Emergency medicine

Case reports Case 1: A 22-year-old man complained that he was "burning up" and collapsed after ingesting drugs at a friend's house. He died soon afterwards at a local hospital, despite attempts at resuscitation. His core temperature was 42oC. At autopsy there was evidence of coagulopathy, with scattered bruises, intra-alveolar haemorrhage, and haemorrhagic pleural effusions, ascites and stomach contents. Toxicological blood analysis revealed a lethal level of PMA (1.3 mg/L), together with 0.02 mg/L of MDMA and 0.21 mg/L of methylamphetamine. No alcohol was detected in the blood. Case 2: An 18-year-old man died at his home after ingesting a number of "ecstasy" tablets over five hours, both at a dance club and at home. Two hours after death the core temperature of the body was 39oC. Autopsy revealed focal pericardial haemorrhage, pulmonary congestion and renal tubular necrosis. Toxicological blood analysis showed a lethal level of PMA (1.7 mg/L), with 0.1 mg/L of MDMA and 0.06 mg/L of methylamphetamine. No alcohol was detected in the blood. Case 3: A 19-year-old man died in hospital 40 hours after being brought to the emergency department in respiratory arrest with a body core temperature of 41.6°C. He had taken "two or three capsules" of street drugs of an uncertain nature, both at a "rave" party and then at a friend's home the following day. According to witnesses, he had been advised to take PMA for an enhanced effect after taking MDMA. Laboratory investigations revealed evidence of rhabdomyolysis, with a serum myoglobin level of 328 960 g/L (normal level, < 150 g/L), disseminated intravascular coagulation and marked hyperkalaemia (7.7 mmol/L; normal range, 3.5–5.0 mmol/L). At autopsy there was evidence of coagulopathy, with epicardial petechiae, pulmonary haemorrhage, haemorrhagic gastric and intestinal contents, and haemorrhagic serous cavity effusions. There was also oedema and necrosis of skeletal muscle and renal tubular necrosis. Toxicological blood analysis revealed a lethal level of PMA (0.98 mg/L), with 0.32 mg/L of MDMA. No alcohol was detected in the blood. Analysis of capsules found with the patient revealed PMA with no other amphetamine derivatives. Death from amphetamine use is a well recognised occurrence, with most reported fatalities involving the use of 3,4-methylenedioxymethamphetamine (MDMA, or "ecstasy"). In 1998, a series of six cases of death due to an unusual amphetamine drug, paramethoxyamphetamine (PMA), was reported in South Australia.1 The only other comparable report of deaths due to PMA was that of nine deaths in Ontario, Canada, in the early 1970s.2 In 1998, our group warned that, although PMA substitution for MDMA appeared at the time to be a local Australian problem, there was a possibility that the manufacture and sale of PMA could occur in other countries. Unfortunately, this prediction has been proved accurate, with recent reports of PMA-related deaths in the United States, Europe and Canada.3-5 Initially, it was assumed that PMA was created as a contaminant during the synthesis of MDMA and was being disguised and substituted for MDMA by local dealers attempting to offload the drug.1,6,7 However, this is now considered unlikely, as the chemical precursors of PMA and MDMA are different,3,4 and information received concerning Case 3 (described here) suggests that capsules containing only PMA are being marketed specifically to augment the effects of MDMA. This is an extremely dangerous development, as it is well recognised that PMA has a much greater propensity to produce adverse effects than other ring-derivative amphetamines.6 Death in each of the cases described here was due to PMA toxicity with hyperthermia. PMA levels of higher than 0.3 mg/L and MDMA levels higher than 0.6 mg/L have been found in cases where deaths were attributed to these drugs.1

Roger W Byard MD · Nicholas G Rodgers MB BS · Ross A James FRCPA · Chris Kostakis BSc(Hons) · Andrew M Camilleri BSc(Hons)

To the Editor: Lamberth stated in his case report that Antarctic tourist ships should be equipped to provide life support, as well as better screening and education of Antarctic tourists.1 I recently travelled to both the Arctic and Antarctic as a medical officer on small ships, caring for seven passengers injured in a helicopter crash in the remote Russian Arctic and a 12-year-old with diabetic ketoacidosis in the Drake Passage, as well as numerous people with minor ailments. To compare these ships with large tropical cruise liners is unrealistic. Ships' medical supplies are selected with an appreciation of the casemix. A study of 16 Antarctic trips in 1997 and 1998 found that most problems were respiratory tract complaints, acute soft tissue injuries and complaints, sea sickness and dermatological problems.2 Few major incidents have been reported, and equipment for advanced life support is tailored to this. Paralysing agents and ventilators are not supplied. A single doctor with no nursing staff cannot safely care for a ventilated patient for 72 hours, as suggested by Lamberth, and the additional staff needed for this would be a huge additional expense for a very rare occurrence. While some ingenuity and adaptability may be required, the equipment supplied is adequate for the vast majority of events. Safety and preventive medicine are very much part of the ship's doctor's role. Most doctors give a brief lecture as part of the initial briefing of passengers. Seasickness, appropriate medication and safety on the ship are usually part of this. The passengers are predominantly elderly and, in my experience, many are fulfilling a long-held ambition to travel to the polar regions. Reputable companies require a fitness-to-travel assessment from passengers' general practitioners before the trip is confirmed. This assessment is tailored to potential problems in remote regions. I believe that excluding people from the wonders of polar travel on the basis of age or previous coronary artery disease would be a terrible shame, while accepting that there will always be a risk in travelling to remote locations. Having shared in the 90th birthday celebration of a woman with chronic obstructive pulmonary disease in the Arctic, I hope that I will still be able to enjoy such experiences at that age.

Eve R Merfield FACEM

To the Editor: Lamberth raised some worthwhile issues about small-ship adventure tourism to Antarctica in his recent case report describing the death of an 82-year-old tourist.1 This occurred in 1999, the season I started as medical director for the leading polar adventure tour company that chartered the vessel involved. I have some comments and an update. The former Soviet oceanographic research vessel was converted in the 1990s to carry 78 passengers. She had a two-bed infirmary and a procedure room with Russian and German medical supplies for passengers and crew, and carried a German- and English-speaking Russian doctor experienced with passenger ship medicine. The tour operator provided additional medical supplies and an emergency physician. Ventilatory support could have been provided, although not to the standard of a contemporary Australian intensive care unit. Polar adventure operations are very different from "tropical" cruise lines, which generally operate their own ships from home ports and cater for up to 3000 passengers with very different expectations.2 Operators require that prospective passengers submit a medical information form and a declaration from their personal physician that they are fit for the journey. The 82-year-old who died was a retired physician who did not declare the extent of his limitations, and who acted as his own medical advisor. His is the only death I am aware of after seven years' involvement in the industry. The medical declaration form has been modified and now addresses the risk factors identified by Lamberth. Prospective clients with questionable health are referred to the medical director. However, operators cannot verify declarations of good health, and physicians have been known to collude with passengers to avoid risk of rejection. Furthermore, "ageism" is as unacceptable as sexism and racism. I was present on the first passenger-circumnavigation of Antarctica in the company of several octogenarians and a 90-year-old, and on the first circumnavigation of the Arctic Ocean, with other octogenarians and a 92-year-old. Short trips to the Antarctic Peninsula are very different from scientific expeditions; Lamberth's suggestion that advising doctors should consider scientific expedition criteria is inappropriate. The International Association of Antarctic Tour Operators (<www.iaato.org>) is a voluntary association of competing adventure eco-tour operators whose purpose is to self-regulate the industry and to develop good standards. Standards for provision of medical supplies and capabilities are under development by this association.

Chris H Curry

In reply: I welcome Curry and Merfield's interest and comments. The patient described in my case report1 was not, as Curry states, "a retired physician". Nor did he provide his own health assessment, but had his assessment form filled out by another physician. Unfortunately, this form, along with those of 60 other passengers, was not made available to any doctor before embarkation. Curry confirms that many older passengers are travelling to Antarctica.2 Merfield's experiences attest to the potential for serious (including multiple casualty) incidents in this remote location. I agree that ageism per se is unacceptable. Rather, the issue is the provision of adequate facilities to deal with potential problems or, alternatively, warning as to the hazards. Advertising for Antarctic cruises emphasises the medical facilities provided. The public may not realise that a doctor with minimal equipment cannot deliver the same care available in a First World hospital. Curry's assertion that ventilation could have been provided illustrates this. Ventilation is more than placement of an endotracheal tube. It is ludicrous to suggest that, without oxygen, paralysing drugs, positive end-expiratory pressure or means to suction the copious thick secretions, hand-bagging for 36 hours while crossing the heavy seas of the Drake Passage might have altered the tragic outcome for this patient. I recommend a book by Levinson, a seasoned polar physician, and Ger on health aspects of polar tourism.3 They have collated the findings of a conference held on this topic at Cambridge in the United Kingdom in 1995. The book addresses what Levinson describes as "the often inadequate medical care which exists in these regions". He notes "major concerns . . . expressed by travel experts, the American Medical Association, the American College of Emergency Physicians, and other professional organisations."3 The survey by Curry and Johnston found that illnesses among their company's Antarctic tourists in 1997 and 1998 included cardiac arrest, acute myocardial infarction, severe pneumonia, diabetic ketoacidosis due to seasickness, haematemesis, anaphylaxis, ruptured ectopic pregnancy and acute appendicitis. The fact that polar trips are short does not seem to protect against potentially lethal diseases. Given the stress of this travel and the nature of the population involved, maybe the contrary applies.

Paul G Lamberth FACEM

To the Editor: In their case report entitled "Dangerous bodies", Nocera and colleagues described a case of poisoning with aluminium phosphide tablets,1 which generate the fumigant gas phosphine when exposed to moisture.2 The foul odour emanating from the patient alarmed hospital staff, leading to evacuation of the emergency department. After the patient died, they sealed his body in an impervious suit and bin. It was buried, without autopsy, using earth-moving equipment — it being considered too dangerous to do this by hand. The burial was filmed for television. The article sought to highlight risks to hospital staff from poisoned patients and indicated that phosphine gas emanating from this patient could be toxic before it was able to be smelt. Despite stated fears of extreme toxicity, no air samples were collected for analysis, and the sole symptom among staff was nausea (not unexpected given the smell). In parts of India, where wheat is commonly stored in the home before being ground into flour, aluminium phosphide tablets are widely available for household use to stem insect attack on the grain.3,4 Ingestion of these tablets is a common way to attempt suicide, with perhaps as many as 15 000 cases per year, two-thirds of which are fatal. The hospital in the city of Chandigarh, in northern India, treats about 50 cases per year. The breath of patients who have ingested aluminium phosphide has a characteristic garlic-like odour. Diagnosis is based on history and a positive result (blackening) on tests of the patient's breath with paper moistened with fresh silver nitrate solution. Hospital staff take no special precautions during resuscitation, and surviving patients are managed with routine supportive care. Autopsies are routine. No threat is perceived by hospital staff. Metal phosphides have been safely used by trained people in Australia for decades. They are Schedule 7 poisons and so require an expensive permit for purchase. Consequently, their use for suicide is rare. Nocera and colleagues understandably reacted with caution to an unusual situation. However, we consider that, in documenting their experience, they overstated the risk. Because of the legal and ethical issues involved in patient care in a situation of alleged risk, we consider that risk estimates should, when possible, be based on available evidence rather than theoretical possibilities. In general, apart from a few highly toxic, mainly anticholinesterase compounds that can be absorbed through the skin (eg, sarin and tabun), there are no known poisons that will seriously endanger hospital staff routinely caring for patients in an emergency department. Competing interests: The authors have no association with companies that manufacture or market aluminium phosphide, and had no financial support for preparation of this letter. In reply: In our article, we clearly stated that the emergency department was evacuated on the instructions of officers from the New South Wales Fire Brigades.1 The officers then placed the patient's body within a fire brigade hazardous materials encapsulated suit and, when that began to distend with phosphine gas emissions from the body, into a hazardous materials recovery bin. In contrast, Christophers and colleagues state that staff at the hospital in Chandigarh, India, take no special precautions in antemortem or postmortem care of patients who have taken aluminium phosphide tablets. I am disappointed that they provide no data on air sampling for phosphine gas during this care to justify this practice. Our case highlights the problems confronting emergency department staff with a critically ill patient and an unknown chemical hazard. In this case, the chemical hazard was not correctly identified for over 30 minutes. The risk cannot be estimated, as suggested by Christophers and colleagues, until the chemical agent and its vapour concentration are correctly identified. Retrospective determinations cannot be used to guide the immediate emergency department response, or to determine what personal protective equipment is needed by staff during the initial confusion of a hazardous materials incident. In addition to organophosphates, over 30 chemical agents have the potential to be used as chemical weapons. Furthermore, the toxicity profiles of many industrial chemicals are unknown or incomplete. We do not believe that any hospital or emergency department staff should be exposed to avoidable danger during antemortem or postmortem care of patients, or that healthcare institutions should be exempt from their statutory obligations under occupational health and safety legislation.

Allen J Christophers · Surjit Singh · David G Goddard · Antony Nocera FACEM, MSc (Emergency Planning and Disaster Management)

Riding waves on a bodyboard, or boogie board (bodyboarding), is a popular seaside pastime. Abdominal injuries have not previously been reported from this activity. We report the cases of three adolescents who sustained major blunt abdominal injuries while bodyboarding. The three patients were seen between February 1998 and March 1999 at hospitals serving large beachside communities in Queensland. The circumstances of the accidents suggest that the method in which a bodyboard is usually ridden places a rider at risk of abdominal injury. Clinical recordsPatient 1A 14-year-old boy was "dumped" by a wave onto a sandbank, causing his board to be driven against his upper abdomen. Over the next few hours he experienced worsening left-side abdominal pain. On presentation, six hours after the injury, he was pale and in pain. His pulse was 120/minute and blood pressure was 110/60 mmHg. He had marked tenderness in the left upper abdominal quadrant with guarding. A computed tomography (CT) scan of the abdomen revealed a full-thickness laceration of the spleen, extending into the hilum (Box 1). The patient was managed by active observation, and did not require surgery or blood transfusion. Subsequent scans revealed healing of his injury by three months. Patient 2A 12-year-old boy presented with abdominal pain 16 hours after being hit from behind by a large wave while attempting to ride it to shore. The nose of his board was caught on the sandy sea floor, driving one of the base corners of the board into his upper abdomen. On examination, he was pale with a pulse of 130/minute and blood pressure of 100/60 mmHg. His abdomen was tender in the right upper quadrant with guarding. A CT scan of the abdomen revealed a large laceration to the right lobe of his liver, with a significant amount of free intraperitoneal fluid (Box 2). The patient was observed closely in hospital for one week without adverse sequelae. Subsequent ultrasound scans showed resolution of his injury by four months. Patient 3A 15-year-old girl was thrown off balance by a wave while riding her bodyboard. She immediately experienced abdominal pain, which became increasingly severe. She recalled the board making contact with her abdomen during the fall. On presentation, within two hours of the fall, she had severe abdominal pain, right shoulder tip pain and light-headedness when standing. On examination, her pulse was 130/minute and blood pressure was 90/50 mmHg. She had signs of generalised peritonitis and there were no bowel sounds. An ultrasound scan of the abdomen revealed a large amount of free fluid in the peritoneal cavity. No definite injury to the liver, spleen or kidneys was detected. As gastrointestinal tract perforation could not be excluded, a laparotomy was performed. This revealed 500 mL of fresh blood in the peritoneal cavity as a result of a superficial liver laceration. Haemostasis was achieved initially by packing, and then by the application of topical thrombostatic agents. No other significant injuries were noted. The patient made a very good recovery and was discharged home four days after admission. DiscussionThere are very few reports of injuries associated with bodyboarding. A literature review revealed only one report of injuries (facial) sustained during this activity.1 There are anecdotal accounts of injuries as a result of bodyboarding misadventures, including severe spinal injuries, on bodyboarding-related forums on the Internet.2 Bodyboards can also pose a hazard to other swimmers in the surf.3 A bodyboard rider lies with the upper part of the body on the board, parallel to the sea floor, placing the base of the board against the ventral trunk. Should the rider be thrown off balance and the nose of the board strike or be caught on the sea floor or sandbank, the base of the board can be driven with considerable force into the upper abdomen (Box 3). Although most boards have a concave curvature of the base, the two corners can potentially inflict significant blunt injuries, as evidenced by Patient 2. As they lie parallel to the sea floor, riders are also less able to protect themselves when thrown onto the sea floor or a sandbank. Injuries from conventional surfboarding are well documented.4-6 Lacerations make up a high proportion of surfboard-related injuries,5 reflecting surfboard design and configuration (sharp nose, fins). Blunt trauma would be expected to predominate in bodyboarding, as bodyboards have less sharp edges and have a relatively softer consistency. Bodyboarding is also more popular, especially among children and teenagers. Although many bodyboarders are very skilled (a professional circuit exists), bodyboarding is an activity in which most beachgoers can partake. The boards are readily available, and less skill and swimming ability is required to catch a wave than in conventional surfing. As there have been no previous reports of abdominal injuries associated with bodyboarding, we are unable to determine how commonly they occur. Our experience may be unique, but, given the popularity of the pastime with young people, we suspect that this association may be under-reported. Bodyboarders, as well as their medical attendants, need to be made aware of the potential for abdominal injuries during what most would consider a benign beachside activity. Altering the design of boards, such as rounding off the base corners or increasing the pliability of the core material, might help prevent such injuries occurring. However, this suggestion may not be welcomed by bodyboarders themselves, as it might be impossible to make such alterations without adversely affecting the performance of the boards. 1: Computed tomography scan of the abdomen of Patient 1, a 14-year-old boy A full-thickness laceration of the spleen, extending into the hilum, is visible. 2: Computed tomography scan of the abdomen of Patient 2, a 12-year-old boy A large laceration of the liver is visible, with a significant amount of free intraperitoneal fluid. 3: Proposed mechanism for abdominal injury while bodyboarding

Kelvin L Choo MB BS, FRACS · Deborah M Bailey MB BS, FRACS · John B Hansen MB BS, FRACS

Objectives: To study the incidence of and factors associated with single-vehicle rollover (SVRO) accidents in the "Top End" of the Northern Territory (NT); to identify factors associated with major injury and death from SVRO accidents.Design: Retrospective analysis of records from the NT Department of Transport and Works' police database, Royal Darwin Hospital's trauma database, coroner's records, and case notes from public hospitals in the Top End.Study population: All patients involved in SVRO accidents in the Top End between 1 January 1996 and 31 December 1997 whose accident was documented by the police, who attended a public hospital, or who died.Main outcome measures: Types and incidence of all accidents; details of the accident scene, vehicle features, and population groups associated with SVRO accidents; factors associated with major injury and death.Results: SVROs accounted for 30% of all accidents and 29% of all injuries and deaths (441 people) in the whole of the NT over the study period. Some of the factors associated significantly more frequently with SVRO accidents were (i) occurrence of the accident on a straight, dry, unsealed road; (ii) presence of a vehicle defect; (iii) travelling at excessive speed; and (iv) the person being male, aged 41–50 years, of Aboriginal descent. Among the 147 people who were admitted to hospital or died from SVRO accidents in the Top End, major injury occurred significantly more frequently if the person was under the influence of alcohol, was not wearing a seatbelt and was ejected; if the accident occurred in a rural area; and if the vehicle was speeding. Major injuries occurred in 21% (31/147), and death was more likely in those with head, chest and neck injuries.Conclusion: SVRO accidents are a major cause of morbidity and mortality in the Top End of the NT. Effective methods of limiting speeding, drink-driving and driver fatigue should be sought. Populations most at risk should be targeted.

