydration). Most cases of envenomation by jellyfish causing Irukandji syndrome occur some distance from medical care, with helicopter or medical response often too late to treat the early pain and hypertension. As intravenous nitrates are effective in reducing hypertension, sublingual nitroglycerine spray may help control blood pressure until skilled medical aid is available. Research on venom from Carukia barnesi caught in the Cairns region shows it acts as a presynaptic neuronal sodium channel agonist, strongly stimulating noradrenalin release, and causing many clinical features of the Irukandji syndrome.9 Venom studies on carybdeid jellyfish are urgently needed to develop preventive strategies and effective treatments for Irukandji syndrome, including an antivenom.

Peter J Fenner MD, FRCGP · John C Hadok MB BS, DA(UK), Dip IMC, FIMC, RCS(Ed), FACRRM

The logic is simple, but the implementation difficult and the costs potentially astronomical. Simple, because the cause is usually ventricular fibrillation (VF), which, if corrected within one minute, leads to survival in well over 90% of patients.1 Implementation is difficult because of the 10% fall in survival for every minute that passes from onset of VF until a defibrillator can be used.1 Astronomical cost is anticipated if all people at high risk of VF were to be offered an implantable defibrillator,2 or if the conventional ambulance service were geared up to provide a response time of less than five minutes in metropolitan areas. Novel approaches are required, as the average Australian ambulance response to cardiac arrest is 8–10 minutes even in metropolitan areas, and the survival to discharge for VF is generally less than 10%. A new initiative is presented on page 305 of the Journal — Smith et al report the experience in Melbourne, where fire fighters have been trained to defibrillate, fire trucks are equipped with defibrillators, and a three-tier response (ambulance, intensive care ambulance, and fire vehicle) is made to 000 calls for suspected cardiac arrest.3 The Victorian Government and the Victorian Department of Health are to be complimented on trying a new approach, as are the emergency service officers who participated. But the results are disappointing, despite overall mean response time of 6.0 minutes and time to defibrillation of 8.8 minutes. Of 2942 events, 1331 patients were in cardiac arrest and considered for resuscitation, but just 155 were in VF. From these, there were 26 known survivors, of whom 10 received initial care from fire fighters and 16 from ambulance paramedics. Of the 10 initially treated by fire fighters, possibly half would not have survived with the later arrival of an ambulance. The low prevalence of VF (12% of all [155 of 1331]; 36% of presumed cardiac arrests [155 of 430]) contrasts with the 100% prevalence at the Melbourne Cricket Ground,4 suggesting that there was substantial delay in calling 000. In the Melbourne experience for three-tier response, costs were not estimated, but must include the wage margin negotiated with fire fighters, the cost of training and equipping vehicles, and any overtime worked. A rough estimate for a possible five lives saved among almost 3000 calls reported by Smith et al is more than $1 million. The question arises, is there a better way? In the United States, emergency medical services are usually provided by town or city fire departments. However, except in model cities like Seattle, response times are similar to or longer than those in Australia, and survival rates correspondingly bad. In Rochester, Minnesota (home of the Mayo Clinic), defibrillators are carried in police vehicles. As in Melbourne, these vehicles respond to an emergency (911) call and have reduced response time to five minutes, with overall survival boosted to more than 40%.5 This system has been tried in other US cities and rural areas, but without the same commitment or success. Regrettably, in most instances, the overall survival rate remains less than 10%, and could be worse in an environment where security is more intense and access more difficult. Is there another way to tackle this problem? Clearly, we can identify high-risk individuals and insert a pacemaker/defibrillator (as in US Vice President Dick Cheney), but at high cost, and with benefit to a small fraction1,2 of the more than 10 000 people who suffer cardiac arrest outside hospital each year in Australia. Most cardiac arrests are unexpected and occur in people with little or no apparent risk.1 A different way was first suggested by Frank Pantridge, who initiated the "coronary ambulance" concept. In 1968, he developed a small portable defibrillator, which he suggested be located like a fire extinguisher in buildings and public places.6 His idea fell flat, since the device could be used as a weapon, but has regained credibility with development of semi-automatic defibrillators that can only be activated if a person is in VF.7 These defibrillators were introduced into all ambulances in New South Wales in 1990, then into the Qantas aircraft fleet in 1991,8 then much more widely. The high survival rates for VF at the Melbourne Cricket Ground (71%),4 Chicago (O'Hare) Airport (75%)9 and Las Vegas casinos (53%)10 are attributable to very early use by first responders (St John volunteers, airport staff, passers-by, or security officers), who can initiate defibrillation well within the time it takes for conventional emergency services to arrive. What then is the current status of "public access defibrillation" — the fire extinguisher approach? The program has the blessing of the American Heart Association and the International Liaison Council on Resuscitation, which have been promoting it with increasing enthusiasm since 1990. In Australia, it has been promoted by St John Ambulance (the most experienced voluntary body), the Heart Foundation, and the Australian Resuscitation Council. In the US,7 state legislation has been introduced to permit early implementation, and federal legislation has been passed to provide defibrillators for isolated areas, and to require installation of defibrillators for "public access", with key staff trained, into all major federal buildings and into all passenger aircraft with one or more cabin attendants by mid-2004. In the United Kingdom,11 more than 800 defibrillators have been deployed in public places and another 3000 placements planned — and key staff trained — under a government initiative. Australia, regrettably, has fallen behind. The NSW Ambulance Service provided key advice in development of the original Laerdal semi-automatic defibrillator, while Qantas was the pioneer in the sky and set the benchmark for aircraft and airports in 1991. The National Health and Medical Research Council (NHMRC) has, to date, not seen cardiac arrest as a health priority, despite more than 10 000 lives lost yearly and a potentially high salvage rate. Currently, St John Ambulance Australia has a proposal before the federal government for a program with strong community links and has a belated chance to match or better what is happening in the US, the UK and elsewhere. The Melbourne experience reported in this issue may be disappointing, but it is an important step by the Victorian government, emergency services and medical personnel, who have already achieved recognition for other initiatives in pre-hospital care. We have new tools and we need to implement them to address the most common cause of sudden unexpected death in our community.