P John Treacy MD, FRACS · Kerrie Jones BMBS, FACEM · Carole Mansfield RN

Neuromuscular paralysis and death up to four days after removal of ticks is well documented and apparently unique to Australian tick envenomation.1-5 Generally, obvious symptoms and signs are present at the time of tick removal. In contrast, onset of local neurotoxicity many hours after tick removal has not, to my knowledge, been reported previously in the medical literature. Clinical recordA 48-year-old man with tick infestation was referred to our hospital emergency department by his general practitioner. The patient complained of lumps on his scalp (present over the previous few weeks), lethargy, myalgia, unsteadiness on his feet and numb lips. He stated that he spent a lot of time walking in bushland around his home. His friend's dog had recently died from tick paralysis. Multiple engorged ticks were evident on the man's face, scalp, neck, back and limbs. An engorged tick was removed from his left cheek, but there were no intra-aural or peri-aural ticks. He had multiple associated urticarial lesions and generalised lymphadenopathy. His pulse was 114 beats/minute, blood pressure 148/100 mmHg and he had a temperature of 37.5°C. Neurological examination revealed no cranial-nerve deficits. In particular, there were no motor or sensory deficits of the face. The numbness of the lips, which the patient had earlier described, had now resolved. His gait, muscle power, tone and reflexes were normal. Light touch and pinprick sensations in his limbs were also normal. Forty-four ticks (41 females [32 engorged] and 3 males) were removed with forceps (see Box), carefully avoiding pressure on the ticks' abdomen, which is thought to trigger expression of venom.1,3,5 The species was later formally identified as Ixodes holocyclus (Mr Bruce Dixon, Senior Microscopist, Olympus Imaging Unit, Parasite Identification and Diagnostics Program, Adelaide University, personal communication). In view of the magnitude of the infestation, the patient was asked to return the following morning for reassessment. A review 20 hours after tick removal revealed left facial-nerve palsy. In addition to the lower motor neurone motor deficit, the patient complained of altered sensation over his left cheek and upper lip, and subjective loss of light touch and pinprick sensation from the left cheek to the upper lip were demonstrated. As tick venom has not been shown to affect sensory-nerve conduction, the most likely explanation is that this apparent dysaesthesia is akin to that seen with idiopathic Bell's palsy, in which patients commonly complain of altered sensation in what is purely a disorder of the motor neurone. The phenomenon appears to relate to altered proprioception. No other neurological abnormality could be detected and there were no residual ticks found after a thorough search. The facial paralysis took seven days to completely resolve. After two weeks the patient felt well and had resumed his previous activities. He was advised to ask a friend or relative to check him thoroughly for ticks after spending any time in the bush. DiscussionOf the 19 identified species of Australian tick in the Ixodes genus,6 only three have been shown to secrete paralytic toxins.7 With the exception of one case of I. cornuatus envenomation,8 all human cases of paralysis in which the tick was identified were due to I. holocyclus. The structure of the protein neurotoxin, also known as holocyclotoxin, has not been elucidated. It is secreted from the massive salivary glands of engorged female ticks late in the feeding cycle. Like botulinum toxin, holocyclotoxin is thought to act presynaptically at the neuromuscular junction to inhibit acetylcholine release.9 In Australia there have been 20 reported deaths from tick envenomation, all before 1945. Ticks have caused more deaths than any other Australian arachnid, including the funnelweb spider (Atrax robustus) (13 attributable deaths) and the redback spider (Latrodectus hasselti) (14 deaths).10 Tick paralysis has been frequently misdiagnosed, and this envenomation syndrome must be included in the differential diagnoses of any patient presenting with an ascending symmetrical paralysis. Generalised paralysis most commonly affects children under three years, but there are three documented fatalities in Australian adults due to tick envenomation.10 Late discovery of ticks hidden on the scalp or in bodily creases and orifices is a recurring, and often lethal, theme.1,11 The diagnosis may not be immediately apparent, and any child with ataxia or progressive weakness should be carefully examined for ticks. Cases of isolated local paralysis, usually facial, are less commonly reported.1,4,12-14 Usually, the palsy is present at the time of tick discovery, and, in the case of facial-nerve palsy, the tick is found most often behind the ear or within the external auditory meatus. Cases of isolated facial palsy have lasted three days to three weeks.4,12,13 I am aware of one other case of delayed-onset facial-nerve paralysis in a child secondary to tick envenomation. This resolved spontaneously within a few days (Dr Bill Whyndham, Registrar, Emergency Department, Gosford Hospital, personal communication). A case of median-nerve palsy caused by local (axillary) I. holocyclus envenomation has also been described (Dr Bill Whyndham, personal communication, from a presentation to the Australasian College for Emergency Medicine Winter Symposium, Lorne, VIC, July 1999). Local paralysis is a well documented, albeit unusual, complication of tick envenomation. The case described here emphasises the potential for late onset of paralysis, even many hours to days after removal of the tick(s), and the need to closely follow up any patients with symptoms suggesting tick envenomation. Admission for several days' observation of children with any signs of neurotoxicity should be considered. Ticks removed from the patient.

Mark K Miller BMed, FACEM

To the Editor: The report by Mangion et al1 draws attention to a serious risk in the environment. The general public has been increasingly protected against the risk of harm from domestic products by a combination of legal liability actions and government regulation. Thus, the continuing availability to the general public of hydrofluoric acid (HF) in concentrations that are hazardous is something of an anachronism. While we applaud Mangion and colleagues for raising the issue of HF burns, we feel that their article is deficient in failing to mention a number of important points. Topical calcium gluconate has been shown to be more effective in treating HF burns if the preparation contains dimethyl sulfoxide (DMSO).2 There is a great risk of blindness with ocular exposure to HF. Slow local injection with 10% calcium gluconate using fine needles, titrating its effect against the patient's pain, is a well described technique. This is another treatment option that could have been tried. Nail removal, described by Mangion et al as an "extreme measure", is, unfortunately, often required. It is less likely to be required with the application of DMSO/calcium gluconate solution and retrograde ischaemic intravenous injection of calcium. Local excision of contaminated tissue may be required after exposure to concentrated solutions. Management should be a team effort from the first moment, involving an intensivist/toxicologist and surgeon, as burns surgeons are trained in the care of HF exposure, and surgery is often needed. The availability, packaging, and labelling of preparations containing HF have recently been changed. Since 1 December 2001 it has no longer been possible for the general public to purchase any HF preparation stronger than 1%. All preparations now carry prominent labelling drawing attention to the risk of blindness if even dilute solutions of HF get into the eyes. Containers are now less easy to open by children. These changes have been introduced by the National Drugs and Poisoning Committee of the Therapeutic Goods Administration as a result of an independent review and lobbying by the Australian and New Zealand Burn Association (ANZBA). The ANZBA guidelines for referral to a specialised burns unit include chemical burns. The peculiar challenge posed by HF burns emphasises the need for the guidelines to be more widely disseminated. Currently, the New South Wales Department of Health has adopted the guidelines, so this policy is official throughout New South Wales.

Hugh C O Martin · Michael J Muller

Emergency Medicine (EM) was recognised as a principal specialty in Australia in 1993, and the development of EM has had a profound effect on the way healthcare is delivered in Australia. Most major Australian hospitals now have 6–12 full-time emergency physicians. The Australian Medical Workforce Advisory Committee has estimated that more than twice the current number of EM physicians will be needed by 2007.1 Within five years from now, major emergency departments (EDs) will have 16-hour, 7-day cover (some will have 24-hour cover). Subspecialisation will occur in toxicology, retrieval, disaster medicine, paediatric emergency medicine and hyperbaric medicine, and academic EM will grow rapidly. Prevention. The many presentations in EM provide fertile ground for surveillance in injury prevention and other areas. Data collected and computerised at the time of attendance provide great opportunities for monitoring of disasters and epidemics and for disease identification and surveillance. Some EDs are undertaking disease prevention programs, giving telephone advice and conducting quality assurance programs related to ambulatory care that should have a major impact on disease presentation and prevention. Training. Improvements in training and experience for emergency physicians and the reduced reliance on junior medical staff in EDs have significantly improved early diagnosis and reduced initial adverse events and times to critical therapies. Most routine ED laboratory tests and some imaging (eg, using ultrasound and portable computed tomography) will soon be performed at the bedside, although there are issues surrounding cost and reliability. Interventions. Little has changed in cardiopulmonary resuscitation over the past 30 years. High-dose adrenaline has been found to have no advantage over the standard dose, and there is some doubt about whether adrenaline is useful at all. Time to defibrillation remains the key to advanced life support for cardiac arrest. Easy-to-use automatic external defibrillators, which will eventually be accessible to the wider community, will improve survival after out-of-hospital cardiac arrests. EM physicians have developed great expertise in managing poisoning and envenomation, and five toxicology admitting services have been established nationally. This has reduced the frequency of the need for decontamination and antidote administration and reduced admission rates and length of stay, without increasing morbidity or mortality. Doctors managing an acute poisoning anywhere in Australia can rapidly get expert advice by calling Poisons Information Centres (on 131126), at which medical consultant support is largely provided by emergency physician toxicologists. Modifications to hospital and ED systems in recent years have enabled earlier intervention.2 For acute coronary syndromes, the early administration in the ED of aspirin, β-blockers, thrombolytic agents and platelet glycoprotein IIb/IIIa antagonists is improving outcomes. Glyceryl trinitrate and angiotensin-converting enzyme inhibitors improve outcomes in pulmonary oedema. The use of low molecular weight heparins has enabled most patients with venous thromboembolism to be managed at home with daily injections and has reduced mortality in patients with unstable angina. Non-invasive ventilation for respiratory conditions such as asthma and chronic airways limitation can prevent endotracheal intubation, reduce length of stay and reduce mortality. The most significant advance in EM has been formalisation and application of triage. The Australasian Triage Scale (ATS) is now used in all Australasian EDs, usually as part of a real-time patient tracking and reporting system. It has become the cornerstone of departmental clinical management, casemix measurement and interdepartmental workload comparisons, and has been applied in incentive bonus payment schemes in New South Wales and Victoria.3 The ATS is widely used as the basis of ED audit and quality improvement.4 It enables comparisons of very large patient populations, and has extraordinary research potential. System changes in EDs have led to integration of specialised teams for reception of emergency patients, and research and training in team dynamics in several areas, especially trauma. The development of clinical pathways (for asthma, chronic airways limitation and abdominal pain), chest pain units and nurse-based analgesia have reduced time to essential treatment, ED length of stay and unnecessary tests. Specialised observation medicine units run by EDs have had a significant impact on hospital lengths of stay for many illnesses.5 The ED is also a critical focus for developing out-of-hospital programs, integrating components of acute hospital care such as intravenous therapy, nursing support, specialist consultations and physiotherapy. Continuing improvements in EM are likely over the next five years.

George A Jelinek MD, FACEM · Lindsay M Murray MB BS, FACEM · Peter A Cameron MD, FACEM

Plastic surgery has seen many changes in the past five years. Advances in our knowledge of genetic coding, growth factors, and tissue engineering offer the potential for new treatment options in the near future. Prevention. Craniofacial surgery has undergone an explosion of new discoveries over the past five years, which has the potential to lead to dramatic improvements in diagnosis and treatment of craniofacial disorders. Recent studies have demonstrated that mutations in the genes that code for fibroblastic growth factor receptors (FGF-R) are at least partially responsible for both syndromic and non-syndromic craniosynostoses.1 To date, four FGF-R subtypes have been identified. These tyrosine kinase transmembrane proteins function as high-affinity receptors for fibroblast growth factors and have been implicated in the regulation of cellular proliferation, differentiation, chemotaxis and apoptosis. Clinical applications of these findings are currently limited to genetic testing for some of the common craniosynostosis syndromes, but the hope is that these conditions will one day be treated with a combination of minimally invasive procedures and gene therapy. In a similar way, the complex cascade that determines upper-limb development is being unravelled. A number of important protein signals have been discovered and their role in upper-limb growth may provide therapeutic options in prevention of upper-limb anomalies. Diagnosis. Malignant melanoma is one of the most common cancers in Australia, with the estimated risk of developing a melanoma before the age of 75 years in Australia being one in 26 for men and one in 36 for women. Management of melanoma saw dramatic changes through the 1990s, in particular with regard to safe excision margins. However, it remains an intense area of research. Studies are now in progress to look at the role of sentinel-node biopsy. This technique, first described in 1992,2 involves identification of the first draining lymph node from the primary melanoma site using a combination of radioactive tracer and patent blue dye. The technique has already been shown to be a good indicator of spread of melanoma to draining lymph nodes. This could provide prognostic information and direct adjuvant therapies, potentially treating early disease spread. It has the advantage of causing less morbidity than traditional block dissections. Currently, sentinel-node biopsy should be considered for any melanoma thicker than 1 mm, but only in the context of a controlled clinical trial. Intervention. Chronic and other difficult-to-manage wounds remain a huge treatment challenge and cost burden to the community. One of the greatest advances has been the development of low-pressure dressings.3 These dressings consist of a non-collapsible evacuation tube connected to a sub-atmospheric pressure system, which is embedded within medical-grade reticulated polyurethane ether foam dressing. This technique removes excess interstitial fluid, increases vascularity, decreases bacterial colonisation and aids the natural tendency of the wound to contract. Additionally, it is only changed every 72 hours, thus decreasing labour costs and patient discomfort. Another area of wound care that is being developed and used by plastic surgeons is the determination of the precise biochemical processes that control wound healing. Already, the roles of a number of growth factors and cytokines have been defined. It is envisaged that during the 21st century new treatments will be developed to change cell function in a favourable way with the addition of positive growth factors and the removal or inhibition of negative growth factors. Some clinical trials have already been conducted using platelet-derived growth factor.4 Biochemical modification of wounds will have implications not only for treating chronic wounds, but also in preventing or controlling scarring. Bioresorbable plating systems represent an enormous development, particularly in the area of craniofacial surgery. Previous systems consisted of plates and screws made of stainless steel or Vitallium. Although these materials provide rigid fixation, have excellent tissue compatibility, and are corrosion resistant, they are permanent unless surgically removed, and thus carry long term potential for infection, migration and limitation of growth. Polyglycolic acid and poly-l-lactic acid fixation systems maintain their strength long enough to allow healing, and are then broken down completely by the body, thus eliminating these long term complications. Tissue engineering is one of the most exciting advances, and may lead to a new era in medicine: the potential to create new tissues or induce their regeneration. The basic requirements for this process are cells, a scaffold for the cells to grow on, and cellular signals or growth factors, which differentiate and stimulate cell growth. For the new tissue to be incorporated into the body, a blood supply then needs to be established. Although plastic surgeons have been "engineering" tissues for decades, these new developments raise the possibility of manufacturing tissues and organs ex vivo. This technology is already used in the area of burns surgery to create skin replacements when donor sites are limited by the extent of the injury.

Richard J Bloom MB BS · Kirstie MacGill MB BS, FRACS

Crisis Death in Antarctica Antarctic tourism is flourishing, but Antarctic cruises are often more physically demanding than typical "tropical" cruises. An 82-year-old Antarctic tourist died of probable septic shock secondary to lower respiratory tract infection six days after sustaining a suspected vertebral fracture in a minor fall from an inflatable boat. This case highlights the need for Antarctic cruise ships to be equipped to provide life support and for better screening and education of prospective Antarctic tourists. Paul G Lamberth MJA 2001; 175: 583-584 Clinical record - Discussion - References - Authors' details - - More articles on Travel, aviation and underwater medicine Antarctic tourism has increased rapidly in recent years, possibly because the collapse of the Soviet Union has made available a fleet of icebreakers.1 The combination of cruise ship conditions and the hostile, remote environment portends health risks for travellers. Doctors on scientific expeditions to the Antarctic report dealing with a range of major medical problems, including acute abdomen requiring laparotomy,2 ruptured intracranial aneurysm,3 70% thermal burns,4 and intestinal haemorrhage requiring a multinational rescue operation.5 Although the health needs of workers in Antarctica have been documented, little is known of the requirements of unscreened tourists. I report the death of an Australian tourist on an Antarctic cruise. Clinical record An 82-year-old Australian man boarded a Russian ice-strengthened vessel in Ushuaia, at the southern tip of Argentina, for a two-week cruise to the Antarctic Peninsula. During traverse of the notoriously rough Drake Passage on Day 2, he took dimenhydrinate and hyoscine for motion sickness. On Day 3, he had a minor fall while disembarking from an inflatable boat, leaving him with back pain which he treated with paracetamol and dextropropoxyphene. His only complaint to the ship's doctor (myself) at the time was wheezing induced by the cold air. On Day 5, he missed breakfast and was found lying on the floor of his single cabin. He explained that he had been unable to get up after a fall 12 hours before. I examined him carefully, with the only positive findings being dry mucosae and exquisite localised midline vertebral tenderness elicited at T9. He had a past history of smoking-related chronic airflow limitation, treated with bronchodilators and corticosteroids, and osteoporosis. The working diagnosis was a crush fracture of a lower thoracic vertebra, for which I gave him further analgesia. The following afternoon, subtle disorientation was noted, progressing over four hours to stupor with hypotension, poor peripheral perfusion and tachypnoea. Examination revealed left basal crackles and right-sided wheeze. The right calf had become tender. Intravenous resuscitation with 10% hydroxy-ethyl starch increased his blood pressure to 125/65 mm Hg, and urine output to 40-50 mL/h. Ceftriaxone (1 g) and gentamicin (320 mg) were administered with dexamethasone (4 mg intravenously) in lieu of regular bronchodilator therapy. On Day 8, the stupor persisted. Lung auscultation revealed left basal crackles correlating with a region of dullness to percussion. There was profuse purulent sputum. The patient's insurer agreed to meet the expense of evacuation, but a plan to fly him from the nearby Russian base on King George Island to Punta Arenas in Chile was abandoned when the weather deteriorated. After discussion, the Russian captain's initial plan to leave the patient at the Russian base, which was apparently less well equipped than the ship's hospital, was dropped in favour of returning to Ushuaia at full speed. That evening, the patient developed bilateral ocular deviation to the right, poor peripheral perfusion and periodic respirations. Crystalloid was administered to treat poor perfusion and falling urine output. Lansoprazole, for stress-ulcer prophylaxis, and aspirin, for a probable left leg venous thrombosis, were also given. On Day 9, the patient remained febrile, with normal heart rate and blood pressure. Enteral fluids (2000 mL per day) with sucrose (80 g) and sodium chloride (4 g) were tolerated, with gastric aspirates under 20 mL and normal bowel sounds. That afternoon, his breathing became intermittent, he developed oliguria and bradycardia, and died at 1730 hours. The ship reached Ushuaia 16 hours later. No autopsy was performed, and the body was cremated in Argentina. Discussion The final diagnosis was septic shock secondary to lower respiratory tract infection. The patient may also have had a deep venous thrombosis with possible pulmonary embolism. Contributing factors were chronic airflow limitation, back pain due to a thoracic crush fracture complicating osteoporosis secondary to frequent corticosteroid use, immobilisation and dehydration. Cold air exacerbating bronchospasm probably also contributed, while impairment of balance and cognitive function by anticholinergic medications may have been a factor in the patient's falls. This case illustrates the fundamental principle of incident analysis — a number of seemingly minor factors can combine to produce a disaster that was not predicted from any one precipitant alone.6 The case also raises issues for Antarctic tourism: Medical stocking of ships: As the areas explored can be several days' journey from modern healthcare facilities, there is an argument that ships' hospitals should be able to provide life support for 72 hours. This is not the case on most Antarctic cruise ships, despite travel companies advertising medical supervision as a feature. In contrast, the major "tropical" cruise lines provide advanced medical facilities appropriate to the elderly and infirm nature of many of their clientele. Medical equipment on Antarctic cruises should include intravenous fluids for resuscitation and maintenance and, ideally, a portable ventilator and monitoring device, such as a pulse oximeter. Ships' doctors require a high level of critical care skills to undertake advanced life support at sea. Many ship's doctors now working in Antarctica are Australian emergency physicians. Furthermore, the risks of anticholinergic medications for motion sickness, especially in the elderly, need to be better appreciated. Disturbed balance, sedation and cognitive impairment are a deadly combination in an unfamiliar environment. NASA (the National Aeronautics and Space Administration) advises promethazine for microgravity motion sickness.7 It is believed that promethazine, unlike hyoscine, dimenhydrinate and other common anti-motion-sickness agents, relieves symptoms without impairing adaptation. Therefore, during prolonged exposure, promethazine can be ceased as travellers get their "sea legs". Screening and education of prospective passengers: Factors that increase risk during Antarctic travel include: Moderate to severe reactive airway disease, especially if precipitated by cold air. Caution should be advised for those with chronic airway disease with severe fixed obstruction (FEV1 < 1.0 L/s) or requiring frequent courses of corticosteroids. Decreased mobility or balance problems, because of the need to negotiate steep companionways in heavy seas.8 Conditions with potential complications that would be difficult to treat in a remote environment, such as coronary artery disease, pregnancy and insulin-dependent diabetes. Poorly controlled mental illness. Provision of information on motion sickness, cold environment risks, and hazards such as falls may help passengers look after their own health. Appropriate health and accident insurance should be mandatory. A nihilistic philosophy that requires tourists to accept their own risks does not take into account the impact of illness or injury on other passengers, who may seek legal remedy from the tour operator. Improved surveillance of passengers travelling alone: Passengers in single cabins appear to be at increased risk of adverse events. The failure to detect my patient's predicament until 12 hours had elapsed may have been a crucial factor in his death. A simple system of surveillance would be possible, with passengers on their own reporting to a nominated crew member twice daily. The increase in adventure tourism by the elderly is a significant health challenge. Tour companies should consider developing a standard to equip ships for life support. A well-prepared aeromedical evacuation plan would mitigate this responsibility. Physicians advising prospective passengers should consider the rigorous screening that scientific expeditions apply to participants, and the equipment and training they provide in preparation for medical emergencies.9 Tourists swimming in an active volcano, Deception Island, Antarctic Peninsula. References Prociv P. Health aspects of Antarctic tourism. J Travel Med 1998; 4: 210-212. Priddy RE. An "acute abdomen" in Antarctica. The problems of diagnosis and management. Med J Aust 1985; 143: 108-111. Pardoe RA. A ruptured intracranial aneurysm in Antarctica. Med J Aust 1965; 1: 344-350. Alcorn GB. My Antarctic practice. Med J Aust 1992; 157: 253-258. Poki MT, Semmens K. Intestinal haemorrhage in Antarctica: a multinational rescue operation. Med J Aust 1979; 2: 275-277. Mendick M. What went wrong? Analysis. the little things add up. Flight Safety Aust 2001; 5(4): 14. Cowings PS, Toscano WB, DeRoshia C, et al. Promethazine as a motion sickness treatment: impact on human performance and mood states. Aviat Space Environ Med 2000; 71: 1013-1022. Carter JW. Shipboard medicine on package cruises. BMJ 1972; 1: 553-556. Lugg DJ. Antarctic medicine. JAMA 2000; 283: 2082-2084. Authors' details Department of Emergency Medicine, Canberra Hospital, Canberra, ACT. Paul G Lamberth, FACEM, Emergency Physician, and Consultant, Shock Trauma Service. Reprints will not be available from the author. Correspondence: Dr P G Lamberth, Canberra Hospital, Yamba Drive, Garran, ACT 2606. palamATozemail.com.au Make a comment

Paul G Lamberth

Crisis So this is Christmas For many, Christmas is a time of religious celebration and joyous family reunions, while for those separated from family and friends it can be a time of great loneliness. For others it can be a time of great grief as loved ones die on our nation's roads. Steven R Doherty MJA 2001; 175: 585-586 On the last "normal" working day before Christmas 2000 many hospital departments were in wind-down mode. Office parties, long lunches and early pre-Christmas drinks promoted an atmosphere of relaxation before the festive season holidays. Emergency departments rarely have such luxuries, although, on this particular day, a buffet was spread out in the tea-room. The local paper that morning screamed out headlines about the carnage on country roads. In the preceding 48 hours, in separate crashes in our area, one woman had been killed and a pregnant woman had been flown to Sydney with spinal injuries. The police were hoping that these would be the last major incidents in our region over the festive season. Just after lunch the emergency physician on duty asked if I could leave intensive care and help in the emergency department. There had been a car accident about 50 km away. Initial reports were that there were three vehicles with three dead, a baby on its way by helicopter, a man in shock at the scene and an elderly couple coming by road. The "unknown male" baby arrived accompanied by paramedics. He was probably about three months old with an obviously fractured humerus, conscious and crying loudly. He had a lot to cry about. His parents were both killed in their small hatchback vehicle. In the newspaper photograph the following day, their car was unrecognisable. He had been in a child restraint in the back seat and appeared to have no other major injuries. However, he was transferred to a paediatric facility because of concerns about occult injuries, and was subsequently ventilated for a closed head injury. The paramedic advised us that the "man in shock" was really a man with a few orthopaedic injuries. The elderly couple had only minor injuries, but one of them had had ischaemic chest pain. The medical retrieval unit then phoned to say that the "man in shock" was being flown to a tertiary centre and wouldn't be coming to us. The elderly couple arrived and I started to assess them. The woman had been driving at the time of the accident. The baby's parents in the car in front never had a chance. An oncoming car just suddenly drifted across the road and drove them backwards. The driver of that vehicle died too. The elderly woman tried to avoid the wrecks, but clipped into them. She had a bruised knee and, after a series of investigations, went home. Her husband's ischaemic pain had settled, but he had a painful and tender neck, although nothing wrong according to his x-rays. Just before the "man in shock" arrived — it seemed he wasn't going to a tertiary centre after all — Santa came in. One of the local general practitioners has traditionally dressed as Santa and brought in gifts, usually of the liquid and chocolate variety, for emergency department staff working over Christmas. I think he realised as soon as he pushed open the resuscitation room doors that he'd come at a bad time. The "man in shock" was the passenger in the car that drifted. He was 22 years old and had open fractures of his right hand and right ankle and a fractured left radius. He had no more serious injuries. He verified the story told by the elderly woman. His brother, who had turned 26 three days previously, had been driving. After the casualties were sorted out the bodies started to arrive. The dead parents had names, the baby had a name. Before the baby's transfer, and long after the others had left, the nurse who had received him into the emergency department was still there, stroking his hair and waiting for the retrieval team. He would never again know the sound of his mother's voice, never again suckle at her breast. Some time before this, the mother of the two brothers had phoned. The police had given her the news. With a broken voice she asked me about her other son. It was some consolation to be able to tell her that he was battered and bruised, but not in any real danger. A female resident, 20 weeks pregnant with her first child, arrived for the evening shift. She wasn't involved with any of the patients, but was upset by the whole event. She asked me if things like this get harder as you get older. I don't know if they do or not. Does experience harden or mellow you? I told her that I believed these events became harder after you had your own children. Your own children give you a perspective on life you never knew existed. You understand the mother's grief on a more tangible level. You understand the changes this baby will face on a more tangible level. The solemn staff went about their work; counsellors were called to see the survivors of the crash and their relatives, as well as the staff. Only a month before I had spoken at the Australasian College for Emergency Medicine annual scientific meeting. I presented on the differences between rural and city trauma. Fatigue, speed and alcohol are all more frequently associated with car smashes in country areas. These vehicles were all doing about 100 km/h, and all undertaking long trips. The baby and his parents were on a journey of 978 km, the two brothers 513 km, and the elderly couple 859 km -- massive distances in anyone's language. At the meeting I also presented 1999 Roads and Traffic Authority (RTA) figures; in New South Wales 572 people were killed and 26 748 people were injured in motor crashes. Sixty-five per cent of fatalities occurred in country areas, where only 30% of the population live (Mike Adams, Traffic Accident Research Unit, RTA). The police and the RTA preach preventive driving all the time. Yet hundreds of people still die on our roads. The incidence increases every holiday season, with Christmas no exception. Perhaps, though, at Christmas, the impact of the road toll, repeatedly tallied on our televisions and in our newspapers, hits harder. In the 2000 Christmas and New Year break, 77 people died on Australian roads, 39 in NSW. Notwithstanding the work of the police and the RTA, the medical profession, and emergency physicians in particular, are in a great position to become more proactive in road trauma prevention. Programs need to be developed, starting with children in our schools, and they need to be repeated at various stages of their progress through school. Indoctrination? Perhaps, but something needs to be done. We need to develop a society that knows the dangers of driving and understands the main contributors to road crashes, most of which are not "accidents". Christmas 2001 is approaching, and sadly the same horror stories will occur somewhere this year. They will keep recurring. For some this will be the real Christmas. A Christmas of tragic loss or painful memories. Are we, as a profession, doing enough to lessen this trauma? Authors' details Emergency Department, Tamworth Base Hospital, Tamworth, NSW. Steven R Doherty, MB BS, FACEM, Emergency Physician. Reprints will not be available from the author. Correspondence: Dr S R Doherty, Emergency Department, Tamworth Base Hospital, PO Box 83, Tamworth, NSW 2340. srdohertATmpx.com.au; sdohertyATdoh.health.nsw.gov.au Make a comment