Michael F O'Rourke MD, DSc

The Emergency Medical Response (EMR) program is a Victorian Government initiative in which fire fighters trained in cardiopulmonary resuscitation and equipped with automatic external defibrillators are dispatched to suspected cardiac arrests simultaneously with ambulance paramedics across metropolitan Melbourne. During the first 12 months (February 2000 to February 2001) of the expanded EMR program, 2942 events involved simultaneous dispatch of ambulance paramedics and fire fighters. In 430 events, patients had suffered a cardiac arrest of presumed cardiac cause, and resuscitation was attempted by the emergency medical services. Fire fighters provided the initial defibrillation to 41 (26.5%) patients presenting in ventricular fibrillation. Survival to hospital discharge for bystander-witnessed ventricular fibrillation cardiac arrests was 21.8%. The mean emergency services (fire and ambulance) response time to cardiac arrest patients was 6.03 (SD, 1.65) minutes. The mean time to defibrillation for ventricular fibrillation patients was 8.75 (SD, 2.07) minutes.

on behalf of the Emergency Medical Response Steering Committee

To the Editor: I would like to compliment Coiera et al for their very interesting article about communication in an emergency department.1 Nearly a third of communication events were classified as interruptions, thus having an adverse effect on communication within the department. In trying to reduce this level of interruption, perhaps it is time to rethink the role of the on-call emergency physician in an emergency department. In most large Australian emergency departments, the emergency physician is also the admitting officer, who is responsible for coordinating the non-elective admissions of the day. This involves being readily available for external and internal phone calls, usually by mobile phone. Thus, as well as the normal clinical workload of an emergency physician, he or she needs to respond immediately to the summons of a mobile phone — a recipe for interruptions and less efficient communication. It is not optimal for the person who has clinical responsibility for the emergency department to also be the person through whom most of the communication is channelled. One possible solution is to channel calls about patients whom the referring doctor considers definitely need assessment in the emergency department to non-medical clerical staff. They could enter the details in a computerised "expected patients" database, which would be available for viewing by emergency department staff. Only calls about patients where there is some uncertainty, and advice calls, would be channelled to the emergency physician on call. This would facilitate both planning of the emergency department workload and also provide access to advice for the referring doctor. This change in process would reduce the number of phone calls received by the on-call emergency physician — and thus the number of interruptions — and improve overall communication within the emergency department.

Alan E O'Connor · Antony Nocera · Thomas Hamilton · Enrico W Coiera

To the Editor: Coiera et al1 should be congratulated for highlighting the excessive communication workloads of emergency department clinical staff, and the potential for these to be a source of errors and adverse events. However, their article fails to discuss the confounding variables, making it difficult to assess the validity of the communication strategies the authors propose to remedy the problem, or the applicability of their findings to other institutions. Emergency department overcrowding results from lack of access to hospital beds.2,3 Situations in which the number of patients exceeds the number of available beds (as depicted in the emergency department shown on the cover of the same issue of the Journal) are of particular concern, and would be expected to be a significant factor in the communication workload of clinical staff. Furthermore, many emergency departments do not have ward clerks, which means emergency department clinical staff perform the functions delegated to ward clerks in other hospital areas. The lack of direct telephone access to patients in the emergency department means that telephone calls from family members to a patient have to be directed through clinical staff. This increases the exchange of information between clinical staff, especially when the emergency department is overcrowded and patients are moved within the department to accommodate new patients. It is not clear, from the communication workload identified in Box 3,1 whether these factors were relevant in the institutions surveyed. In addition, Coiera et al do not indicate the seniority of the six doctors they studied. This is important given that the ratio of staff specialists to registrars or junior staff in emergency departments may be two to three times that of inpatient wards, increasing the number of times staff specialists communicate to junior medical staff in the emergency department. Finally, there is no mention of the adequacy of nursing staff numbers during the survey periods. If there were a lack of nurses, or if there were nurses on duty who normally do not work in the emergency department, one would expect an increase in communication between nurses. When emergency department infrastructure is so stressed, important studies, like that of Coiera et al, need to describe their findings in context, because of the likelihood of communication problems emerging as a result of health system failures.

Enrico W Coiera PhD, FACMI

To the Editor: I was interested in the report by Coiera et al1 about communication in the emergency department and the accompanying editorial by Vincent and Wears2 (from the United Kingdom and the United States, respectively, where, incidentally, the practice of emergency medicine differs significantly from that in Australia). In no other discipline is facility in communication between doctors, nurses, patients and relatives, as well as colleagues in other departments, of greater importance, given the paucity of information at presentation and the time constraints for assessment, management and appropriate referral — all within a time frame of a few minutes to several hours, depending on the severity of the presenting complaint. Vincent and Wears allude to the "fluidity and complexity of the clinical environment" and rightly suggest that studies need to be designed to embrace a "need to appreciate clinicians' decision making and cognitive load". It was therefore disappointing that, after so much effort, Coiera et al did not correlate their data with severity of clinical condition and/or outcome (eg, requiring resuscitation, assessment for possible admission, treatment solely in the emergency department, or discharge to outpatients clinic or home, to name but a few possible groupings). These may, of course, be intended for future publication. Regrettably, it is not stated how much input, if any, in the design and conduct of the study was obtained from staff in the unidentified emergency departments, and their contribution goes largely unacknowledged. As Richardson3 has pointed out, the active participation of at least one member of the emergency medicine staff (preferably senior and experienced) in such studies enhances motivation in staff busy with other priorities, and facilitates cooperation and collaboration (which can thereafter properly be recognised in co-authorship). There is also a danger that in the current litigious climate an inadvertent emphasis on "errors and poor outcomes" may prejudice the real benefits of the worthwhile objective of assessing the nature, relevance and value of improved communication between those engaged in clinical practice. Nonetheless, it is encouraging to deduce from this report that, in emergency departments, doctors and nurses regularly speak to each other, presumably with an optimal outcome for the patient in mind. For one who spent two decades as head of a busy, metropolitan emergency department, it is reassuring to find, in a discussion of informatics, advocacy2 for a return to the "white board", which, even today, remains the mainstay of patient information and tracking in many emergency departments.

Alan E O'Connor

In reply: We know little about communication systems in healthcare, and our study is still only one of a handful that quantify communication processes. Consequently, the aim of our pilot study, as well as reporting specific emergency department communication patterns, was to develop a robust general observational methodology, and measures of communication load.1 With the evidence that communication load is an issue, the next stage in the research would be to design studies to identify variables that could, in principle, affect communication load, as suggested by both Nocera and Hamilton. Indeed, there are many such variables — staff level and experience, organisational structure, clinical task, patient acuity, communication infrastructure, departmental policy, etc. The difficulty we will face is to control for many of these variables, and this will require longitudinal studies and samples from multiple sites. Hence, we are not yet able to make specific recommendations about interventions to "improve" communication in emergency departments. Indeed, there are no benchmarks against which to compare these data, so we cannot even say whether the data reflect good practice. Given these uncertainties, we agree with Nocera that it is too early to say which interventions would be appropriate to the specific circumstances of emergency departments, and we made no specific recommendations ourselves, but rather summarised commonly suggested interventions. Nocera and O'Connor also suggest other interventions which in their clinical experience may improve communication loads in emergency departments. It is likely that the variability of organisational settings will mean most such interventions will need to be customised to local conditions and needs. Hamilton is correct to highlight the tension in reporting data on organisational performance, and the risks of these data being misinterpreted or misused. Given these risks and the lack of comparative benchmarks, we explicitly chose not to comment on performance, nor to identify the organisations or participating clinicians. However, we would not have been able to carry out the study without the full cooperation of the staff at both hospitals, and, while they remain anonymous, we are deeply indebted to them for their willingness to welcome us into their workplace, volunteering to be subjects, and allowing us to observe them as they carried out their work.