Steven R Doherty

Childhood injuries Drowning and near-drowning in Northern Territory children Karen M Edmond, John R Attia, Catherine A D'Este and John T Condon MJA 2001; 175: 605-608 For editorial comment, see Pitt and Cass Abstract - Methods - Results - Discussion - Acknowledgements - Competing interests - References - Authors' details - - More articles on Paediatrics Abstract Objective: To compare incidences of drowing for children in the Northern Territory (NT) with those in Queensland and the rest of Australia. Design: Descriptive, retrospective, population-based analysis of death and hospitalisation data for drowning and near-drowning. Setting and participants: Children aged 0-14 years resident in Australia from 1983 to 1998. Main outcome measures: Age-standardised average annual incidence of drowning (1983-1998) and near-drowning (1994-1997) in children aged 0-4 and 5-14 years in the NT, Queensland and the rest of Australia. Results: The average annual incidence of drowning and near-drowning from 1994 to 1997 for children aged 0-4 years in the NT (67.82 per 100 000) was significantly higher than for Australia (24.45 per 100 000) (incident rate ratio [IRR], 2.77; 95% CI, 1.40-4.91) and for Queensland (32.55 per 100 000) (IRR, 2.13; 95% CI, 1.05-3.94). The proportion of children aged 0-4 years drowning or near-drowning in swimming pools from 1994 to 1997 was also significantly higher in the NT (83%) than Australia (64%) (difference, 0.19; 95% CI, 0.086-0.30) and Queensland (65%) (difference, 0.18; 95% CI, 0.069-0.29). From 1983 to 1998, the incidence of drowning in NT children aged 0-4 years increased by 0.4% per year (IRR, 1.004; 95% CI, 0.994-1.070), compared with a 5.0% reduction per year (IRR, 0.950; 95% CI, 0.937-0.963) in Australian children. Conclusions: The incidences of drowning and near-drowning in the NT are higher than in the rest of Australia and show no significant decrease. The NT should improve its measures for prevention of childhood drowning. In Australia, childhood drownings are second only to road trauma as a cause of injury death in children younger than 15 years.1,2 Encouragingly, the overall incidence of childhood drowning in Australia appears to be decreasing.1,3 However, drowning death rates are higher in the Northern Territory (NT) than the rest of Australia.1,4-6 There is also some evidence that rates of drowning in the NT are not decreasing as fast as those in the rest of Australia.4,5 However, there are no published studies that compare rates of near-drowning in the NT with rates in the rest of Australia. There are also no published analyses of NT drowning trends. Risk groups for drowning include children aged 0-4 years,1,3 children living in cities with high swimming pool to population ratios,7-10 children living in hot climates,3,8 children living in areas with lack of isolation pool fencing,11-14 and Indigenous children.4,5,7 However, there are no published NT data concerning these risk groups. The proportion of NT children drowning in swimming pools is also currently unknown. This study was designed to determine how incidences of childhood drowning and near-drowning in the NT compare with rates in the rest of Australia and in Queensland (another State with a similar climate and similar numbers of domestic swimming pools per capita as the NT). We aimed to stratify our analysis according to specific risk groups (children aged 0-4 years, children aged 5-14 years, children drowning in swimming pools, and Indigenous children). We also planned to compare the proportion of NT children aged 0-4 years who drowned or nearly drowned in swimming pools with Queensland and the rest of Australia. The study was designed as a descriptive, retrospective, population-based analysis of hospital morbidity and mortality data for drowning and near-drowning, identified by International classification of diseases, 9th revision, clinical modification (ICD-9-CM) codes15 in children aged 0-14 years. Methods Definitions A drowning incident was defined as a non-intentional episode in which immersion of a child in water was followed by death. A near-drowning incident was defined as a non-intentional episode in which immersion of a child in water was followed by admission into hospital and the child subsequently surviving. A case was only included as a drowning or near-drowning if it was identified by specific ICD-9-CM external (E) cause codes (830, 832, 919.0-910.9) or the ICD-9-CM disease code for near-drowning (994.1).15 E-codes classify environmental sites, events, circumstances, and conditions as the cause of injury, and include a code for swimming pool drowning.15 Data collection Mortality and hospital morbidity data for all cases of drowning and near-drowning were obtained from the Australian Institute of Health and Welfare (AIHW). Mortality data were available for 1983-1998, but hospital morbidity near-drowning data were available for 1994-1997 only, because of the introduction of casemix funding and changes in ICD-9-CM coding.16 Population denominators for the NT, Queensland and the rest of Australia were the estimated resident population data for each year published by the Australian Bureau of Statistics (ABS).17 NT Indigenous population data were the estimates of the NT Indigenous population published by the ABS.18 Data analysis Crude incidences of drowning and near-drowning for the NT, Queensland and the rest of Australia were standardised year by year within 0-4 and 5-14 years age groups using the indirect standardisation method and the Australian population as the reference population.19The annual number of cases was assumed to follow a Poisson distribution.20 Changes in annual drowning death rates from 1983 to 1998 were investigated using the Mantel test for trend and a Poisson regression model which included terms for year. NT average annual incidences of age-standardised drowning and near-drowning were compared with Queensland and the rest of Australia using incident rate ratios (IRR) and 95% confidence intervals. An IRR was defined as the ratio of two incidences. The difference between proportions of children drowning or nearly drowning in swimming pools in the NT, Queensland and the rest of Australia was compared using tests of difference between two proportions and 95% confidence intervals. Stata software was used for statistical analysis.21 Ethical approval This study was approved by the Joint Institutional Ethics Committee of the Royal Darwin Hospital and the Menzies School of Health Research. Results Drowning Forty-two NT children drowned from 1983 to 1998. There was no significant change in the incidence of drowning over this period in NT children aged 0-4 or 5-14 years (Boxes 1 and 2). In contrast, rates of drowning in Australian children reduced significantly each year in children aged 0-4 years (Boxes 1A and 2). Rates in Australian children aged 5-14 years also reduced each year, but the Poisson regression rate ratio for trend per year did not reach statistical significance (Boxes 1B and 2). The average annual incidence of drowning in NT, Australian and Queensland children from 1994 to 1997 is shown in Box 3. Near-drowning The NT incidence of near-drowning for children aged 0-4 years was higher than the Queensland rate, but not statistically significant, while the rate for children aged 5-14 years was similar to the Queensland rate (Box 3). Swimming pool drowning and near-drowning The proportion of children aged 0-4 years drowning or near-drowning in swimming pools from 1994 to 1997 in the NT (83%) was higher than in Queensland (65%) (difference, 0.18; 95% CI, 0.069-0.29) and the rest of Australia (64%) (difference, 0.19; 95% CI, 0.086-0.30) (see Box 3 for incidence). Indigenous status In the NT, non-Indigenous children aged 0-4 years had higher rates of drowning and near-drowning (73.19 per 100 000) than Indigenous children (56.63 per 100 000) (IRR, 1.29; 95% CI, 0.53-4.47), although this was not significant. Non-Indigenous children aged 5-14 years also had higher rates of drowning and near-drowning (7.27 per 100 000) than Indigenous children (5.41 per 100 000; IRR, 1.34; 95% CI, 0.81-5.42). Rates of swimming pool drowning in the NT were also higher in non-Indigenous children aged 0-4 years (24.89 per 100 000) than Indigenous children (14.04 per 100 000) but this difference was not significant (IRR, 1.77; 95% CI, 0.91-6.22). Only five of 40 children (13%) aged 0-4 years who drowned in a swimming pool in the NT from 1983 to 1998 were Indigenous. Discussion This study describes the extremely high incidence of drowning and near-drowning in children in the NT. Incidences were higher than in the rest of Australia and showed no significant decrease despite reductions in the rest of Australia. Rates in the NT are among the highest recorded worldwide.3-5Indigenous children in the NT had lower rates of drowning and near-drowning than non-Indigenous children, as well as lower rates of swimming pool drowning, although the differences were not statistically significant. Case numbers of fresh water drownings were too small to allow statistical analysis. Some studies describe rates of drowning and near-drowning in Native American children to be two to three times those of non-Native American children.7,10 However, Australian studies report rates of Indigenous child drowning mortality similar to those reported here.4,5 Reporting of Indigenous status in the NT is accurate, in contrast to other Australian States and Territories.1 Near-drowning urban and rural hospital referral patterns are similar and are unlikely to have contributed to the difference in Indigenous and non-Indigenous rates. Reduced exposure of Indigenous children to domestic swimming pools is a possible explanation. Further prospective research is required to clarify these issues. There are many reports of the high rates of drowning in children aged 0-4 years.1,2,9,11 In our study, children aged 0-4 years in the NT, Queensland and the rest of Australia had rates of drowning and near-drowning 5-10 times higher than children aged 5-14 years. Young children in the NT appeared to be at greatest risk, with rates of drowning and near-drowning nearly three times higher than the rest of Australia and Queensland. Rates of swimming pool drowning in children aged 0-4 years in the NT were more than twice the Australian and Queensland rates and among the highest in the world.2,8,9,11 The proportion of children drowning in swimming pools in the NT was also statistically higher than in Queensland and the rest of Australia. Drowning rescue and resuscitation protocols in the NT are similar to those in the rest of Australia. One possible explanation for the differences between NT and Queensland rates of swimming pool drowning is that Queensland introduced statewide pool fencing legislation in 1992, while pool fencing laws in the NT are still inadequate. All the NT swimming pool drowning deaths reported in this study occurred in pools with non-Australian Standards fencing (NT coroner, personal communication). There is no standard legislation for pool fencing in the NT. Only one jurisdiction (encompassing less than 10% of the population) requires fencing according to Australian Standards. Other reasons for the disparity between NT and Queensland rates of drowning could be differences in exposure to water, differences in exposure to swimming pools, or differences in parental supervision. Further prospective research is needed to investigate the role of these different risk factors. We may have underestimated rates of drowning and near-drowning, as retrospective data were used and case ascertainment relied on coded cause of death/hospitalisation. We may also have under-reported NT rates of near-drowning, as the ratio of near-drowning to drowning in the NT (2:1) was lower than Australia (9:1) and Queensland (9:1). Smaller numbers of NT drowning and near-drowning cases also produced considerable variation in annual NT data. However, statistical analyses, including Poisson regression, enabled analysis of trend over time. In response to this study and other reports, NT injury prevention groups are planning to expand their drowning prevention campaigns. This will include lobbying the NT government to enact isolation/four-sided pool-fencing legislation. More public awareness campaigns are also planned. These will be directed towards the need for effective pool fencing, parental supervision of young children, and cardiopulmonary resuscitation skills, and will include other measures that can assist in preventing drowning in young children. Kidsafe NT also intends to use the information from this study to develop a prospective drowning surveillance system. This system will be used to evaluate drowning prevention interventions and to further investigate NT risk factors for childhood drowning, including the role of swimming pool fencing. Acknowledgements Kidsafe, Child Accident Prevention Foundation of Australia, NT branch, provided the funding for the data extraction by the Australian Institute of Health and Welfare. Competing interests None declared. References Moon L, Rahman N, Bhatia K. Australia's children: their health and well being 1998. Canberra: AIHW, 1998. (AIHW Catalogue No. PHE 7.) Pitt WR. Increasing incidence of childhood immersion injury in Brisbane. Med J Aust 1986; 144: 683-685. Cass DT, Ross F, Lam LT. Childhood drowning in New South Wales 1990-1995: a population based study. Med J Aust 1996; 165: 610-612. Vimpani G, Doudle M, Harris R. Child accident mortality in the Northern Territory. Med J Aust 1988; 148: 392-395. Silva DT, Ruben AR, Wronski I, et al. Excessive rates of childhood mortality in the Northern Territory. J Paediatr Child Health 1998; 34: 63-68. d'Espaignet ET, Kennedy K, Paterson BA, et al. From infancy to young adulthood: health status in the Northern Territory, 1998. Darwin: Territory Health Services, 1998. Spyker DA. Submersion injury epidemiology, prevention and management. Pediatr Clin North Am 1985; 32: 113-125. Pitt WR, Balanda KP. Childhood drowning and near-drowning in Brisbane: the contribution of domestic swimming pools. Med J Aust 1991; 154: 661-665. Geddis DC. The exposure of pre school children to water hazards and the incidence of potential drowning accidents. N Z Med J 1984; 97: 223-226. O'Carrol PW, Alkon E, Weiss B. Drowning mortality in Los Angeles County 1976-1984. JAMA 1988; 260: 380-383. Fergusson DM, Horwood LJ. Risks of drowning in fenced and unfenced domestic swimming pools. N Z Med J 1984; 97: 777-779. Carey V, Chapman S, Gaffney D. Children's lives or garden aesthetics? A case study in public health advocacy. Aust J Pub Health 1994; 18: 25-32. Millner N, Pearn J. Will fenced pools save lives? A 10 year study from Mulgrave Shire, Queensland. Med J Aust 1980; ii: 510-511. Intergov-WA, Intergovernmental Working Party on Swimming Pool Safety. Preschool drowning in private swimming pools. Perth: Health Department of Western Australia, 1988. US Department of Health and Human Services. The international classification of diseases. 9th revision. Clinical modification (ICD-9-CM). 3rd ed. Bethesda, Md: DHHS, 1989. Langlois JA, Buechner JS, O'Connor EA, et al. Improving the E coding of hospitalizations for injury: do hospital records contain adequate documentation? Am J Public Health 1995; 85: 1261-1265. Australian Bureau of Statistics. Population by age and sex, Australian States and Territories. Canberra: ABS, 1997. (Catalogue no 3201.0.) Australian Bureau of Statistics. Experimental estimates of Aboriginal and Torres Strait Islander population 1991 and 1996. Canberra: ABS, 1997. (Catalogue no 3230.0.) Pagano M, Gauvreau K. Principles of biostatistics. 1st ed. California: Wadsworth, 1993. Frome EL, Checkoway H. Epidemiologic programs for computers and calculators. Use of Poisson regression models in estimating incidence rates and ratios. Am J Epidemiol 1985; 121: 309-323. Stata Statistical Software [computer program]. Version 5.0. Texas: Stata Corporation, 1997. (Received 23 Feb, accepted 30 Jul, 2001) Authors' details Territory Health Services, Casuarina, NT. Karen M Edmond, FRACP, MMedSc (ClinEpid), Community Paediatrician. Centre for Epidemiology and Biostatistics, University of Newcastle, Newcastle, NSW. John R Attia, FRCPC, PhD, Senior Lecturer; Catherine A D'Este, PhD, Senior Lecturer. Menzies School of Health Research, Casuarina, NT. John T Condon, FAFPHM, MPH, Research Scholar. Reprints will not be available from the authors. Correspondence: Dr K M Edmond, Research Fellow in Paediatric Epidemiology, London School of Hygiene and Tropical Medicine, 50 Bedford Square, London, WC1B 3DP, UK. karen.edmondATlshtm.ac.uk. Make a comment 1: Age-standardised annual incidence of drowning for the Northern Territory and the rest of Australia, 1983 to 1998 Back to text 2: Drowning trend analysis for children in the Northern Territory and the rest of Australia, 1983-1998 Poisson regression Mantel test for trend rate ratio for trend per year (95% CI) χ2 (degrees per year of freedom) P for trend per year NT children 0-4 years 5-14 years 1.004 (0.994-1.070) 0.981 (0.883-1.078) 0.02 (1) 0.15 (1) 0.895 0.696 Australian children 0-4 years 5-14 years 0.950 (0.937-0.963) 0.911 (0.889-1.067) 53.73 (1) 66.08 (1) Back to text 3: Average annual incidence of drowning and near-drowning for the rest of Australia and Queensland compared with the Northern Territory, 1994-1997 Northern Territory Australia Queensland Number Incidence* Incidence* IRR† (95% CI‡) Incidence* IRR (95% CI) Drowning 0-4 years 16 22.61 3.71 6.17 (1.60-16.68) 5.77 3.92 (0.94-12.48) 5-14 years 1 3.21 0.62 5.26 (0.12-33.48) 0.82 3.91 (0.08-39.28) Near-drowning 0-4 years 32 45.21 20.69 2.19 (1.18-4.37) 26.78 1.69 (0.70-3.52) 5-14 years 7 5.56 2.55 2.20 (1.26-8.30) 5.36 1.03 (0.12-4.14) Drowning and near-drowning 0-4 years 48 67.82 24.45 2.77 (1.40-4.91) 32.55 2.13 (1.05-3.94) 5-14 years 8 6.44 3.61 1.78 (1.21-6.58) 6.12 1.04 (0.12-4.08) Swimming pool drowning and near-drowning 0-4 years 40 56.51 15.65 3.61 (1.70-6.77) 20.69 2.74 (1.24-5.47) 5-14 years 1 3.20 1.03 3.08 (1.75-18.7) 2.63 1.22 (1.29-8.23) * Incidence per 100 000 children. † Incident rate ratio. Back to text