Alan E O'Connor

Chemical, biological and radiological (CBR) incidents have the potential to shut down emergency departments that do not have an adequate CBR response. Secondary contamination also poses a threat to the safety and wellbeing of staff and other patients. On activation of a CBR response, "clean" and "contaminated" areas should be clearly marked, and all patients decontaminated before being allowed into the emergency department or outpatients department. Personal protective equipment (PPE) is needed for all staff. Staff using PPE must be monitored for signs of heat illness. Stocks of coveralls, bags for contaminated clothes, plastic sheeting for radiological incidents, barriers for crowd control, and selected drugs should be obtained. Staff required include medical, nursing, security, clerical, orderlies, patient care assistants and other staff, depending on the type of threat. An on-call roster that allows regular rotation of staff is needed. All hospital personnel should understand the response plan, and recognise that the emergency department and hospital is a community asset that requires protection.

Gim A Tan DRANZCOG, FACEM · Mark C B Fitzgerald FACEM, MRACMA

Objective: To evaluate an intervention developed to improve test-ordering practice.Setting: Public hospital emergency department with an annual census of 42 500. The study comprised a six-month pre-intervention stage (November 1998 to April 1999), which was compared with a similar post-intervention period (November 1999 to April 2000), and trends were examined over an 18-month post-intervention period (May 1999 to October 2000).Intervention: The intervention comprised three integrated components: implementation of a protocol for test ordering; education program for medical staff; and audit/feedback process.Main outcome measure: Test utilisation (assessed as cost per patient).Results: There was a 40% decrease in the ordering of investigations in the emergency department (95% CI, 29%–50%), with test utilisation falling from a mean of $39.32/patient to $23.72/patient. The decrease was similar for both laboratory and imaging tests and was sustained for the duration of the 18-month follow-up.Conclusions: Our intervention appears to have produced long term modification of test ordering in the emergency department of a public teaching hospital.

Peter J Stuart MB BS, FACEM · Shelley Crooks BA(Hons.Psych) · Mark Porton BAppSc

In cases of multiple impalement injury, the extent of damage to the body can be underestimated. A 26-year-old man sustained a fivefold impalement injury after falling three metres onto metal reinforcement rods. When the emergency medical services arrived at the scene, the patient was in severe distress, pale with clammy and moist skin, increased respiratory and heart rate and tenderness in the lower abdomen. Motor and sensory responses were normal. The emergency physician would not permit the steel rods to be cut until adequate fluid resuscitation (lactated Ringer's solution 1500 mL and hydroxyethylstarch 1000 mL) and analgesia (ketamine hydrochloride 50 mg) were established. During the extrication process, the patient was covered with a blanket and supported from the back (Figure A). Within 53 minutes of the fall, the patient was admitted to the emergency department. Abdominal x-ray indicated that two rods had entered the abdominal cavity (Figure B). Surgical investigation revealed, in addition to laceration of the right femoral artery, major trauma to the abdomen (perforated rectum, jejunum and duodenum, incomplete rupture of the spleen, and injury to the head of the pancreas). The patient recovered from severe infection of the abdominal cavity with concomitant septicaemia, and was discharged from hospital three months later. Multiple impalement is a potentially life-threatening injury that requires perfect cooperation between technical and medical personnel on the scene.1-3 Stabilisation of vital functions, analgesia, and extrication must be performed simultaneously. On-site emergency management must be judged on an individual basis. The question arises whether a scoop-and-run policy — with presumably shorter prehospital treatment time — is justified. In cases involving prolonged rescue, manipulation, or even removal, of the impaling objects has been reported as an exception to the general rule that an impaling object should remain in situ while the patient is transported to an operating theatre.4,5 In our patient, removal of the impaling objects was especially tempting, as successful compression of bleeding vessels from outside the body was anticipated. However, intra-abdominal injury was clearly underestimated at the scene. Major injuries to the upper abdomen by protruding rods were not clinically suspected before operation. This shows that the entry site does not necessarily reveal the extent of damage to the body. A: The patient was supported from behind while the penetrating rods were cut. B: Rods were found to have penetrated the abdomen. This was not suspected until the patient had reached the hospital.

Wolfgang Lederer MD, DTM · Hans C Jeske MD · Kroesen Gunnar MD

Struan Sutherland, an Australian pioneer in medical research on envenomation and an expert on the management of envenomated victims, died on 11 January 2002. As Head of Immunology Research at the Commonwealth Serum Laboratories (CSL), he was the force behind the development of the antivenom to the Sydney funnel-web spider. Born in Sydney on 17 June 1936, Struan was raised in Bendigo and educated at Bendigo High School. He graduated in medicine from the University of Melbourne in 1960, and from 1962 to 1965 served as a Surgeon-Lieutenant in the Royal Australian Navy. Struan started work at CSL in 1966, and in the following year was appointed foundation Head of Immunology Research, a position he held for 28 years. His interest in venoms was sparked in 1967 by the deaths of a young soldier bitten by a blue-ringed octopus and of a child bitten by a Sydney funnel-web spider. He renewed research into finding a spider antivenom, but it was not until 1980 that the research team finally succeeded. This was a remarkable scientific achievement — many others had tried and failed in this endeavour. Struan also developed techniques that have made the medical management of envenomation in Australia the best in the world. He invented the pressure-immobilisation technique of first-aid, which revolutionised the management of snakebite world-wide. He also developed a snake venom detection kit that enabled doctors in Australia and Papua New Guinea to determine which snake antivenom should be administered to a victim. In recognition of his achievements, he was awarded the AMA Prize for Medical Research in 1977 and the James Cook Medal of the Royal Society of NSW in 1984. Struan was a prolific author, publishing over 300 scientific articles and book chapters. His book Australian animal toxins was the standard medical textbook on envenomation, and he co-authored other books, including the best-selling Venomous creatures of Australia. Struan served the medical profession and the public selflessly. He was always available to give advice at any time of day or night on management of envenomated victims. He was dedicated and passionate about things that mattered, and prepared to fight for a principle. His departure from CSL in 1994 was precipitated by the closing of the antivenom research program when the organisation was privatised. His outspoken view that antivenom research should continue and that the public good was more important than profitability led to many heated clashes with management. After leaving CSL, with the help of Professor Jim Angus he established the Australian Venom Research Unit within the Department of Pharmacology at the University of Melbourne. Struan was a generous, kind person. He married three times, and was devoted to his children and grandchildren. Visitors to his home would be plied with produce from his hydroponic garden, another of his passions. His autobiography, A venomous life, tells the story of his life with characteristic candour and dry wit. A variant of Parkinson's disease eventually slowed him down, but, although confined to home, he continued writing. Struan was honoured posthumously in the 2002 Australia Day awards as an Officer of the Order of Australia.

James Tibballs MD MBA FANZCA

Ethics and putting the patient first are the primary considerations in deciding what is acceptable advertising of medical services by doctors Type "cosmetic surgery" into your Internet search engine and several hundred thousand sites will appear. All enthuse about the benefits and increasing popularity of their techniques. They identify and detail medical practitioners qualified to work their miracles on the human body. Few negatives are to be found in such promotional material, and much of the hype is not dissimilar to that used to market other lifestyle products. This is but part of the global rise of the entrepreneurial approach to healthcare. Cosmetic surgery is in demand because of the changing culture and attitude of patients. For some in today's world there is a need to satisfy a desire for what, in times gone by, would be unrealistic expectations — changes to their bodies to enhance their appearance — at least in their own eyes. If we take the definition used by the New South Wales Committee of Inquiry into Cosmetic Surgery, "cosmetic surgery" is any cosmetic procedure "performed to reshape normal structures of the body or to adorn part of the body, with the aim of improving the consumer's appearance and self-esteem". It "is initiated by the consumer, not medical need", and "excludes reconstructive surgery".1 This lies outside the traditional boundaries of medicine, which saw the profession dedicated to saving lives, healing and promoting health.2 Cosmetic surgery is not rebatable under Medicare, nor covered by health insurance. There are relatively few referrals. However, it does provide a service for which consumers are prepared to pay. Traditionally, the medical profession has prohibited advertising in its codes of ethics. The traditional view is that doctors should develop a reputation for excellence based on a reputation among their peers, rather than by the advertising of their services directly to the public. This minimises the opportunity for patients to be misled by claims of superiority of a technique or individual. Particularly in Australia and the United Kingdom, general practitioners have long been "gatekeepers" to specialist services. This role has helped maintain quality care for patients and has probably helped to contain overall costs in the healthcare system. But with the demise of paternalism, both in society and in the professions, this way of doing things has attracted increasing criticism. Undoubtedly, this forms part of the rationale for applying trade practice law to the health sector and to advertising by doctors, and to the interpretation of such law by the Australian Competition and Consumer Commission. Under federal law in Australia the Trade Practices Act 1974 (Cwlth) now permits advertising, unless it is likely to mislead or deceive. Direct advertising by doctors to the public is now lawful. The article by Ring in this issue of the Journal (page 597)3 asks if ethical standards are a casualty in the promotion of cosmetic surgery, and shows that this specialty is being seen as part of the beauty industry rather than a procedure for meeting health needs. The promotional strategies used do not sit well within the medical environment. The beauty industry promotes a body image that draws on vanity rather than on health. It creates expectations linked to perpetual youth, which can feed insecurities in people of both sexes, and contributes to a youth culture which treats with contempt the results of the ageing process.2 On the other hand, people who wish to change their image are now being informed that there are treatments available. The World Medical Association Declaration on the Rights of the Patient says that, "The patient has the right to self-determination, to make free decisions regarding himself/herself. The physician will inform the patient of the consequences of his/her decision".4 Should not patient autonomy include the freedom of adults to purchase these treatments, as long as the advertising surrounding them remains within the ethical boundaries of truthfulness? Where should the boundaries lie between medicine as traditionally defined, and lifestyle-modification medicine? The Australian Medical Association (AMA) Code of Ethics encourages doctors to promote the health and well-being of their patients and prohibits doctors from behaving in their own self-interest. It also says that doctors have "a responsibility to their patients to recommend only those diagnostic procedures necessary to assist in the care of patients and only that therapy necessary for their well being".5 Many patients would say that changing their image through cosmetic surgery is for their well-being, as it would improve their quality of life. It is a personal decision based on personal perceptions. If we consider that cosmetic surgery is part of medicine, then the advertising and promotion of such procedures must adhere to the ethical guidelines of the medical profession. The AMA believes that, as a general principle, advertisements must be honest, must not exploit patients' vulnerability or lack of medical knowledge, and should provide only factual information. Any advertisement for a doctor's services should present information that is reasonably necessary for making an informed decision about the appropriateness and availability of the medical services offered.6 In recognition of the need for a middle ground between the traditional ban on advertising and the current deregulated environment, the Medical Practitioners Board of Victoria has produced draft guidelines which will provide clear guidance for doctors who wish to advertise their services. A summary of the guidelines is presented in the Box.7 Summary of the Medical Practitioners Board of Victoria's draft guidelines for medical advertising7* Ban the use of "before and after" photography, which is common in advertisements for cosmetic surgery. Limit advertising to a factual statement of services offered. Warn against the creation of "unwarranted or unrealistic" patient expectations of treatment. Continue the ban on the use of patient testimonials. Prohibit advertising which encourages inappropriate use of medical services and contains information or language which could cause fear or distress or make people believe their health may suffer from not using a medical service. * Reproduced with permission. Whether we agree with changes in contemporary views which have allowed doctors to enter the free market of advertised services, or prefer the traditional culture, the one interwoven thread which must run unbroken through the fabric of medical practice is that of standards of ethical practice and the primacy of the patient.

Trevor J Mudge MB BS, FRACOG · Dorothy A Dashwood BEd, GradDipAdmin

Objective: To explore, among middle-aged women, the relationship between having ever had cosmetic surgery and the frequency of use of other health services.Design: Retrospective analysis of cross-sectional survey data from the Women's Health Australia (WHA) study.Setting and participants: A nationally representative sample of the "mid-aged" (45–50 years) cohort of women who participated in the 1996 WHA baseline postal survey. Responses were received from 14 100 women (a response rate of 54%).Results: Seven per cent of women reported ever having had cosmetic surgery. After adjusting for demographic variables, multivariate analysis confirmed that women who had had cosmetic surgery were significantly more likely to use health services more frequently (eg, surgical procedures, consultations with specialists and alternative healthcare providers). Cosmetic surgery was also associated with a greater number of chronic illnesses and use of medication for anxiety and sleep problems.Conclusion: Further research is needed to determine whether cosmetic surgery is directly related to health conditions or to attitudinal or psychosocial variables. Such research should examine whether alternative interventions may be more cost-effective in dealing with the issues that motivate women to seek cosmetic surgery.

Rafat Hussain MB BS, PhD · Margot Schofield MClinPsych, PhD · Deborah Loxton BPsych(Hons)