Karen M Edmond · John R Attia · Catherine A D'Este · John T Condon

Bites and stings Prospective study of jellyfish stings from tropical Australia, including the major box jellyfish Chironex fleckeri Gerard M O'Reilly, Geoffrey K Isbister, Paula M Lawrie, Greg T Treston and Bart J Currie MJA 2001; 175: 652-655 Abstract - Methods - Results - Discussion - Acknowledgements - Conflict of interest - Reference - Authors' details - - More articles on Insects, bites and stings Abstract Objective: To determine the immediate and delayed effects of jellyfish stings, and correlate these with microscopic identification of jellyfish nematocysts. Design: Prospective study of patients presenting with jellyfish stings. Participants and setting: 40 people presenting with jellyfish stings to the emergency department of a teaching hospital in tropical Australia between 1 August 1999 and 31 July 2000. Main outcome measures: Clinical diagnosis (sting by Chironex fleckeri, "Darwin carybdeid" or other jellyfish, or "Irukandji" syndrome); clinical severity; delayed hypersensitivity; and sticky-tape sampling and microscopic identification of nematocysts. Results: Patients were aged 2-50 years, with eight aged under 15 years; 23 were male. Presentations were consistent with C. fleckeri sting in 28 cases, Darwin carybdeid sting in five, and Irukandji syndrome in four. Sticky-tape sampling was done in 39 patients and was positive for C. fleckeri nematocysts in 23 and for non-C. fleckeri nematocysts in six, with nematocysts not detected in 10 (including all four with Irukandji syndrome). All microscopically confirmed C. fleckeri stings had typical clinical presentations. None of the stings were life-threatening, and no antivenom was given. Delayed hypersensitivity reactions were seen in 11 of the 19 patients (58%) followed up after stings positive for C. fleckeri nematocysts. Conclusions: Although most jellyfish stings presenting to Royal Darwin Hospital were caused by C. fleckeri, severe envenomation was rare. There was a strong association between clinical features and sticky-tape identification of nematocysts. Delayed hypersensitivity was common after C. fleckeri stings. Box jellyfish stings have historically been an important cause of mortality and morbidity in coastal tropical Australia.1-3 The most common cause of sting presentations to the Royal Darwin Hospital (NT) is the major box jellyfish Chironex fleckeri (Class Cubozoa; Order Chirodropidae)4-6(Box 1A). It is responsible for most severe cases of jellyfish envenomation.1-4 Clinical manifestations include immediate local pain with visible linear tentacle marks and, in severe stings, systemic effects with cardiorespiratory arrest possible within minutes.1-4,6-8 However, fatalities are rare, and the clinical spectrum is not evident from published case reports, which mostly present fatal or near-fatal cases. In addition, it is not clear whether delayed hypersensitivity, which has been reported after other jellyfish stings, is a feature of C. fleckeri stings.1The "Irukandji" syndrome has been associated with stings by Carukia barnesi (Class Cubozoa; Order Carybdeidae)9,10 (Box 1C), although other jellyfish may cause a similar syndrome.11C. barnesi has rarely been found in the Northern Territory (P Alderslade, Curator of Coelenterates, Museum and Art Gallery of the Northern Territory, Darwin, NT, personal communication), and the Irukandji syndrome is less common than in far north Queensland.10,11 Other jellyfish species appear to cause some stings in the Darwin region.1,4 These include the "Darwin carybdeid",1 a four-tentacled jellyfish larger than C. barnesi, which appears to cause less severe skin damage than C. fleckeri. We conducted a prospective study of all jellyfish-sting presentations to Royal Darwin Hospital over 12 months in 1999 and 2000. Our aim was to determine the immediate and delayed effects of all marine stings, and to correlate these with microscopic identification of jellyfish nematocysts using the sticky-tape sampling technique.6 Methods The study included all patients who presented to the Royal Darwin Hospital after a jellyfish sting between 1 August 1999 and 31 July 2000. The study was approved by the Joint Institutional Ethics Committee of the Royal Darwin Hospital and the Menzies School of Health Research. Patients were assessed and treated in the Emergency Department according to the Royal Darwin Hospital protocol12(Box 2). Clinical and demographic details were entered prospectively, along with details of hospital management, on a standardised form. Details included investigations (eg, electrocardiography [ECG]), type and effect of analgesia (topical [ice], oral [eg, aspirin or codeine], or parenteral [morphine or pethidine]) and whether C. fleckeri antivenom was administered. The clinical diagnosis was classified as typical or not typical of C. fleckeri sting according to known features (immediate and persistent local pain, linear sting marks and absence of generalised pain, which is seen in Irukandji syndrome).1,3,11 Sticky-tape sampling During the initial presentation, the sting site was sampled for nematocysts using the sticky-tape technique developed in Darwin.6 Transparent sticky tape was applied to the site and then transferred to a microscope slide for examination at x 100 to x 400 magnification. This allows nematocysts of C. fleckeri to be distinguished from those of other jellyfish on the basis of morphology (Box 1B and 1D). Presence of C. fleckeri or other jellyfish nematocysts was determined by one of the authors (P M L) and verified by another (B J C). Follow-up We telephoned patients about three weeks after initial presentation to ask about persistent or delayed effects, especially emergence of a pruritic rash at the site of the initial sting. Results Forty patients presented to Royal Darwin Hospital with jellyfish stings in the 12-month study period. They were aged two to 50 years (median, 21 years), with eight aged under 15 years; 23 were male. Seasonal variation in stings is shown in Box 3. Of the 40 stings, 28 (70%) were clinically typical of C. fleckeri, and 12 (30%) were not typical. Four of the latter were consistent with Irukandji syndrome (minimal local erythema, and delayed systemic symptoms, especially pain), and five with Darwin carybdeid sting (less severe skin pain and markings, with some "overlap" Irukandji features, such as abdominal pain). A typical C. fleckeri sting is shown in Box 4A. Sticky-tape sampling Sticky-tape sampling was done in 39 patients and was positive for nematocysts in 29 — C. fleckeri in 23 and carybdeid-appearing nematocysts in six. Sampling was negative for nematocysts in 10 patients, including all four with Irukandji syndrome. Correlation between microscopic findings and clinical presentation is shown in Box 5. All microscopically confirmed C. fleckeri stings had typical clinical presentations. Of the six patients with carybdeid-appearing nematocysts, five had presentations consistent with Darwin carybdeid envenomation, while one was more consistent with C. fleckeri. Management None of the 40 patients had documented arrhythmias on ECG, or pulmonary oedema. None was treated with pressure-immobilisation bandages or C. fleckeri antivenom, and there were no deaths. Of the 23 patients with stings positive for C. fleckeri nematocysts, one required parenteral analgesia and nine oral analgesia. In five, pain responded to topical ice alone, and eight required no pain relief. None of these patients required admission. Maximum length of tentacle marks was 5 m, followed by 4 m; both patients had severe local pain. Three of the patients with Irukandji syndrome and one stung by an unidentified jellyfish (no nematocysts detected on sticky-tape sampling) required admission for analgesia. Follow-up Twenty-nine patients were followed up, including 19 whose stings were positive for C. fleckeri nematocysts. Of these 19, 11 (58%) had delayed hypersensitivity reactions. These comprised an itchy red maculopapular rash dotted along the initial tentacle contact points consistent with papular urticaria, occurring 7-14 days after first presentation (Box 4B). These reactions resolved spontaneously in seven patients and after treatment with oral antihistamine and topical corticosteroid cream in four. Discussion This is the largest prospective study of C. fleckeri stings to date. Most previously published cases describe fatal or near-fatal stings, and some authors quote mortality rates up to 20%.13 Our study does not support this high mortality rate and showed that most stings were not severe, consistent with previous Northern Territory findings.5-7Although most C. fleckeri stings are minor and not life-threatening, the potential exists for severe systemic envenomation and even death. It is a concern that, despite considerable public education, eight of our cases were in children. The last 10 deaths from C. fleckeri envenomation in the Northern Territory were all of children, most recently a three-year-old girl from a remote Aboriginal community in February 1996.4 In January 2000, a five-year-old boy died soon after a jellyfish sting near Yarrabah, in north Queensland, presumed to be from C. fleckeri.14 In the past, considerable attention has focused on the use of antivenom in C. fleckeri envenomation.3,8,15-17 Indications have been cardiac arrest and arrhythmias, analgesia or cosmesis, although evidence supporting the efficacy of antivenom remains limited.7 None of our patients received antivenom, as none had cardiac toxicity, and severe local pain was controlled with appropriate analgesia. Nevertheless, it is crucial that antivenom is available for early use in life-threatening situations with arrhythmias or cardiorespiratory arrest. None of our patients had pressure-immobilisation bandages applied. These bandages are not recommended in the Northern Territory, as they potentially increase nematocyst discharge and are unlikely on theoretical grounds to prevent venom absorption.7,12,18 Delayed skin eruptions have been reported after jellyfish stings, although C. fleckeri has not been specifically implicated.19-21 These eruptions typically occurred at the site of the original sting after five days or more, and were pruritic and painless.1 Their histological features were generally consistent with delayed (type IV) hypersensitivity reactions.20 They are likely to be a response to retained foreign material, such as nematocyst thread or other cellular substances injected into the dermis, but specific antigens have not been identified. In our study, over half the patients followed up after stings positive for C. fleckeri nematocysts had delayed skin eruptions clinically resembling papular urticaria, similar to those reported after other jellyfish stings.19-21 This confirms that delayed cutaneous hypersensitivity reactions are common after C. fleckeri stings. Corticosteroid cream, with or without systemic antihistamines, may help relieve symptoms of delayed reactions.1,7 Correlation of sticky-tape sampling with clinical presentation suggests that there were no false-positive identifications of C. fleckeri nematocysts. The false-negative rate is unknown. However, as the test was negative for nematocysts in only three cases that appeared clinically typical of C. fleckeri envenomation, correlation with clinical findings appears good. While all the non-C. fleckeri nematocysts detected were carybdeid in appearance, degenerate C. fleckeri nematocysts may sometimes appear similar. Further description and classification is needed of the Darwin carybdeid and other local jellyfish yet to be identified. Clinical features of most of the carybdeid nematocyst-positive stings differed from those of both C. fleckeri stings and the Irukandji syndrome. The Darwin carybdeid appears to cause local pain from tentacle marks, but this pain is less severe than in C. fleckeri stings. The Darwin carybdeid also causes some "overlap" systemic symptoms, similar to those of a mild Irukandji syndrome. Two earlier stings with these features were confirmed to be caused by the Darwin carybdeid through capture and examination of the jellyfish, as well as microscopic identification of nematocysts1 (Currie BJ, unpublished data). Finally, although life-threatening envenomation is uncommon, we should continue to pursue public education and prevention policies vigorously. Deaths from severe C. fleckeri envenomation will inevitably occur while people, especially children without protective clothing, enter tropical waters in Australia. Acknowledgements We would like to acknowledge support from the Cooperative Research Centre for Aboriginal and Tropical Health; from the National Health and Medical Research Council Centre of Clinical Excellence grant to the Northern Territory Clinical School, Royal Darwin Hospital; and the staff of the Emergency Department, Royal Darwin Hospital, particularly Carole Mansfield and Marg St Leone. We would also like to acknowledge Phil Alderslade (Northern Territory Museum, Darwin) for assistance and for the photograph of the Darwin carybdeid. Conflict of interest There was no specific funding for this study and no conflict of interest. References Williamson JA, Fenner PJ, Burnett JW, Rifikin JF. Venomous and poisonous marine animals. 1st ed. Sydney: University of New South Wales Press, 1996. Williamson JA, Callanan VI, Hartwick RF. Serious envenomation by the northern Australian box-jellyfish (Chironex fleckeri). Med J Aust 1980; 1: 13-15. Williamson JA, Le Ray LE, Wohlfahrt M, Fenner PJ. Acute management of serious envenomation by box-jellyfish (Chironex fleckeri). Med J Aust 1984; 141: 851-853. Currie BJ. Clinical toxicology: a tropical Australian perspective. Ther Drug Monit 2000; 22: 73-78. Currie BJ, Khanh DM, Alderslade P, et al. Jellyfish envenomation in the Northern Terrritory of Australia. Toxicon 1992; 30: 501. Currie BJ, Wood YK. Identification of Chironex fleckeri envenomation by nematocyst recovery from skin. Med J Aust 1995; 162: 478-480. Currie B. Clinical implications of research on the box-jellyfish Chironex fleckeri. Toxicon 1994; 32: 1305-1313. Lumley J, Williamson JA, Fenner PJ, et al. Fatal envenomation by Chironex fleckeri, the north Australian box jellyfish: the continuing search for lethal mechanisms. Med J Aust 1988; 148: 527-534. Barnes JH. Cause and effect in Irukandji stingings. Med J Aust 1964; 1: 897-904. Little M, Mulcahy RF. A year's experience of Irukandji envenomation in far north Queensland. Med J Aust 1998; 169: 638-641. Fenner PJ, Williamson JA, Callanan VI, Audley I. Further understanding of, and a new treatment for, "Irukandji" (Carukia barnesi) stings. Med J Aust 1986; 145: 569-574. Currie B. Box-jellyfish in the Northern Territory. N T Dis Control Bull 1998; 5: 12-14. Guenin DG, Auerbach PS. Trauma and envenomations from marine fauna. In: Tintinalli JE, Ruiz E, Krome RL, editors. Emergency medicine — a comprehensive study guide. 4th ed. New York: McGraw-Hill, 1996: 868-873. Lill J. Fatal sting. Box jellyfish kills boy, 5. The Cairns Post 2000 Jan 25: 1. King GK. Acute analgesia and cosmetic benefits of box-jellyfish antivenom. Med J Aust 1991; 154: 365-366. Beadnell CE, Rider TA, Williamson JA, Fenner PJ. Management of a major box jellyfish (Chironex fleckeri) sting. Lessons from the first minutes and hours. Med J Aust 1992; 156: 655-658. Holmes JL. Marine stingers in far north Queensland. Australas J Dermatol 1996; 37 Suppl 1: S23-S26. Pereira PL, Carrette T, Cullen P, et al. Pressure immobilisation bandages in first-aid treatment of jellyfish envenomation: current recommendations reconsidered. Med J Aust 2000; 173: 650-652. Reed KM, Bronstein BR, Baden HP. Delayed and persistent cutaneous reactions to coelenterates. J Am Acad Dermatol 1984; 10: 462-465. Pierard GE, Letot B, Pierard F. Histologic study of delayed reactions to coelenterates. J Am Acad Dermatol 1990; 22: 599-601. Burnett JW, Cobbs CS, Kelman SN, Calton GJ. Studies on the serologic response to jellyfish envenomation. J Am Acad Dermatol 1983; 9: 229-231.(Received 20 Apr, accepted 13 Aug, 2001) Authors' details Royal Darwin Hospital, Darwin, NT. Gerard M O'Reilly, MB BS, Emergency Registrar; currently, Emergency Registrar, Alfred Hospital, Melbourne, VIC. Geoffrey K Isbister, BSc, MB BS, Emergency Registrar; currently, Toxicology Registrar, Department of Clinical Toxicology and Pharmacology, Newcastle Mater Hospital, Newcastle, NSW. Greg T Treston, DTMH, DIMCRCS, FACEM, Director of Emergency Department; currently Consultant, Emergency Department, John Flynn Hospital, Tugun, QLD. Menzies School of Health Research, Darwin, NT. Paula M Lawrie, BSc, Technical Officer. Bart J Currie, FRACP, FAFPHM, DTMH, Head of Tropical Medicine and International Health Unit; and Professor in Medicine, NT Clinical School, Darwin, NT. Reprints will not be available from the authors. Correspondence: Professor B J Currie, Tropical Medicine and International Health Unit, Menzies School of Health Research, PO Box 41096, Casuarina, NT 0811. bartATmenzies.edu.au Make a comment 1: Common Northern Territory jellyfish and their nematocysts Chironex fleckeri A. B. Nematocysts from C. fleckeri (original magnification, x 400; sticky-tape preparation; no stain). "Darwin carybdeid" C. D. "Darwin carybdeid" nematocyst (original magnification, x 1000; eosin stain). Nematocysts from C. fleckeri are usually elongated ellipses (cigar-shaped), while those from carybdeid (four-tentacled box-jellyfish) species are usually less elongated and more lemon-shaped or round. Back to text 2: Protocol for hospital treatment of Chironex fleckeri stings in the Northern Territory 1. If necessary, attend to airway, breathing and circulation and give oxygen. 2. Apply vinegar to the stings for at least 30 seconds to inactivate remaining nematocysts. 3. If patient is unconscious or has life-threatening cardiac or respiratory decompensation or significant arrhythmia, administer at least one ampoule of antivenom intravenously (20 000 units per ampoule, diluted 1:10 with an isotonic crystalloid solution such as Hartmann's solution or isotonic saline, given over 5-10 minutes). In a life-threatening situation where response remains inadequate, up to three ampoules may be given consecutively. 4. Cardiopulmonary resuscitation should be continued in a patient with ongoing cardiac arrest until after further therapy with antivenom (at least six ampoules total dose if available) and consideration of cardioactive drugs. 5. For non-life-threatening stings (no cardiac or respiratory decompensation), use ice-packs for initial pain relief, together with oral or parenteral analgesia if necessary (pethidine, 1 mg/kg up to 50 mg adult dose initially, or morphine, 0.1 mg/kg up to 5 mg initially, but can be repeated). For pain not relieved by ice-packs and narcotic analgesia, administer one ampoule of antivenom intravenously as above. Back to text 3: Jellyfish sting presentations to Royal Darwin Hospital, 1999-2000 Back to text 4: Chironex fleckeri stings A. Severe sting on Day 2. B. Hypersensitivity reaction seen 10 days after a sting. Back to text 5: Correlation between clinical presentation and nematocyst identification in 39* jellyfish stings Nematocyst appearance Presentation Chironex fleckeri Other jellyfish† Not detected Typical of C. fleckeri (n = 27)* 23 1 3 Not typical 0 5 7 "Irukandji" syndrome (n = 4) 0 0 4 Other (n = 8) 0 5 3 * Nematocyst sampling was not performed in one patient with a typical C. fleckeri presentation. † All non-C. fleckeri-appearing nematocysts were consistent with carybdeid nematocysts, although degenerate C. fleckeri nematocysts may sometimes look similar. Back to text

Gerard M O'Reilly · Geoffrey K Isbister · Paula M Lawrie · Greg T Treston · Bart J Currie

Letter Eye exposure to squashed spiders MJA 2001; 175: 671 To the Editor: I read with great interest the letter from Isbister and Balit describing ocular reactions to squashed daddy longlegs spiders.1 As an arachnophile, I think it is a great pity that people go around squashing these harmless beasts that are very efficient at catching and eating real pests such as mosquitoes and flies. Living in a house that is well populated with daddy longlegs, I would like to enlighten readers on my own method of removing these harmless spiders from the house without harming either myself or the spider. This is the "open fist" method. The spider can be easily caught by placing the hand over and around the spider, leaving a small amount of space in the "open fist". It can then be removed from the house and released into the garden. I have used this method successfully on at least 20 occasions without suffering any bite or reaction. Long live daddy longlegs! John E Stuart Paediatrician, John Hunter Children's Hospital, Locked Bag 1, Hunter Mail Centre, NSW 2310. jstuartATdoh.health.nsw.gov.au Isbister GK, Balit C. Eye exposure to squashed spiders [letter]. Med J Aust 2001; 175: 391-392. Make a comment

John E Stuart

MJA 2001; 175: 672 To the Editor: In these days of increasing globalisation of medicine, it is refreshing to realise that there are some uniquely antipodean case scenarios. I wish to report two patients who presented to the emergency department with multiple injuries caused by a single kangaroo. Although there have been previous reports of kangaroos causing injury, this is usually in the passive capacity as an immovable obstruction to a moving vehicle.1 I do not believe there have been any reports of a single kangaroo causing injury to two people at the same time by actively inflicting injury, resulting in a need for hospital treatment. Patient 1: A 32-year-old man intervened in a fight between his dog and a grey kangaroo. The dog escaped, but the kangaroo then turned on the man, inflicting several deep abrasions to his chest, trunk and back, and a bite to his left forearm. X-rays revealed no underlying fractures, and the skin abrasions were treated conservatively. Prophylactic antibiotics and a tetanus booster were administered, and the patient was discharged. Patient 2: While driving past, a 50-year-old man saw the attack described above. He stopped to assist, and grabbed the tail of the kangaroo to distract its attention. The man was thrown to the ground, and sustained bruising to the right shoulder and upper arm. X-rays revealed no fracture, but the arm was immobilised in a sling for symptomatic relief of pain. The kangaroo escaped without injury. These two cases should serve as a warning that intervening in fights between animals poses the risk of injury, and that one kangaroo is easily capable of injuring two humans at the same time. Caution is required if approaching these animals in the wild. Alan E O'Connor Emergency Physician, Emergency Department, The Canberra Hospital, Yamba Drive, Woden, ACT 2606 Alan. O'ConnorATact.gov.au Whittle IR. Beware of boomerangs and kangaroos. Med J Aust 1980; 2: 347. Make a comment