Within the past five years, medical practitioners have seen major changes to the ways in which they are entitled to promote their services in Australia. The current approach was formalised as a result of the State-by-State deregulation of advertising by doctors through concerted action by the Australian Competition and Consumer Commission (ACCC), which did so in order to enable equal opportunity to all businesses in compliance with the National Competition Policy.1,2 Box 1 outlines the current conditions for medical advertising. In 1998, the then Head of the NSW Health Care Complaints Commission (HCCC) sounded a cautionary note about the risks to the medical profession from a shift to "competitive principles", and the potential effects of this in compromising the traditional medical ethics that have guided the behaviour of members of the profession "since Hippocrates".1 Concerns about implications for the profession have also been expressed by the Australian Medical Association (AMA), with one of the key points in its current position statement on advertising and endorsement being that: "The promotion of a doctor's medical services as if the provision of such services were no more than a commercial product or activity is likely to undermine public confidence in the medical profession."4 Evidence that some practitioners of cosmetic surgery were in the vanguard of the profession in promoting their services in this way was presented to the New South Wales Inquiry into Cosmetic Surgery conducted in 1999 by the NSW HCCC. The Committee of that Inquiry concluded that a number of the promotional practices "may be in breach of professional standards and fair trading laws".5 Two years on, the ways in which a subset of plastic and other cosmetic surgeons continue to promote their practice2,6 require the medical profession to consider, fair trading laws aside, some important questions about the implications of such commercial strategies for both the cosmetic surgery sector, and for the profession as a whole. It should be noted that the term "cosmetic surgery", as used in this article, is in accordance with its definition by the NSW Committee of Inquiry into Cosmetic Surgery. Key points of that definition are listed in Box 2. Are ethical standards a casualty in the promotion of cosmetic surgery?Doctors strive to prolong life, and have earned some of the credit for the fact that we are living in a society that is ageing healthily as our life expectancy continues to grow. It is therefore somewhat anomalous that the public face of cosmetic surgery includes promotions which play on the insecurities associated with the superficial consequences of ageing. Specifically, there is considerable evidence that the highly profitable tactic of targeting the appearance of ageing as an undesirable quality is being exploited by some medical practitioners, using methods similar to the beauty industry's approach of stigmatising this normal bodily process. The allegation that doctors have made a substantial contribution to the reconstruction of ageing for profit is, of course, not new.7,8 By 1990, in America, Naomi Wolf (in her book The beauty myth7) had described a key marketing strategy for cosmetic surgery — namely, classifying ageing as ugly, and ugliness as a disease for which cosmetic surgery practitioners had the most effective treatment.7 She also questioned whether such exploitation of women's insecurities about their appearance was "subject to the ethics of the genuine medical profession".7 These are now matters that also need to be examined in the Australian context. This can be done on the basis of examples of anti-ageing strategies drawn from Australian media and attributed to Australian medical practitioners. The following examples fall into two categories: textual references, and the use of enhanced and idealised images that could be construed as misleading. The majority of the examples come from recent issues of Australian Cosmetic Surgery Magazine.9 This is a quarterly publication distributed through newsagents since 1998 (by which time, it should be noted, advertising by doctors had been deregulated in the three most populous States in response to the requirements of the ACCC10). Key aspects of this magazine are that: Many of the articles are identified as being authored by, or substantively based on interviews with, named medical practitioner contributors. Many of the contributors also have an advertisement within the magazine, either on the same page as one of those articles, or in another part of the magazine. The contributors are introduced in an illustrated list at the front of the magazine.9 It is relevant to note that, while there are substantial and often publicly aired areas of professional conflict between different categories of surgeons who practise cosmetic surgery,5,11 they use similar promotional strategies within the covers of Australian Cosmetic Surgery Magazine.9 Text messagesTypically, negative comments about the appearance of ageing have focused on aspects of the face and skin (usually, but not always, in reference to women). Box 3 shows examples of the ways in which some doctors have characterised normal bodily changes as undesirable changes in appearance. In each of the articles from which the quotes were drawn, the doctor offered cosmetic solutions to the targeted features. Enhanced and idealised imagesSince the linking of questionable anti-ageing images and cosmetic surgery was raised in Australia in 1998,12 quite a lot has happened, and nothing much has changed. Examples of "ideal" and enhanced images used in magazines were presented to the 1999 NSW Inquiry into Cosmetic Surgery.5 The key elements of the images that were presented included a number of tactics that are standard practice in the beauty industry. They have, however, been specifically criticised as being neither appropriate nor acceptable promotional strategies for medical practitioners. The NSW Inquiry, for example, concluded that advertising practices that "may be in breach of professional standards and fair trading laws" included: "use of models, implying the model has had the procedure or that the procedure can achieve the results (with or without a disclaimer)"; and " 'before-and-after' photographs that have been enhanced, or are different in size, colour or pose, or give a misleading impression of long-term effects of a treatment".5 One of the outcomes of the Inquiry was the recommendation for development of a guide by the ACCC and the HCCC "on the application of fair trading laws to the promotion of health services".5 When the guide was published, both of the above practices were specifically targeted as potentially misleading.3 It is therefore highly significant that, over a year after the publication of the guide, many of the same, or very similar, kinds of photographs were still being used. Examples of such illustrations can be seen in magazine advertisements and in a more neutral and widely accessible form of commercial media, the Yellow Pages telephone directories. Some advertisements for cosmetic surgery, for example, include photographs of youthful and idealised female features, or enhanced "after" pictures. These images provide a graphic demonstration of the gulf between the promotion of cosmetic surgery and the promotion of other areas of medical practice at this time. Where does cosmetic surgery belong?"Anti-ageing" is one of the most powerful contemporary marketing devices used by the beauty industry. Essentially, it involves exploiting the insecurities wrought by the appearance of ageing, and is a part of the broader strategy of promoting idealised or enhanced standards of appearance as an incentive for buying cosmetic products and services.7 It has a long-established history of targeting women, and, more recently, men, and functions under the socially accepted banner of caveat emptor. The issue here, however, is not whether such tactics are a good or a bad thing or to make any such moral judgements. It is the question of their place within the practice of medicine, as conventionally defined; that is, as "the science or practice of the diagnosis and treatment of illness and injury and the preservation of health".13 Concerns about the place of cosmetic surgery have, in fact, been raised by some of its practitioners. For example, the NSW Inquiry into Cosmetic Surgery cited the Australian Society of Plastic Surgeons (ASPS) as expressing "concern about the promotion of an attitude that cosmetic surgery is just another beauty product".5 A member of the ASPS placed the blame for this attitude on "women's magazines, regrettably, and the media generally".5 However, as the examples cited in this article suggest, "the media" may only be part of the problem, and it is noteworthy that, at the same Inquiry, a cosmetic surgeon described his area of practice in the following terms: "You have to recognise that cosmetic surgery is the nearest thing you're going to get to retail medicine — or retail surgery. You're not treating sick people, we're not treating people who need to have pathology addressed. This is the surgical or medical end of the beauty industry".14 Certainly, there is evidence that the ASPS is right in its reported perception of how the media is currently constructing cosmetic surgery. Recent editions of the magazines Good Medicine and the Australian Women's Weekly (AWW), for example, both classified anti-ageing features involving cosmetic surgery solutions in the "beauty" and "fashion and beauty" sections of their respective contents pages.15,16 Each of the ensuing feature stories expanded on the legitimacy of that location. The introductory text to the Good Medicine article, "Lift your spirits", stated that: "Sophisticated medical technology is making cosmetic surgery an increasingly popular beauty option for many thousands of Australians who want to give themselves a much-needed boost of confidence."17 AWW's story, "Stop the clock", presented a range of "cosmetic fixes", stating in its introduction: "Even the most effective anti-ageing creams can only do so much — that's why an increasing number of women are turning to cosmetic surgeons and dermatologists for high-tech treatments."18 Statements such as these suggest that "anti-ageing" cosmetic surgery and allied procedures are being socially classified as a beauty want rather than a health need. This classification also applies more broadly to the practice of cosmetic surgery as a whole, and is, in fact, consistent with the definition of cosmetic surgery given earlier in this article as the basis for the NSW Inquiry into Cosmetic Surgery.5 At this early phase of deregulated advertising by doctors, the nature of cosmetic surgery, and the perhaps consequent way in which some of its practitioners have adopted commercial strategies from the beauty industry, has clearly opened up some interesting areas of debate for the medical profession as a whole. Should current promotions of cosmetic surgery be a focus of professional concern?First of all, there is the issue of cosmetic surgery itself, and the extent to which some ways of promoting this burgeoning area of medical practice meld with accepted visions of what being a doctor is all about. Do such visions include the application of medical technology, techniques and procedures to consumer needs which have been defined as "non-medical",5 and with what may be seen as some of the sophistry of commercial advertising techniques? More specifically, does the profession see the latter aspects of such applications as simply an extension of core business for doctors, or a worrying expansion into a grey area of mixed allegiances and hazy ethical boundaries that need to be examined? What are the implications of commercially structured promotional strategies for the tradition of "Trust me, I'm a doctor"?It could, more broadly, be argued that the way in which cosmetic surgery is being promoted by some practitioners in Australia today makes it an important test case for how the medical profession and the community want to see the future direction of the profession develop. The AMA's concerns, cited at the beginning of this article, about the potential for such promotional strategies to "undermine public confidence in the medical profession"4 need to be taken seriously. Would the continuing and potentially expanding use of such strategies presage a decline in the role of trust within a doctor–patient/client/consumer relationship? And would any such decline be of concern to the medical profession, or just be seen as a natural and acceptable consequence of a progression towards the more commercialised practice of medicine? 1: Advertising: what doctors can and can not — and should and should not — do* The National Competition Policy requires that "strict controls on advertising" have to be eased "where anticompetitive effects do not have countervailing public benefits". However, the subsequent changes in the laws do not result in a "free for all where anything goes". Advertising and other promotional activity must comply with: the rules of the Commonwealth Trade Practices Act 1974, which prohibits a range of misleading, deceptive and unconscionable conduct, and misrepresentations; the relevant State and Territory Fair Trading Acts; and "any specific medical and health practitioner regulations that remain". Some equivocation applies, however, with regard to the distinction that the Trade Practices Act draws between misleading content and "puffery or self-evident exaggeration". While there is a reluctance at the legal level to elevate puffery "to the status of potentially misleading conduct", it is recommended that – in the case of complex areas such as medical and health care – puffery "should be avoided or used with extreme caution". This echoes a broader caveat laid down for practitioners: that consumers "are best protected when they are fully informed and when medical and health professionals maintain professional and ethical standards". * Drawn from a 2000 guide to the Trade Practices Act 1974 (Cwlth) for health and medical professionals.3 2: Current parameters of cosmetic surgery Cosmetic surgery: is any cosmetic procedure "performed to reshape normal structures of the body or to adorn parts of the body, with the aim of improving the consumer's appearance and self-esteem"; "is initiated by the consumer, not medical need"; and "excludes reconstructive surgery which is . . . [generally] performed to improve functions, but may also be done to approximate a normal appearance".5 3: Quotes from cosmetic and plastic surgeons* ". . . lower face and neck . . . is the area where the by-product of ageing is most obvious with defects such as 'turkey neck', double chin, jowl fat and platysma bands. This area is most susceptible to gravity pull and is usually regarded as the ageing area . . ." ". . . as a natural part of the ageing process, most people develop deposits of fat underneath the eye and on the eyelid which make them appear older than they are . . ." [included for its curious logic]. ". . . as we age, the globe of the eye tends to descend and fall backwards due to gravity and subcutaneous fat fades away. This causes the eyelids and folds around the eyes to become crepey [sic] and wrinkled giving an untidy and withered appearance . . ." * From publicly available magazines published in 2000 and 2001.