Alan E O'Connor

Raina K Plowright As a veterinarian working on an Adélie penguin research program, I was to spend six months on an island off the coast of Mawson Station in the Australian Antarctic Territory. During a field training exercise on my third day at Mawson, I fell into a crevasse with my four-wheel-drive quad bike and was crushed between the bike and the crevasse wall six metres below the rim. I had hypothermia and abdominal injuries, and underwent two emergency surgical procedures at Mawson Station. Sixteen days after the accident, I was evacuated by helicopter and ship. Here, I describe my experiences. The Antarctic plateau is a crevasse-riven mass of ice rising steeply behind Mawson Station. While riding across sastrugi (ridges in the ice formed by frozen accumulations of blown snow) on the plateau, I slowed to avoid skidding on a snowdrift that was barely visible in the glare. The front wheels of my quad bike reached the other side of the drift, but spun on blue ice. There was a deafening sound, like shattering glass, then ice and metal rushed past me as I plummeted down the walls of the crevasse and was crushed into the ice by the oppressive weight of metal. When everything stopped, I opened my eyes and found I couldn't breathe. I was wedged vertically in a narrow part of the crevasse, pinned between the bike and the ice wall 30 metres from the bottom. The 250 kg bike was crushing my abdomen and thorax against the ice, my chest flattened by the seat, the petrol tank against my lower body. Four-wheel-drive quad bikes being driven across sea ice. (Photograph courtesy of Kym Newbery) At that moment death seemed violently and terrifyingly close. The enormous weight of the bike was squeezing the life from me and I thought that I had only minutes to live. I knew something was very wrong where the bike was crushing my abdomen. Warm urine dribbled down my freezer suit and I could no longer feel my legs. The possibilities that crossed my mind included spinal injury and paraplegia, but I was unafraid, as a chance of life as a paraplegic was preferable to dying. Westbay and the area where I fell into the crevasse: a view from Mawson Station. (Photograph courtesy of Kym Newbery) Rescue By the time rescuers descended into the crevasse 90 minutes after my fall, I thought that I couldn't manage the extraordinary effort of moving air into my lungs any longer. As the bike was lifted off me I was crushed back into the ice and a white curtain of unconsciousness descended. It took six people over 15 minutes to haul me out of the crevasse using a "Z"-pulley rigged with ropes secured to an oversnow vehicle. I recall lying in a stretcher. Madeleine Wilcock, the station doctor, was peering down at me and asking what day it was, an oxygen mask was placed over my face and I was breathing rapidly, gulping for air, and I remember thinking, "I'm breathing! I'm breathing!". The stretcher was lifted onto the back of a utility, which started bumping over the ice, while I stared at the blue sky thinking, "I'm still breathing, I'm alive". Triage I have vague memories of painful needles being pushed into my arms and abdomen, uncontrollable shaking from the ice at my core and nausea that suddenly swept over me causing me to vomit a liquid like coffee grounds. I knew this was altered blood, but my mind refused to make the next logical step and question why I would be vomiting digested blood. There was a frantic effort to find Jason the electrician, as he was the only one of the 44 expeditioners on station who shared my Rh negative blood type. When Bryan Walpole walked in, with his cheerful hello, the relief of his familiarity was so overwhelming that Madeleine noticed a drop in my highly elevated pulse rate. Bryan had been the ship's doctor on my voyage to Antarctica on the Aurora Australis. The ship was still within helicopter range, and Bryan had been rushed 140 nautical miles over the sea ice to Mawson. It was extremely important to me, and for my morale, to see someone familiar taking control over a situation in which I had none. "We have to operate" The next morning Bryan announced that they had to operate. The thought of postoperative pain on top of discomfort and nausea I could already barely tolerate was devastating. I didn't even know if the station had surgical facilities, or if Madeleine or Bryan had surgical experience. It did not occur to me to ask them why I needed surgery. However, my haemoglobin level had fallen from 140 g/L to 100 g/L overnight, my pulse rate was rising, and I had developed abdominal pain. The only diagnostic tools available were haematological and biochemical tests, and x-rays. Thus, it was necessary to open me up to see if there was continued bleeding. There was also concern that I may have had a perforated gut, as I had been vomiting altered blood. It was a lonely and daunting experience being wheeled into an empty, sterile room under bright surgical lights. At least the lights indicated that they had an operating theatre. My anaesthetist, his beard covered in a mask, sat at the head of my bed. I had met him just two days previously; he was an electronics engineer with only two weeks training in anaesthetics at The Royal Hobart hospital 12 months earlier. My nurses were a carpenter and a diesel mechanic. I recall being terrified -- too sick and narcotised to interact or understand; the situation was completely out of my control. I remember someone explaining that the anaesthetic was being injected and a mist washed over me and I couldn't see or breathe. I could hear instruments being dropped onto metal trays and people talking around me, but I felt unable to breathe. My neck had been cranked to one side and the discomfort was excruciating. Then something was placed down my throat, and the air that I was desperately craving flowed into my lungs. I needed another breath and I strained to inhale, but my body wouldn't respond. I realised that I was paralysed and experiencing anaesthetic awareness and the doctors were about to operate while I was still conscious. I started screaming and screaming but I couldn't open my mouth to make a sound. With the most enormous effort I tried to move my arms and open my eyes to show them that I was fully conscious, but nothing I did made me move. However, I must have lost consciousness, as I felt no pain during the surgery, and my next memory was of regaining consciousness on a wave of nausea. Someone was holding a bowl to my mouth, and as I vomited I felt a sensation like sutures ripping through the tissues in my abdomen. The surgery was over and I was wheeled back into my hospital room. During exploratory laparotomy, they found a mesenteric tear with some bleeding vessels, which were ligated, and a large retroperitoneal haematoma, about which they could do nothing. There were also crushing injuries to my small intestine. Dr Madeleine Wilcock putting an oxygen mask on me immediately after the first operation. (Photograph courtesy of Jason Reinke) My care team The next seven days were a blur of unbearable suffering, surrounded by the extraordinary compassion and dedication of Madeleine Wilcock, my doctor (Bryan was required to return to the ship), who understood my suffering as if she were going through it too. This was complemented by the diligence and kindness of my three dedicated (bearded) nurses, who were there 24 hours a day and would do anything for me. Their combined love and concern enveloped and helped me during those awful days. During long sleepless nights in the care of the nurses my veterinary skills were often useful, in ways such as guiding them in fixing blocked intravenous lines or giving injections. At first I was nervous about a diesel mechanic or a carpenter trying to give me intramuscular injections, but then I noticed that they were even more terrified than I. I learned how stressful it is having to endure and anticipate multiple painful procedures each day, and would have preferred all dressing changes, catheter changes, injections and other painful events to be finished in one go. I appreciated Madeleine's efforts to relieve my pain, such as administering local anaesthetic before inserting a cannula. I decided that I would take great care to avoid inflicting pain on my patients in the future. No visitors Madeleine understood that I was unable to cope with visitors and allowed only Lyn (my biologist colleague, and one of only two other women on the station) to visit every day to read emails, which were important for maintaining my morale. I appreciated Madeleine's sensitivity, as I found interaction with people almost unbearable. Moving, and especially speaking, caused the nasogastric tube to irritate my pharynx and induced gagging and vomiting. I was anxious for people to leave. If they remained for any length of time, I needed their reassurance that they didn't expect me to answer or to look at them. I needed them to acknowledge and empathise with my suffering, the awful nausea, and the pain that vomiting caused me, as well as the exhaustion from lack of sleep, and the demoralising affliction of the nasogastric tube. No medical details, please Uncharacteristically, despite my usual curiosity and medical background, I had no interest in my medical details. I was unable to process any information. My entire focus was on existing. Until I was well again I didn't ask what the outcomes of the surgery were. I could not think about the accident, full stop. Flashbacks were immediately pushed out of my mind, and it wasn't until the nausea had subsided and the nasogastric tube had been removed that I was ready to face the full psychological trauma of the accident. My past veterinary patients As I lay in the white hospital room, watching the opaque grey world of a passing blizzard through my tiny porthole, I remember thinking, "My God, this is what sick people feel like". This new insight into suffering was particularly harrowing when I related it to all of those animals which had sat in the back of their cages, unmoving and unresponsive: I now understood what they may have been experiencing. I was certain that I would never work as a veterinarian again; I never wanted to face anything -- human or animal -- that felt as sick and uncomfortable as I did then. A slow recovery Traumatic pancreatitis -- diagnosed during further surgery after my return to Melbourne -- and recurrent forceful vomiting contributed to delayed wound healing. Eleven days after my operation my wound completely dehisced, and the next day I underwent further surgery for abdominal wall repair at Mawson Station. The Aurora Australis was turned around from its position in the Southern Ocean to bring me home. This was a major disappointment, as I was so much looking forward to recovering among the people who had cared for me and to continuing working on the island with the penguins. However, as well as the risk of further complications, supplies of drugs, cannulas, and fluid administration kits were running very low. Moreover, there was no total parenteral nutrition and my body had wasted away. Six days after the second operation I was 12-13 kg lighter than before my accident. The Aurora Australis, which turned back to bring me home (Adélie penguins in the foreground). (Photograph courtesy of Kym Newbery) On returning to Australia, I spent two weeks at a rehabilitation hospital in Melbourne undergoing intensive physiotherapy for right lumbar plexopathy. Two months after the accident I underwent an incisional hernia repair and bowel resection because of adhesions. I have been fortunate and grateful to make a complete recovery. Madeleine Wilcock and my nurses, Garry Watson, Jason Reinke and Nick Mortimer, were awarded the Australian Antarctic Medal for their extraordinary efforts while I was under their care. I would like, once again, to express my deep gratitude for their dedicated, skilful and untiring efforts to nurse and restore me. I will always remember my journey to Antarctica by the aura of love and compassion and care that contained me during those critical days of recovery from the crevasse fall. Authors' details Wentworth Falls, NSW. Raina K Plowright, BVSc(Hons), Veterinary Surgeon. Reprints will not be available from the author. Correspondence: Ms R K Plowright, PO Box 241, Wentworth Falls, NSW 2782. rainapATozemail.com.au

Raina K Plowright

Bites and Stings Pressure immobilisation bandages in first-aid treatment of jellyfish envenomation: current recommendations reconsidered Peter L Pereira, Teresa Carrette, Paul Cullen, Richard F Mulcahy, Mark Little and Jamie Seymour MJA 2000; 173: 650-652 Abstract - Introduction - Methods - Results - Discussion - References - Authors' details - - More articles on Emergency medicine Abstract Objective: To evaluate whether applying pressure equivalent to that of pressure immobilisation bandages (PIB) causes release of additional venom from discharged jellyfish nematocysts. Design: In-vitro experiment -- the venom beads released from electrically activated Chiropsalmus sp. nematocysts were viewed under direct microscopy before and after applying 40 mmHg pressure (replicating the pressure of PIB); and saline washings of discharged nematocysts before and after applying pressure were tested for toxicity (time to ventricular standstill after injecting into live prawns). Results: Applying 40 mmHg pressure caused the venom beads to visibly increase in size, consistent with pressure expressing further venom from the discharged nematocysts. First washings of the nematocyst shafts before compression produced ventricular standstill in prawns within 60 seconds (n = 3); second washings did not produce standstill during 540 seconds of observation (n = 3); and washings after applying 40 mmHg pressure showed a return of toxicity, with ventricular standstill in all prawns within 180 seconds (n = 3). Conclusion: Discharged nematocysts are by no means empty and harmless. Applying pressure results in further release of nematocyst venom. The currently recommended practice of applying PIB in the initial treatment of patients stung by a jellyfish may exacerbate the envenomation, and thus should not be recommended. Introduction The application of pressure immobilisation bandages (PIB) in the first-aid treatment of jellyfish envenomation remains controversial. It is currently recommended by the Australian Resuscitation Council,1 by the Queensland Surf Life Saving Association2 and the Queensland Ambulance Service,3 but not by authorities in the Northern Territory.4,5 The evidence to support the use of PIB is anecdotal,6 and its use is a direct extrapolation of PIB use in elapid snakebite. In snakebite, its beneficial effects have been proposed7 and supported by published case reports.8,9The effect of PIB is to retard the dissipation of snake venom into the circulation by impeding lymphatic flow. This protects target tissues by confining the toxin to the affected limb until the patient is treated with antivenom. In snakebite, the venom is released into the tissues and the delivery apparatus (the snake's fangs) does not remain at the bite site. By contrast, in jellyfish stings, the venom is delivered by specialised cells (nematocysts) which have barbed shafts that adhere to the skin. Unless the nematocysts have entirely discharged their venom, applying pressure (as with PIB) has the potential to worsen the envenomation. Our anecdotal experience is that patients with jellyfish stings whose first aid includes PIB have more severe and prolonged symptoms. Furthermore, no scientific evidence supports the use of PIB in the treatment of box jellyfish stings.10 We designed an experiment to test the hypothesis that applying direct pressure to discharged nematocysts releases further venom. Methods Tentacles from live Chiropsalmus sp. (a closely related species to the box jellyfish Chironex fleckeri) were collected and placed on human amniotic membrane, which in turn was placed over the open end of a glass cylinder (4.5 cm in diameter and 5.5 cm in depth). To cause the nematocysts to discharge, we applied a 6 volt, 3 ampere direct current charge across the tentacles for two seconds. Such electrical augmentation is currently used to collect venom from jellyfish for antivenom production.11 After removal of the tentacles, the membrane was inverted, leaving the nematocyst bodies lying within the cylinder and their penetrating shafts directed externally through the membrane. An aneroid sphygmomanometer (bladder removed) was then attached to the other end of the cylinder (Box 1) to apply pressure to the discharged nematocysts. We used a pressure of 40 mmHg, as pressures of between 40 and 70 mmHg from PIB have been found to obstruct lymphatic flow in simulated snake envenomation.12 Through a dissecting microscope (x 100 magnification) small beads of clear fluid were noted on the tips of the shafts (Box 2). With constant visualisation of these beads, 40 mmHg pressure was applied, and a subjective estimate was made as to whether the pressure altered the size of the beads. To confirm the nature of these beads, the shafts from the discharged nematocysts were washed repeatedly with 2 mL of isotonic saline. The first washing was after activation of the nematocysts (A); the second (B) further cleaned the nematocysts; and the final washing (C) occurred after pressure was applied (and released). Live adult prawns (Penaeus mergenensus) were then injected with one of the three washes (0.2 mL intramuscular injection into the second abdominal segment) and their heart rate was observed every 30 seconds for a period of 10 minutes. The time to ventricular standstill was recorded as a measurement of toxicity. Each solution was administered to three prawns. Statistical analysis Statistical analysis was performed using SPSS.13 Differences in the mean time to cardiac death for prawns in each of the three treatments were determined using a balanced one-way analysis of variance with type I sums of squares. Differences between the means of the treatments were determined using least significant difference (LSD) post-hoc analysis. Results The venom beads, viewed under direct microscopy, visibly increased in size on applying 40 mmHg pressure. The heart rates of the nine prawns at time zero (before injection of the washings from the nematocyst shafts) were not statistically different (F2,6 = 1.895; P = 0.230), but there were significant differences between time from injection of the washings to ventricular standstill for the three different washings (F20,65 = 8.53; P < 0.001) (Box 3). Solution A: In the three prawns administered the first washing, ventricular standstill occurred within 60 seconds of injection. Solution B: All three prawns administered the second washing were unaffected by this inoculum during 540 seconds of observation, apart from a minor reduction in heart rate at 60 seconds for one prawn. Solution C: The third washing (after applying pressure), although not as potent as the first washing, caused ventricular standstill within 180 seconds in all three prawns. Discussion Our experiment shows clearly that further venom is expressed by applying pressure (equivalent to that of PIB) to discharged nematocysts. Furthermore, direct visual examination revealed an increase in bead size related to the amount of pressure being applied. This suggests that our simulated PIB caused mechanical expression of nematocyst contents rather than nematocyst reactivation, in which a triggered quantum of venom would be expected. We showed that Solution A (with venom from initially activated nematocysts) produced the anticipated ventricular standstill when injected into prawns. The relatively innocuous nature of Solution B, which did not produce any ventricular standstill, shows that Solution A had effectively cleaned the nematocyst of any substantial amount of venom. Solution C showed a return of toxicity after 40 mmHg pressure was applied. Thus, pressure applied to discharged nematocysts of Chiropsalmus sp. results in further venom being released. Vinegar, presumably through a chemical process, is a potent inactivator of nematocysts' firing mechanism. Not discounting this important function, its role in first aid is limited to inactivating undischarged nematocysts. Any inference that it has a continuing protective effect with discharged nematocysts is probably incorrect, as further expression of venom from discharged nematocysts appears to be mechanical rather than triggered. Given that the physical processes behind nematocyst discharge in all jellyfish are similar, and that nematocyst discharge operates similarly, there is sufficient reason to believe that the use of PIB on any jellyfish sting site may exacerbate the envenomation, irrespective of whether vinegar has been applied. Until evidence to the contrary is available, we recommend that applying PIB is not part of the management of this life-threatening condition. An amended first-aid protocol for jellyfish stings is given in Box 4. References Envenomation -- jellyfish stings. Australian Resuscitation Council. Policy Statement No 8.9.6. Melbourne: Australian Resuscitation Council, July 1996. Fenner P. The marine stinger guide -- dangerous jellyfish and other sea creatures in Australia. Identification and treatment. Brisbane: The Surf Life Saving Association of Australia, Queensland State Centre Inc, 1985. Case management guidelines for poisoning, envenomation, cuboidal jellyfish. Revised May 1998. Queensland Ambulance Service -- clinical practice manual. AL 10, Guideline A 12-6. Brisbane: Queensland Ambulance Service, May 1998. Currie B. Box-jellyfish in the Northern Territory. Northern Territory Disease Control Bulletin, Sept 1998; 5(3): 12-14. Currie B. Clinical implications of research on the box-jellyfish Chironex fleckeri. Toxicon 1994; 32: 1305-1313. Williamson J, Fenner P, Burnett J. Principles of patient care in marine envenomations and poisonings. In: Williamson JA, Fenner PJ, Burnett JW, Rifkin JF, editors. Venomous and poisonous marine animals -- a medical and biological handbook. Sydney: University of New South Wales Press, 1996. 98-118. Sutherland SK, Coulter AR, Harris RD. Rationalisation of first-aid measures for elapid snakebite. Lancet 1979; 1: 183-185. Sutherland SK, Leonard RL. Snakebite deaths in Australia 1992-1994 and a management update. Med J Aust 1995; 163: 616-618. Currie B, Fitzmaurice M, Oakley J. Resolution of neurotoxicity with anticholinesterase therapy in death adder envenomation. Med J Aust 1988; 148: 522-525. Little M, Mulcahy RF. A year's experience of Irukandji envenomation in far north Queensland. Med J Aust 1998; 169: 638-641. Barnes JH. Extraction of Cnidaria venom from living tentacle. In: Russell FE, Saunders PR, editors. Animal toxins. London: Pergamon Press, 1967: 115-129. Howarth DM, Southee AE, Whyte IM. Lymphatic flow rates and first-aid in simulated peripheral snake or spider envenomation. Med J Aust 1994; 161: 695-700. SPSS [computer program], version 9. Chicago, Ill: SPSS Inc, 1999. (Received 3 Jul, accepted 19 Sep, 2000) Authors' details Department of Emergency Medicine, Cairns Base Hospital, Cairns, QLD. Peter L Pereira, MB BS, FACEM, Director of Emergency Medicine, and Director of C-Airmed; Paul Cullen, BMed, FACEM, Staff Specialist; Richard F Mulcahy, MB BS, Staff Specialist; Mark Little, DTM&H, FACEM, MPH&TM, Staff Specialist. School of Tropical Biology, James Cook University, Cairns, QLD. Teresa Carrette, BSc, Senior Researcher; Jamie Seymour, BSc(Hons), PhD, Lecturer. Reprints will not be available from the authors. Correspondence: Dr P L Pereira, Department of Emergency Medicine, Cairns Base Hospital, PO Box 902, Cairns, QLD 4870. peter_pereiraAThealth.qld.gov.au 1: The experiment Pressure of 40mmHg applied to discharged nematocysts across an amniotic membrane to simulate pressure immobilisation bandages applied to jellyfish stings. Return to text 2: The discharged nematocysts Beads of clear fluid on the shafts of the nematocysts (original magnification x 100) after applying pressure. Return to text 3: Heart rate v time after injection Effect of the three injected solutions on the heart rate of prawns, showing time to ventricular standstill. Solution A = first washings of discharged nematocysts; Solution B = second washings; Solution C = washings after applying 40 mmHg pressure to the discharged nematocysts. Return to text 4: Proposed first-aid management of cuboidal jellyfish stings (including species of Chironex, Chiropsalmus, Carukia and any jellyfish causing "Irukandji" syndrome) Ensure rescuer safety Resuscitate patient as necessary Apply vinegar concomitantly (pour onto the site for at least 30 seconds) Gently apply a vinegar-soaked dressing Do not apply pressure immobilisation bandages Transport patient to the nearest medical facility Provide supportive management as required Return to text

Peter L Pereira · Teresa Carrette · Paul Cullen · Richard F Mulcahy · Mark Little · Jamie Seymour

Medicine and the Community Improving services to bereaved relatives in the emergency department: making healthcare more human Aled G Williams, Debra L O'Brien, Kylie J Laughton and George A Jelinek MJA 2000; 173: 480-483 For editorial comment, see Kissane Abstract - What do relatives want? - The best way to break bad news - The Sir Charles Gairdner Hospital ED bereavement protocol - Conclusions - References - Authors' details - - More articles on Emergency medicine Abstract Death and bereavement are often poorly dealt with in emergency departments. Guidelines exist for optimal care of bereaved relatives. Establishing a limited bereavement program in a busy emergency department is quite feasible. Bereaved relatives appreciate a more "human" approach from hospital staff. Ultimately hospital staff also benefit from confronting issues surrounding death in the emergency department. Sudden death in the hospital emergency department (ED) is highly emotionally charged for relatives and staff. It is difficult to deal sensitively with death in a busy ED. Doctors find dealing with relatives difficult because of poor training in communication, fear of being blamed, a perceived "failure" in their skills, fear of expressing emotion, and their own fears about death.1-3 Death may be glossed over as we move to the next patient in the ever-increasing queue. Talking to the family may be seen as a chore and a waste of precious time on a busy shift. In not confronting these issues, however, we risk increasing job dissatisfaction and burnout.4 We also diminish the "human" side of our role as doctors. For relatives, the death of a loved one is difficult enough to cope with when it is expected. Deaths in an ED are often sudden and unexpected; the environment is confusing and unfamiliar; there may be difficulty getting information; and medical and nursing staff are usually strangers. This occurs in an atmosphere of high stress in which access to the patient may be restricted. All of these factors increase the likelihood that relatives will experience an abnormal grief reaction, with associated threats to physical and emotional wellbeing.5-7 Here we review the current literature on care of unexpectedly bereaved relatives and outline the changes we made in improving this service in our hospital's ED. What do relatives want? Relatives feel helpless and uninformed, and their experience is often negative. What they want during this very stressful time has been documented: to receive prompt attention from staff on arrival and frequent updates on their loved one's condition;6,7 to be with the patient before death, including during resuscitation;8 to know that the patient received prompt and appropriate treatment from prehospital and hospital staff;8 to be informed of the death in a compassionate and unhurried manner;7,8 to be assured that the patient's belongings will be properly handled;6,7 to be told what to do next (eg, how to contact an undertaker; when to go home);7 and to have the opportunity for follow-up with the hospital to answer unresolved questions.6,7 The best way to break bad news Most medical staff find breaking bad news to relatives stressful and draining, but we must not underestimate the importance of our interactions. The family will review the events of the day, including attitudes and responses of staff, again and again for months. Relatives' perceptions can profoundly affect their grief response, positively or negatively.5,7,9 Every family is different and each bereavement experience is unique, so some degree of flexibility is essential. There are, however, well established guidelines (for a summary, see Box). Initial contact with the family. Initial contact with relatives is often made over the phone. A senior doctor or nurse should first identify himself or herself and then the relative answering the phone. In general, the relative should not be told over the phone that the patient has died (if this is the case) -- the caller should simply outline events, say that the patient is very ill and ask the relative to come as soon as possible.5,7,9 The caller should try to ensure that there is somebody with the relative or able to drive them to the hospital. If informing relatives by phone is unavoidable10-12 (eg, if they live a long distance away), the caller should make greater efforts to ensure that the relative receiving the call is not left alone (eg, by asking if there is anyone who can be with the person, or offering to call a friend or relative).5 A member of staff should meet the relatives on arrival, confirm their identity and show them to a private area.7,12,13This should be a comfortably furnished room with access to a telephone. If the patient is undergoing resuscitation, a senior member of staff should explain this early and prepare the relatives for the possibility of death.6 A member of staff should offer to contact a priest or other spiritual counsellor. The family should, if possible, be given the opportunity to witness the resuscitation -- many relatives feel strongly that they should be at the patient's side, or may simply want to confirm that everything possible is being done.6,10 Relatives witnessing the resuscitation should be accompanied by a staff member to explain what is happening and answer questions. Keeping the family informed. A member of staff should stay with the family, giving them frequent updates on the progress of resuscitation.5,7,8 Informing the family of the death. This should be done by the doctor responsible for the patient.5,7 The doctor's presence implies that everything possible was done to save the patient's life. Introducing oneself and sitting down indicates a willingness to spend as much time as the family needs. Next it is important to identify who is in the room and what their relationship is to the deceased. (Friends should generally be asked to wait outside.5,10) The patient should be referred to by name as the doctor establishes what the family already knows, then fills in the details, beginning with what happened to the patient before arrival at the hospital.5,7,10 It is quite appropriate to inform relatives of details, such as the fact that the patient was "unconscious and didn't feel any pain".10,14 When informing relatives of the death, use plain English ("is dead" or "died") rather than euphemisms like "passed away", which some people misinterpret.7,12,13 The doctor's next responsibility is to facilitate grieving.5,7 The initial reaction will probably be shock. The doctor should allow some time for this to ease, but then the family should be encouraged to express feelings and ask questions. It may be best to just sit quietly for a while to share their grief.7 Sometimes it is appropriate to use touch, such as placing a hand on the arm to comfort a relative.10,14 After the initial shock, one of three emotions usually predominates:5 Denial -- this initial defence mechanism should be recognised and tolerated. It can allow time to adjust to the reality of death; Anger -- this may be directed at hospital staff. Usually, once expressed, the anger will diminish; Guilt -- this represents an inward expression of anger. Relatives may blame themselves. A simple statement from the doctor, exonerating the family, can provide much relief in the days and weeks to follow. Viewing the deceased. Most families wish to view or hold the deceased and this can facilitate the grieving process.5,7,10,13 If they do not wish to, this should be accepted.7,13 Medical or nursing staff should spend time preparing the family, especially if the body has been mutilated or if medical apparatus has been left in place for postmortem examination. Staff should remain discreetly to answer questions before withdrawing.7,10,13 Identifying "at risk" family members. Some family members are at greater risk of severe grief reaction, or even suicide, than others. Identifying these relatives can be difficult, but severe grief reactions are more likely to occur in cases where:7,10 the death was sudden or violent (eg, due to suicide or homicide); the person who died was a child; the person who died was a spouse or partner (especially if the relationship involved a high level of conflict or over-dependence); the relative feels he or she may have contributed to the death; the relative is particularly vulnerable because of past psychiatric illness or lack of a support network. Relatives at high risk of experiencing a severe grief reaction should be encouraged to have a friend or relative stay for 1-2 days. Relatives openly expressing suicidal intent, or even psychotic reactions, may require urgent psychiatric intervention. Concluding process. The family should be informed if a postmortem examination is needed. In Australia, coroner's department counselling services can be of assistance. The services of a funeral director need to be engaged and the deceased's personal property handed over to relatives. As relatives may forget much of what is said, it is useful to provide a brochure containing information about the grieving process, notes on practical matters and a list of useful phone numbers.11 Hospital staff should answer final questions and inform the family doctor. Many families need to be given "permission" to go home.7,11 Follow-up. Many relatives appreciate contact with the hospital after they leave.7,10,11 They may need further information to help resolve important issues, and they like to feel that the hospital actually cares. The Sir Charles Gairdner Hospital ED bereavement protocol The protocol Our hospital's bereavement protocol developed from a discussion of "death and dying" at one of our registrar teaching sessions, which made us aware that we could be doing much more to help bereaved relatives. We decided to set up a bereavement program using best practice guidelines.7,15,16We aimed to provide a service that was relatively simple and easily absorbed into existing staff workload, of benefit to relatives and not intimidating to staff. It was also important to make the program as unobtrusive as possible for relatives and to provide some continuity with staff who were present at the time of the person's death (there is some evidence of an adverse effect on grieving if these factors are not taken into account17). The main features of our program were: an education package for medical and nursing staff; intervention of a social worker at the time of death or by written referral out of hours; an information brochure for relatives, containing notes on the grieving process and practical issues, and contact details for useful agencies, including the name and number of the ED social worker; timely notification of the family's general practitioner by phone or fax, immediately or by the next working day; a sympathy card sent to the closest relative, handwritten and signed by the doctor and nurse most closely involved; a follow-up phone call by the social worker at one week to assess needs, and an offer for interview with the doctor involved; a further follow-up phone call at six weeks (relatives had been told that they would be contacted at this stage and were free to decline). The program was administered through the Social Work Department, which was responsible for keeping records of when calls were due and for coordination with medical staff. Practical issues to be dealt with included staff education (and overcoming staff resistance to the program), administration, and managing the extra workload for the social worker and medical and nursing staff. Because of the round-the-clock nature of the service, staff education and notification of the social worker sometimes created difficulties, especially at times of staff changeover. Initially, some staff saw the program as overly intrusive and "none of our business", and some vigorously opposed the idea of sending a sympathy card. These problems were largely overcome when positive reactions from families were fed back to staff, or when staff received direct thanks or cards. The initial problem of locating the appropriate medical and nursing staff to sign cards was solved by getting the head of department or the program's consultant to sign. There was minimal additional workload for medical and nursing staff, most of the extra time being that spent with grieving relatives, once or twice a month. Outcomes Of 37 deaths in the ED in the first seven months of the program, three were not referred to the social worker and were not followed up. All 34 remaining families wished to be enrolled in the program and received a call and a card during the first week after bereavement. Two relatives declined a follow-up phone call at six weeks, feeling they had enough support. Others were very happy with the call at six weeks -- one relative commented that she had looked forward to it for days, while another telephoned to rearrange the timing, as she would be away during the sixth week. Three families requested further interviews. We received much spontaneous positive feedback from relatives. Nearly all expressed gratitude verbally, and 10 relatives sent a written thank you as well. There was even an appreciative letter to the editor published in The West Australian newspaper, and one relative volunteered to join the hospital's Women's Auxiliary. Some comments from relatives were: "I thought that my mother had died alone, as I wasn't at her side. When I got the card and phone calls I realised that she had died among caring strangers, and that was a source of great comfort to me." "It was wonderful to get the card from Dr X. I'm glad my mother died at your hospital where everybody cares." "I've told all my friends that, when they die, your hospital is the place to do it."(!!) Tangible benefits of our program are hard to measure. As well as helping in the grieving process, for many people our program gave a positive image of the hospital as an institution which treated them as people with feelings and not just a "number". We hope this helps to make the face of emergency medical care in our community more "human". We believe it was also a beneficial process for staff. Apart from the formal education, which was positively received, many staff members were surprised by the appreciation shown by relatives. Some had assumed that relatives and patients wanted a formal and "professional" approach to bereavement and had sought to maintain "emotional distance". To their surprise, they found that spending time and commiserating with the family and showing a more "human" side were very well received. Conclusions Setting up a bereavement program is not difficult if staff are motivated. Provided the number of deaths per year in the ED is not excessive, the increased workload is small and easily absorbed. Although difficult to quantify, there are benefits to relatives, staff and the hospital. For us, the most important lesson is that relatives want to be treated with compassion by a caring professional. Being more "human" in our delivery of healthcare may just be beneficial for us as well. References Buckman R. Breaking bad news: why is it still so difficult? BMJ 1984; 288: 1597-1599. Schmidt TA, Tolle SW. Emergency physicians' responses to families following patient death. Ann Emerg Med 1990; 19: 125-128. Seravalli EP. The dying patient, the physician and the fear of death. N Engl J Med 1988; 319: 1728-1730. Honigman B, Armstrong J. Life and death. In: Rosen P, editor. Emergency medicine: concepts and clinical practice. 4th edition. St Louis, Missouri: Mosby, 1998: 197-212. Dubin WR, Sarnoff JR. Sudden unexpected death: intervention with the survivors. Ann Emerg Med 1986; 15: 54-57. Parrish GA, Holdren KS, Skiendzielewski JJ, et al. Emergency department experience with sudden death: a survey of survivors. Ann Emerg Med 1987; 16: 792-796. Walters DT, Tupin JP. Family grief in the emergency department. Emerg Med Clin North Am 1991; 9: 189-206. Fanslow J. Needs of grieving spouses in sudden death situations: a pilot study. J Emerg Nurs 1983; 9: 213-216. Soreff SM. Sudden death in the emergency department: a comprehensive approach for families, emergency medical technicians, and emergency department staff. Crit Care Med 1979; 7: 321-323. Edlich RF, Kubler-Ross E. On death and dying in the emergency department. J Emerg Med 1992; 10: 225-229. Von Bloch L. Breaking the bad news when sudden death occurs. Soc Work Health Care 1996; 23: 91-97. Adamowski K, Dickinson G, Weitzman B, et al. Sudden unexpected death in the emergency department: caring for the survivors. CMAJ 1993; 149: 1445-1451. Olsen JC, Buenefe ML, Falco WD. Death in the emergency department. Ann Emerg Med 1998; 31: 758-764. Hamilton GC. Sudden death in the ED: telling the living. Ann Emerg Med 1988; 17: 382. Yates DW, Ellison G, McGuiness S. Care of the suddenly bereaved. BMJ 1990; 301: 29-31. Coolican MB, Pearce T. After care bereavement program. Crit Care Nurs Clin North Am 1995; 7: 519-527. Williams WV, Polak PR. Follow up research in primary prevention: a model of adjustment in acute grief. J Clin Psychol 1979; 35: 35-45. Authors' details Emergency Department, Sir Charles Gairdner Hospital, Perth, WA. Aled G Williams, MB ChB, FACEM, Emergency Physician. Debra L O'Brien, MB BS, FACEM, Emergency Physician. Kylie J Laughton, BA, BSocWk, Emergency Department Social Worker. George A Jelinek, MD, FACEM, Professor and Chairman, Emergency Medicine, University of Western Australia. Reprints will not be available from the authors. Correspondence: Dr A G Williams, Emergency Department, Sir Charles Gairdner Hospital, Verdun Street, Nedlands, WA 6009. aled.williamsAThealth.wa.gov.au Make a comment Recommended actions for medical and nursing staff in dealing with grieving relatives Contacting family Request family's urgent attendance Do not inform of death over phone Arrival of family Show to private room with phone Give prompt update on patient's condition Offer spiritual or other counsellor During resuscitation Stay with family Give regular updates Allow relatives to be with patient After death Inform family in an unhurried manner Facilitate grieving Identify "at risk" relatives Allow deceased to be viewed Concluding process Attend to "formalities" (eg, coroner) Give brochure containing useful information and contact numbers Address final questions Follow-up Contact general practitioner Send sympathy card Make phone call at one and six weeks, as appropriate Allow opportunity for interview with treating doctor to address unanswered questions Back to text