Anne L Ring PhD, GradDipHlthEd

Both men and women are becoming increasingly concerned about their physical appearance and are seeking cosmetic enhancement. Most studies report that people are generally happy with the outcome of cosmetic procedures, but little rigorous evaluation has been done. More extensive ("type change") procedures (eg, rhinoplasty) appear to require greater psychological adjustment by the patient than "restorative" procedures (eg, face-lift). Patients who have unrealistic expectations of outcome are more likely to be dissatisfied with cosmetic procedures. Some people are never satisfied with cosmetic interventions, despite good procedural outcomes. Some of these have a psychiatric disorder called "body dysmorphic disorder".

David J Castle MSc, MD, FRANZCP · Roberta J Honigman BComm, BSocWork, Grad Dip Conflict Resolution · Katharine A Phillips MD

"of insects . . . only the ants were troublesome . . . one green as a leaf and living upon trees where he built his nest . . . by bending the leaves together and glueing them . . . their stings were by some esteemd not much less painfull than those of a bee . . ." Joseph Banks, August 17701 Indigenous Australians co-existed with native ants for thousands of years, using them as food (honey ants) and in medicinal decoctions (green tree ants).2 It was the green tree ant (Oecophylla spp.) that first attacked the white invaders from the Endeavour, and a number of native ant species, in particular the jumper or hopper ant (Myrmecia pilosula), still cause significant morbidity. But a foreign ant has now assumed the role of invader. In this issue of the Journal, Solley et al3 (page 521) describe the first Australian patient with anaphylaxis caused by the venom of the Red Imported Fire Ant (RIFA), Solenopsis invicta, and outline the appropriate diagnostic and management strategies, including successful desensitisation. Where did the RIFAs come from? Why are they a threat to our economy as well as our health? Can they be eradicated? February 22, 2001, was a dark day for Australia with the identification of S. invicta at two sites across Brisbane. This ant has the potential to be one of Australia's biggest ecological disasters, with the ability to have an impact on the economy, the environment and society. The ant itself appears innocuous. It is a small (2–6 mm), reddish-brown ant that is hard to distinguish from many other common ants. Its behaviour sets it apart as one of the world's great invaders. The ants will literally boil out of the nest ready to attack in huge numbers. The sting is painful, which accounts for the name "fire ant". Multiple stings are the rule rather than the exception and can be excruciating. The nest is dome-shaped and the colonies consist of up to half a million ants. S. invicta originated in South America, spread to Alabama in the 1930s and now infests 12 US States. Fire ants are thought to have entered Australia via shipping containers. There are two RIFA epicentres, one on the east of Brisbane around the port area, the other in Brisbane's western suburbs and part of Ipswich. The eastern infestation has been identified by DNA testing and chemical analysis of its venom as being from the United States or northern South America. The western infestation may have originated from Argentina (Dr Robert K Vander Meer, Research Chemist, United States Department of Agriculture/University of Florida, Center for Medical, Agricultural, and Veterinary Entomology, unpublished data, personal communication). Despite this multiple encroachment, the pest seems confined to Brisbane. Ecological modelling shows that the ants are capable of surviving in most parts of Australia, while spread modelling suggests that, if uncontrolled, the ants could spread up to 2 million square kilometres (ie, about a quarter of the area of Australia) over the next 30 years.4 A study of the environmental impact of fire ants5 shows that areas infested with the ant have fewer native ant species, lower total biodiversity and an absence of scincoid lizards. The ants can decimate ground-nesting birds, turtles and frogs, and can damage farm, irrigation and electrical equipment.6 The Australian Bureau of Agriculture and Resource Economics7 estimates that the cost of fire ants over 30 years, if uncontrolled, would be $8.9 billion. Australia's response to this invader is a $123 million, five-year National Fire Ant Eradication Program funded by the Commonwealth and the State governments. What about the medical aspects? It is appropriate to compare the RIFA with our most dangerous native ant, the jumper ant: Jumper ants are distributed throughout Australia; RIFAs have only been identified in the Brisbane area. Both jumper ants and RIFAs grasp the skin with the mandibles and sting repeatedly using a retractile stinger on the end of the abdomen. Stings from jumper ants usually cause a local weal-and-flare, while RIFA stings, because of the high alkaloid content of their venom, invariably result in sterile pustules. These pustules should not be broken. Venom proteins from both ants can result in immediate sensitivity. Two proteins have been cloned and sequenced from jumper ants (Myr p 1–2) and four from RIFAs (Sol i 1–4). There is no cross-reactivity between the main proteins of the two ants. Both jumper ants and RIFAs can cause large local allergic reactions that may need to be treated with oral corticosteroids. Up to 3% of Australians describe systemic allergic reactions to jumper ant stings,8 with most allergic sting reactions reported from Tasmania, Victoria and South Australia. In comparison, 30%–60% of people living in areas infested by RIFAs in the United States are stung, with 0.6%–16% of those stung developing anaphylaxis.6 Patients with anaphylaxis should be referred to an allergist/immunologist, and must carry self-injectable adrenalin. The best device, although expensive and still not subsidised by the Pharmaceutical Benefits Scheme, is the EpiPen Autoinjector (CSL, Melbourne). There is no commercial extract for desensitising patients with anaphylaxis to jumper ant venom. A clinical trial of a jumper ant extract has just been completed in Tasmania (Dr Simon G A Brown, Director, Department of Emergency Medicine, Royal Hobart Hospital, personal communication), but commercial production will not occur without financial help from government or private sector sources. At least three commercial desensitising extracts for RIFA venom are available from the United States. Deaths from anaphylaxis to jumper ant stings9 and RIFA stings6 have been documented. Perhaps, with luck and hard work and lots of money, we might eradicate RIFAs from Australia, but no State in the United States has been successful in such a program once the ant has invaded. In some parts of the southeastern United States, stings by fire ants are the commonest cause of anaphylaxis. Let's hope that that is not the case in Australia in 2030. The cost to our health and ecology would be enormous. Interested readers may wish to refer to two excellent web sites: <http://www.dpi.qld.gov.au/fireants/> (Queensland) and <http://fireant.tamu.edu/> (Texas).

Keith I McCubbin · John M Weiner

Stings from insects of the Order Hymenoptera (bees, wasps and ants) are responsible for numerous anaphylactic events, some fatal.1,2 In Australia, allergic reactions to ant stings have, until now, been caused by native ant species (eg, the jumper ant [Myrmecia pilosula and other Myrmecia spp.],3-5 the greenhead ant [Rhytidoponera metallica], Odontomachus, Cerapachys and Brachyponera spp.). Although ants are found worldwide, the only other ant species commonly reported as inducing anaphylaxis is the Red Imported Fire Ant (Solenopsis invicta Buren),6-9 which is native to Brazil, Paraguay, Uruguay and Argentina.10 This species was accidentally introduced into Alabama in the United States in the 1930s,10,11 and since then has spread rapidly throughout the southern United States, causing economic damage to crops and primary industries, reducing biological diversity, and frequently inflicting severe stings to humans.12 In February 2001, two well established populations of S. invicta ants were discovered in Brisbane (Box 1). The mode of introduction is unknown, although it may have been through the transport of infested sea cargo. It is estimated that the incursion is more than five years old. Currently, S. invicta ants are found over 37 000 hectares of the Brisbane region, covering over 64 000 homes. Here, we describe a patient with anaphylaxis as a result of S. invicta stings, document his treatment and estimate the likely rates of anaphylaxis and mortality should these ants spread across the remainder of Australia. Clinical recordA man, aged 47 years, began work as a gardener at the Port of Brisbane in November 1999. His first Red Imported Fire Ant (RIFA) sting occurred during the summer of 1999–2000. These stings resulted in acute local pain at the sting site, leading to small pustules the following day which took two weeks to heal (a typical reaction, unique to RIFA stings, which occurs in about 85% of cases).10 These reactions were quite different from previous stings by greenhead ants, which left nothing more than local puncture marks. He was then assigned to a work party to search and destroy RIFA nests. In this task he incurred 20 to 30 separate RIFA sting events, which resulted in reactions similar to those described above. He then received two RIFA stings on his knee at the one time. Ten minutes later, he developed extreme pruritus and burning of both feet. This was quickly followed by generalised pruritus, nasal congestion, and acute tightness of his throat and chest with dyspnoea. He was transported quickly to a nearby hospital. On arrival, a rash was present on his trunk and legs, his pulse rate was 84 beats/min, his blood pressure was 131/110 mmHg and his lungs were clear. He was given intravenous saline and 200 mg of hydrocortisone, but not adrenalin. Two hours later, he was discharged well. A review by the Port of Brisbane's occupational physician highlighted this as a sentinel case and the causal agent was identified as RIFA. The patient's usual work duties were altered to avoid further, possibly life-threatening, RIFA stings. He was also provided with the semi-automatic adrenalin device, EpiPen (CSL, Melbourne). Avoidance measures were successful, although he subsequently sustained a number of stings from greenhead ants and wasps without adverse responses. Skin-prick testing with the whole-body extract of S. invicta (supplied by Stallergenes, Paris, France) showed a 10-mm weal to the 1: 1000 dilution, thus confirming the occupational physician's initial diagnosis. As a consequence, he began desensitisation with S. invicta whole-body extract in accordance with accepted treatment guidelines.13 He has now reached the "maintenance phase" of the schedule (ie, 0.5 mL of the 1: 10 dilution). Subsequent to desensitisation, he reported one RIFA sting, which caused only the expected localised pustule. DiscussionAdrenalin is the first-aid treatment of choice for a systemic allergic response with dyspnoea and/or hypotension.14 It achieves the quickest reversal of the adverse events and is very safe in a life-threatening situation. Anyone who has had stinging-insect-induced anaphylaxis should carry an EpiPen (or EpiPen Jr for children; CSL) for immediate first-aid use if hypotension or dyspnoea occurs. Specific desensitisation to prevent future anaphylaxis to RIFA stings in susceptible patients is effective,13 and anyone suspected of RIFA sting anaphylaxis should be referred to an allergist for assessment. Taxonomically, S. invicta is in a different subfamily (Myrmicinae) from that of Australian native ants responsible for anaphylactic events. Furthermore, RIFA venom is unlike that of any other Australian Hymenoptera species. As a consequence, there is a strong possibility that allergic cross-reactivity between species does not occur, as is the case in the United States. Indeed, our patient's experience would support this belief. Therefore, RIFA toxin represents a new risk to a portion of the Australian population not yet aware of this. The biology and epidemiology of S. invicta is summarised in Box 2. In the United States, over 40 million people live in areas infested by S. invicta. Annually, 14 million people are stung, a quarter of whom are expected to develop some sensitivity to RIFA toxin.10 An examination of habitat preferences and estimates of the rate of uncontrolled spread suggest that, unless eradicated, S. invicta will occupy much of arable Australia within 30 years, and therefore exist in close proximity to a large portion of the Australian population. Only areas with extremes of aridity and cold would remain free of these ants. It is reasonable to expect that proportionally similar numbers of people will come into contact with fire ants in Australia and experience similar reactions to their stings. A survey of 1286 practitioners in South Carolina (USA) (population, four million), where fire ants are well established,7 estimated that annually over 33 000 people (94 per 10 000 population) seek medical consultation for RIFA stings, and, of these, 660 people (1.9 per 10 000 population) are treated for anaphylaxis. Direct extrapolation of these data to the Australian situation would suggest that about 140 000 consultations and 3000 anaphylactic reactions are to be expected each year by 2030 if RIFA eradication is not successful. 1: Map of Brisbane, showing areas infested and putatively infested with the Red Imported Fire Ant (Solenopsis invicta) shaded yellow, main roads (grey) and council boundaries (dashed) 2: Biology and epidemiology of Red Imported Fire Ants Red Imported Fire Ants are inconspicuous, reddish-brown ants with no distinguishing features visible to the naked eye. Superficially, they resemble many common native and exotic ant species present in the Brisbane region (Figure 1). They range in size from 2 mm to 6 mm, with many intermediate-sized individuals. Optimum habitats include grassed areas, gardens, sites near flowing and still water and recently disturbed soil. Fire ant nests (Figure 2) are largely subterranean and are conspicuous by an above-ground, dome-shaped mound which can be as high as 45 cm above normal ground level (usually 20–30 cm). Normally, the above-ground part of the nest resembles a mound of excavated soil, 30–60 cm in diameter, but sometimes these are absent. The nests of many native ants have obvious openings through which ants enter and exit. Two forms of Red Imported Fire Ants have been discovered in Brisbane: the monogynous (single-queen) and polygynous (multiple-queen) types. Monogyne colonies maintain territory independently from neighbouring colonies. As a result, the distance between colonies is normally greater than 10 metres, as this avoids unnecessary conflict between neighbouring colonies over territory. However, worker ants from polygyne colonies can not determine whether other fire ant workers or queens they encounter are related to them and, as a result, coalesce to form large, dense supercolonies. These polygyne infestations, which are dominant in Brisbane, present a greater hazard due to the much larger numbers of ants a site can support (thousands of polygyne colonies per hectare instead of hundreds of monogyne colonies per hectare). Both forms defend their territory aggressively and make extensive use of pheromones or chemical signals to recruit other workers, synchronise attacks and initiate stinging. For this reason, multiple stings are the rule rather than the exception (Figure 3 a–d). Their diet is unspecialised and they feed on any available sources of carbohydrates, lipids and protein. Currently, over 37 000 hectares of Brisbane's eastern and south-western suburbs are putatively infested with S. invicta (Figure 1). However, an eradication program has been initiated by the Queensland Department of Primary Industries at a cost exceeding $123 million over the next five years. This program is jointly funded by the Commonwealth Government and all Australian States and Territories. The potential for anaphylactic events in Australia due to S. invicta will be higher than for other native ants due to three key factors: The venom of S. invicta is unusual, being composed largely of alkaloids, but also including four different proteins.15,16 These proteins, as well as the non-protein components of the venom, are each individually capable of inducing anaphylaxis. The polygynous form of S. invicta often completely dominates areas where it has invaded, forming interconnected supercolonies.17 Coupled with grassy areas as its preferred habitat, the probability of contact with humans is high. Aggressive pheromone-driven group defence of territory and the colony results in a high probability of multiple stings. 1: (a) The Red Imported Fire Ant (Solenopsis invicta), and (b) Monomorium sp, a harmless native ant, demonstrating the similarity between the two species (with permission, Macquarie University, School of Biological Sciences). 2: A typical Red Imported Fire Ant mound (with permission, Queensland Department of Primary Industries). 3: Multiple stings (about 150) by S. invicta to the right arm of one of the authors (C V) as a result of accidental exposure in the field. (a) Five minutes after the event, showing raised welts at sting sites; (b) 18 hours after, showing typical pustules; (c) 48 hours after; and (d) seven days after the event.

Graham O Solley MB BS, FACP · Cas Vanderwoude ADipAppSc(For), BAppSc(Hons), PhD · Gregory K Knight MB BS, MPH, FAFOM

Clinical question"Is subcutaneous (SC) or intramuscular (IM) naloxone as effective as intravenous (IV) naloxone in the treatment of life-threatening heroin overdose?" An emergency department clinician was interested in comparing routes of administration of naloxone in light of anecdotal evidence suggesting that various routes may not be equally efficacious in restoring a patient to spontaneous breathing and consciousness. Search questionPatients presenting to an emergency department for the management of a heroin overdose were the focus of the search strategy. The search question was "How long does it take for patients to return to consciousness after administration of naloxone by various routes?". In order to answer this question, a randomised controlled trial comparing the effects of SC or IM versus IV naloxone would be the ideal study design. SearchThe search terms "heroin", "opioid overdose", "naloxone" and "route of administration" were combined to identify relevant English-language articles published between 1966 and June 2000. Databases and websites searched included the Cochrane Library, Best Evidence, PubMed, CINAHL (Cumulative Index to Nursing and Allied Health Literature), Smart Search and Bandolier. Studies other than those set in the emergency department (ie, those conducted in hospital wards or post-anaesthetic care units) were excluded, as the clinician had specified that we limit the search to pre-hospital or emergency department settings. The search yielded only one study that compared SC with IV naloxone for treating opioid overdose in this setting. No studies were found comparing the use of IM with IV naloxone. Summary of findingsIn a comparative study using historical controls, Wagner et al1 compared naloxone administered intravenously or subcutaneously to patients in the community with suspected opioid overdose. The two intervention arms were 0.4 mg IV naloxone and 0.8 mg SC naloxone. The study was conducted sequentially in two phases: the IV phase, from 1 June to 30 June 1996, and the SC phase, from 1 July to 1 September 1996. Ambulance attendants in a regional district of British Columbia, Canada, administered naloxone to people meeting the British Columbia Ambulance Services' criteria for suspected overdose (ie, reduced consciousness, history suggestive of opioid use, and respiratory rate of less than 10 breaths per minute). The protocol also included a second dose of SC or IV naloxone if the first dose was not observed to be physiologically effective. The primary outcomes of interest included the time interval from arrival at the patient's side until the respiratory rate rose above 10 breaths per minute, the time interval from arrival at patient's side to naloxone administration, and the duration of bag–valve–mask ventilation. Overall, there was no significant difference between the two modes of naloxone administration with regard to the time interval between arrival at the patient's side and attainment of a respiratory rate greater than 10 breaths per minute (9.3 ± 4.2 minutes [IV] v 9.6 ± 4.6 min [SC]; P = 0.67). There was also no significant difference in duration of respiratory bag–valve–mask ventilation between administration arms (8.1 ± 6.0 minutes [IV] v 9.1 ± 4.8 minutes [SC]; P = 0.20; 95% CI of difference, –2.53 to 0.53). OutcomeWe submitted the report to the emergency physician, stating that the single study in a community setting demonstrated that IV and SC naloxone administration appeared to be equally effective in returning patients suffering from opioid overdose to spontaneous breathing. However, we advised the physician that the study was subject to a number of biases, including the utilisation of historical controls, a lack of clear randomisation, and the recruitment of fewer patients (74) than the 92 required to achieve 90% power. The physician used the information from our report to change the emergency department's policy — the use of IV naloxone was eliminated to reduce the risk of needle-stick injury to staff.

Jason Wasiak MPH · Ornella Clavisi BSc(Hons) MPH