Aled G Williams · Debra L O'Brien · Kylie J Laughton · George A Jelinek

Editorial The medical emergency team: no evidence to justify not implementing change Given the lack of evidence on the effect of the MET system, what should we do? MJA 2000; 173: 228-229 Any senior doctor, on quiet reflection, will recall times as a junior doctor when his or her treatment of an acutely unwell patient in hospital was less than ideal, either because of lack of knowledge, inexperience, or inadequate procedural skills. Many of these patients had delayed diagnosis and treatment, but survived in spite of (our) incompetence; others "did not do well". This reality has provided material for popular entertainment, including Doctor in the house,1The house of God,2 and the more recent television medical dramas. In the real world, the challenge of ensuring appropriate and effective treatment of acutely ill hospital patients has been politely ignored. There is a prevailing culture of acceptance that it has always been thus, and is an unfortunate result of the need for the young doctors to gain experience. This "blind eye" attitude is becoming harder to sustain in the face of growing evidence of the magnitude of the problem. The high rate of preventable adverse events in hospitals has been well documented in studies such as the Harvard Medical Practice Study3 and the Quality in Australian Health Care Study.4 Further, studies of inpatients admitted to intensive care units have shown that suboptimal diagnosis and treatment before admission is common.5-7 In the face of this evidence, various efforts to improve the performance of junior medical staff have been made. More consultant involvement, formal training of junior medical staff, greater development of acute care guidelines, and cross-specialty audit and peer review have also been supported.6,8 Those not wishing to change can claim there is no evidence to justify changing... Those who wish to change can claim there is no evidence to justify not changing. A different approach, which amounts to a "re-engineering" of the treatment process for acutely ill inpatients, has been the development of the medical emergency team (MET).9 This has been simply described as a renaming of the cardiac arrest team, together with a widening of calling criteria, so that the team can be called (by the ward nurse) for any patient who is acutely unwell. This is a useful summary description, although the MET system includes a number of other important aspects. These include development of evidence-based criteria for diagnosing the acutely unwell patient, formalised training and inservicing for both the team and the ward nurses, ongoing audit and quality improvement, and institutional supervision. The system has some similarities to the trauma team concept, which became generally introduced a decade ago. Since the introduction of portable defibrillation, comprehensive efforts to improve survival after inhospital cardiac arrest have been disappointing in their effect.10 The appeal of a strategy of early intervention is hard to deny. The concept of the MET system is intuitively appealing to many, and has attracted interest locally (in the National Demonstration Hospital Program)11 and internationally.12,13 But does it work? In this issue of the Journal, Bristow and colleagues attempt to provide an answer.14 In a complex study using innovative statistical methods, they have compared patient outcomes in three hospitals, one of which has had the MET system in place for six years. The study has not clearly demonstrated any difference in death rates associated with the MET system; they conclude there may be a reduction in unplanned admissions to the intensive care unit (ICU). There are a number of methodological shortcomings in this study. Comparison of performance between hospitals is difficult, and casemix adjustment is imperfect at best. Casemix adjustment does not include socioeconomic differences in patient population, funding levels, staffing ratios, medical and nursing staff expertise, and "cultural" differences between hospitals. It is notable that the casemix-adjusted death rate differs markedly between the two non-MET hospitals in the study, presumably because of these and other factors. This difference is of such magnitude that any effect of the MET team (if there is one) is likely to be overwhelmed. The rate of "do not resuscitate" orders appears to be higher in the MET hospital. Admission criteria for ICU may differ between hospitals. The MET team appears to be underutilised in the intervention hospital, while the control hospitals that chose to participate in the study may already emphasise the importance of responding to acutely ill inpatients, reducing the potential benefit of the MET system. Other outcomes could be considered, including the effectiveness of treatment for non-ICU patients, and stress or satisfaction among nursing and medical staff. Many of these shortcomings are unavoidable, and the authors have attempted to address their hypothesis using appropriate methods. They are to be congratulated on this courageous attempt to provide an answer to the difficult issue of the effectiveness of the MET system. This study has produced neither a positive nor a negative result -- it has shown how difficult getting a clear result will be. This is disappointing, but is not surprising given the complexity of the study. Even with the best methodology, it may not be possible to quantify the effect of the MET system. Hospitals are "chaotic" systems, and may be impervious to analysis using linear methodology. In this and other areas, it may be futile to attempt to go beyond qualitative research, despite the lack of traditional respectability of non-quantitative methods. This problem has been powerfully discussed by Runciman,15 among others. Given this lack of "evidence" that the MET system achieves different patient outcomes to the traditional "system" of responding to acutely ill patients, what should be done? Medical traditionalists will advocate no change. The MET system bypasses the traditional medical hierarchy, and it may be claimed that this will "deskill" the junior medical staff. The cost of the MET system is unclear, but ICUs will claim that it increases their workload (although it may reduce ICU admissions). Other objections may relate to the internal politics of hospitals: the MET system empowers nursing staff to involve medical officers other than those nominally working for the admitting medical officer who "owns" the patient. Those not wishing to change can claim there is no evidence to justify changing. In contrast, those who support the MET system will claim that the inevitable delays in the hierarchical system and the lack of skills among junior medical staff make the traditional system inherently inadequate. The MET system is claimed to be an appropriate way to deal with this, intuitively more rational, and a more efficient system for ensuring rapid and appropriate interventions for acutely ill inpatients. Institutional supervision, audit and quality improvement is facilitated. Those who wish to change can claim there is no evidence to justify not changing. The debate is not just between these two extremes. There are important issues still to be resolved, such as the appropriate composition and leadership of the MET, skill and training requirements, and the relative merits of the various specialties that could be involved. The debate includes passionate views about the skills of medical registrars, the importance of keeping management of the patient under the sole control of the admitting team (which is presumed to be omnipresent), and the potential for improving the current system by better emergency protocols and staff training. The situation is very reminiscent of the controversy and debate about the introduction of the trauma team. The deficiencies of existing in-hospital trauma care were recognised for many years,16 but the introduction of trauma teams was debated with many of the same arguments now used about the MET.17 What would the patients -- the general public -- think? Outside of hospitals, an untrained lay person can summon ambulances, paramedics and even helicopters for an acutely ill person. Their calls are monitored and recorded. On the patient's arrival in the emergency department, a structured patient triage system is used to optimise efficiency and outcomes. The performance of this emergency system is audited and analysed. In recent years questions in Parliament, Commissions of Inquiry, and (perhaps) contribution to a change of government have followed reports of inadequate speed or quality of response by out-of-hospital emergency services, and in emergency departments. The contrast with the traditional in-hospital system, based on a university-trained nurse summoning the most junior medical officer as the start of an emergency response, and without systematic institutional supervision, audit, and quality improvement, seems incongruous. The general public, increasingly aware of reports of the inadequacies of hospitals, may be bemused by the persistence of the traditional model of emergency response in hospitals, which is little changed from a century ago. The current unsatisfactory situation requires action. The available evidence does not provide clear direction. The MET system is a rational and reasonable change that may improve patient care, and is unlikely to make things worse. Those who support the traditional model should produce evidence on which to base their resistance to change. In the absence of such evidence, the widespread introduction of the Medical Emergency Team system should proceed. Ross K Kerridge Anaesthetist, John Hunter Hospital Newcastle, and Editorial Chair Australian Resource Centre for Hospital Innovation (www.archi.net.au) mdrkkATcc.newcastle.edu.au Gordon R. Doctor in the house. London: Michael Joseph, 1952. Shem S. The house of God. London: Bodley Head, 1978. Brennan TA, Leape LL, Laird N, et al. Incidence of adverse events and negligence in hospitalised patients: results of the Harvard Medical Practice Study I. N Engl J Med 1991; 324: 370-376. Wilson R McL, Runciman WB, Gibberd RW, et al. The Quality in Australian Health Care Study. Med J Aust 1995; 163: 458-471. McGloin H, Adam S, Singer M. The quality of pre-ICU care influences outcome of patients admitted from the ward. Clin Intensive Care 1997; 8: 104. McQuillan P, Pilkington S, Allan A, et al. Confidential inquiry into quality of care before admission to intensive care. BMJ 1998; 316: 1853-1858. Smith AF, Wood J. Can some in-hospital cardio-respiratory arrests be prevented? A prospective survey. Resuscitation 1998; 37: 133-137. Leah V, Coats TJ. In-hospital resuscitation -- what should we be teaching? Resuscitation 1999; 41: 179-183. Lee A, Bishop G, Hillman KM, Daffurn K. The Medical Emergency Team. Anaesth Intens Care 1995; 23: 183-186. Varon J, Marik PE, Fromm RE. Cardiopulmonary resuscitation: a review for clinicians. Resuscitation 1998; 36: 133-145. Commonwealth Department of Health and Aged Care. A qualitative review of the National Demonstration Hospital Program Phase 2. Canberra: Commonwealth of Australia, 1999. Available at <http://www.health.gov.au:80/hsdd/acc/ndhp/ pubs/ndhp2review.htm>. Garrard C, Young D. Suboptimal care of patients before admission to intensive care. BMJ 1998; 316: 1841-1842. Singer M, Little R. ABC of Intensive Care: Cutting edge. BMJ 1999; 319: 501-504. Bristow PJ, Hillman KM, Chey T, et al. Rates of in-hospital arrests, deaths and intensive care admissions: the effect of a medical emergency team. Med J Aust 2000; 173: 236-240. Runciman WB. Qualitative versus quantitative research -- balancing cost, yield, and feasibility. Anaesth Intens Care 1993; 21: 502-505. Hoffman E. Mortality and morbidity following road accidents. Ann R Coll Surg Engl 1976; 58: 233-240. Spencer JD. Why do our hospitals not make more use of the concept of a trauma team? BMJ 1985; 290: 136-138. Make a comment

Ross K Kerridge

Research Rates of in-hospital arrests, deaths and intensive care admissions: the effect of a medical emergency team Peter J Bristow, Ken M Hillman, Tien Chey, Kathy Daffurn, Theresa C Jacques, Sandra L Norman, Gillian F Bishop and E Grant Simmons MJA 2000; 173: 236-240 Abstract - Methods - Results - Discussion - Conclusion - Acknowledgements Authors' details - - More articles on Emergency medicine Abstract Objectives: To evaluate the effectiveness of a medical emergency team (MET) in reducing the rates of selected adverse events. Design: Cohort comparison study after casemix adjustment. Patients and setting: All adult (≥ 14 years) patients admitted to three Australian public hospitals from 8 July to 31 December 1996. Intervention studied: At Hospital 1, a medical emergency team (MET) could be called for abnormal physiological parameters or staff concern. Hospitals 2 and 3 had conventional cardiac arrest teams. Main outcome measures: Casemix-adjusted rates of cardiac arrest, unanticipated admission to intensive care unit (ICU), death, and the subgroup of deaths where there was no pre-existing "do not resuscitate" (DNR) order documented. Results: There were 1510 adverse events identified among 50 942 admissions. The rate of unanticipated ICU admissions was less at the intervention hospital in total (casemix-adjusted odds ratios: Hospital 1, 1.00; Hospital 2, 1.59 [95% CI, 1.24-2.04]; Hospital 3, 1.73 [95% CI, 1.37-2.16]). There was no significant difference in the rates of cardiac arrest or total deaths between the three hospitals. However, one of the hospitals with a conventional cardiac arrest team had a higher death rate among patients without a DNR order. Conclusions: The MET hospital had fewer unanticipated ICU/HDU admissions, with no increase in in-hospital arrest rate or total death rate. The non-DNR deaths were lower compared with one of the other hospitals; however, we did not adjust for DNR practices. We suggest that the MET concept is worthy of further study. Certain in-hospital deaths may be preventable.1-3 Nearly 85% of hospital inpatients who suffer a cardiorespiratory arrest have documented observations of deterioration in the eight hours before the arrest.4,5 Recent studies have demonstrated suboptimal care of hospitalised patients before their admission to the intensive care unit (ICU), and that these patients have a higher mortality.6-8 The authors of these studies urge earlier intervention. One approach to providing an early response to at-risk inpatients throughout the hospital is the medical emergency team (MET),9,10 which replaces the conventional cardiac arrest team. The MET responds to specific clinical criteria (such as bradycardia, tachycardia, hypotension and threatened airway) in order to prevent further deterioration. Others have advocated similar approaches to reduce unexpected hospital deaths and morbidity.11,12 In our study, selected outcomes in a hospital with a MET were compared with outcomes in two hospitals with conventional cardiac arrest teams. These outcomes were rates of cardiorespiratory arrest, unanticipated admission to the ICU or high dependency unit (HDU), death, and deaths where there was no prexisting "do not resuscitate" (DNR) order. Methods This study was a prospective cohort comparison of three hospitals, testing whether an early intervention team, the MET, was associated with fewer adverse events among inpatients, after adjusting for casemix differences. The study was approved by the ethics committees of each participating hospital and the University of New South Wales. Setting The hospitals were similarly sized Australian public hospitals, with bed capacities in the range 380-530. At Hospital 1, the cardiac arrest team was replaced by a MET, which any staff member could call for immediate assistance. Staff could summon the MET if concerned about a patient's condition or if the patient's vital signs exceeded certain levels (Box 1).10 An education program explained the MET's role to all new staff. However, calling the MET when criteria were met was not compulsory. The MET consisted of the ICU registrar and senior nurse, and medical registrar. At Hospitals 2 and 3, the arrest team was paged by nursing or medical staff for cardiorespiratory arrest. The arrest team consisted of the ICU registrar, medical registrar, and ICU or coronary care nurse. Data collection We identified all cardiorespiratory arrest calls, deaths, and ICU/HDU admissions at the three hospitals among patients 14 years and over in hospital during the period from 8 July to 31 December 1996. These were designated "events". Soon after an event, the patient's medical record was reviewed for demographic information. In addition, for cardiac arrests and deaths, documentation of a DNR order before arrest or death was recorded. Each ICU/HDU admission was classified as to whether the patient was admitted to ICU/HDU for the same reason he or she was admitted to hospital. If not, the ICU/HDU admission was defined as unanticipated. For example, a patient admitted to ICU with respiratory distress after a cholecystectomy would be unanticipated. Data were collected by three critical care nurses (one at each hospital) trained in the use of a specifically designed form, which was piloted for two weeks before data collection. The nurses were familiar with the medical record at the three hospitals. Where the information contained in the history was unclear, the attending staff were asked for clarification. Data were entered into a database.13 Data cleaning was performed and any anomalies checked by reference to the datasheet or medical record. Data were then exported to SAS14 for analysis. Outcome measures The primary endpoints were the casemix-adjusted rates of ICU/HDU unanticipated admission, cardiac arrest, death, and deaths without a prior DNR order. These were called "total event rates". For any patient, one event could result in additional events (eg, cardiac arrest followed by unanticipated ICU admission and then death). The "index event" was defined as the event the data collectors considered the first in a series of events. The casemix-adjusted rates of index events were compared between the three hospitals as secondary endpoints. To ensure that any decline in the rate of unanticipated admissions was not caused by excess anticipated admissions, the casemix-adjusted rate of all ICU/HDU admissions was calculated as a control measure. Casemix adjustment Demographic and diagnostic data on the patient population (aged ≥ 14 years) admitted to the hospitals for the period were obtained. The study data were merged by medical record number and date of admission with the complete inpatient statistical data to create a dataset with 50 942 records. This enabled us to identify the admissions for which an event occurred and analyse the data at the patient level. Using simple and multiple logistic regression, we modelled the probability of an event occurring during hospitalisation, adjusted for patient demographics and diagnostic characteristics. Models were derived independently for each total event and for each index event. Parameters were added to the model in a stepwise fashion. To prevent overparameterising the models (where minor, non-significant differences cumulatively hide true differences), when C (equivalent to the area under the receiver operator characteristics curve) reached 0.85 no further parameters were added to the model. This always occurred with fewer than six parameters used. Demographic and casemix independent variables that were tested for use in the models are detailed in Box 2. The models developed used groups of diagnostic categories based on ICD-9-CM codes using the principal diagnosis and the stay diagnosis only.15 The ICD-9-CM code groupings used are available from the principal author (PJB). The performance of the models was assessed by Hosmer-Lemeshow goodness-of-fit tests.16 The risk of an event occurring in a hospital compared with the MET hospital was presented as an adjusted odds ratio with 95% confidence intervals. A level of significance of 5% was used in all statistical tests. Results Hospital demographics Characteristics of all patients (aged ≥ 14 years) admitted to the three hospitals during the study period are shown in Box 3. Hospital 2 had fewer admissions than the other hospitals. Hospital 1 had a higher proportion of male patients admitted, and a lower proportion of admissions from the emergency department (ED). This hospital also had a younger patient population, which is reflected in differences in casemix: Hospital 1 had lower proportions of patients with stroke, severe acute heart disease, gastrointestinal disease, and musculoskeletal and connective tissue diseases, but higher proportions with severe trauma and follow-up care without acute diagnosis (eg, dialysis). The rates of DNR orders in dying patients were 77% in Hospital 1, and 64% and 70% in Hospitals 2 and 3, respectively (P = 0.006). Prevalence and characteristics of events A total of 1510 adverse events (unanticipated ICU/HDU admissions, arrest calls, and deaths) were recorded during the study period for the three hospitals. There were 1100 index events. The prevalence and characteristics of events are summarised in Box 4 for total event rates and Box 5 for index rates. There was a significantly reduced rate of unanticipated ICU/HDU admissions at the MET intervention hospital after casemix adjustment (for both the total event rate and the index rate). After adjustment, Hospital 2 had 49 (95% CI, 20-87) more unanticipated ICU/HDU admissions over a six-month period, and Hospital 3 had 92 (95% CI, 47-146) more, compared with Hospital 1. The rate of all ICU/HDU admissions was lower at Hospital 1 than at one control hospital, and trended to lower than at the other. There was no statistically significant difference in cardiac arrest rate or death rate after casemix adjustment. The casemix-adjusted death rate in patients where there was no documentation found of a DNR order was significantly higher at Hospital 2, translating to 27 (95% CI, 7-53) extra non-DNR deaths. Model performance Box 6 presents an example of the odds ratios after addition of the most significant variables in the multiple logistic regression models derived from the data for the total arrest data. It shows the C statistic as each variable was added to the cardiac arrest model. In the cardiac arrest models, the variables that were adjusted for were emergency admissions, age over 74, heart disease, lung disease and infectious disease as diagnoses. In the total death models, the terms adjusted for were emergency admissions, age over 74, single day stay emergency admissions, and cancer and infectious disease. The same demographic variables were used in the index death model, although in the total non-DNR death model both age ≥ 75 and age 65-74 were used in the model. In the unanticipated ICU/HDU models, the variables adjusted for were single day admission, emergency admission, and cancer and gastrointestinal disease diagnoses. The total unanticipated ICU/HDU model also included the variables stroke and infectious disease as diagnoses. All models satisfied the Hosmer- Lemeshow test.16 Discussion Rationale for our methods In this study, we attempted to determine if the MET system was associated with a reduced rate of adverse events among inpatients. To do this, we compared the rates of adverse events between three hospitals after casemix adjustment.17-19 This method was chosen as we decided that randomisation at the patient level was impractical. A random pattern of response to calls would probably have dissuaded staff caring for patients from calling the MET. Randomisation by ward would have risked contamination bias and engendered problems of casemix, as wards differ in the nature of their patients. Historical comparison at Hospital 1 between a period before and a period after introduction of the MET team was impractical, as the team had been trialled and evolved for six years before the study. The models we used appear to adequately fit the data, according to the Hosmer-Lemeshow goodness-of-fit tests, and with good model performance measured by C statistics. However, multiple methods of casemix adjustment are possible, and these may give divergent results. This is a limitation of casemix adjustment methodology.20 To avoid concealing real differences by excessive modelling, parameters were added stepwise by multivariate analysis until the models reasonably represented the data. The terms which appeared in the final models were usually those that could be expected to influence the outcomes. Thus, advanced age and emergency admissions were factors in the death and cardiac arrest models. The cardiac arrest models also included the terms for heart disease, lung and infectious disease. Infectious disease was an unexpected variable and was also significant in the total death model. Other differences (such as levels of hospital funding, ICU/HDU capacity, the number and seniority of medical and nursing staff, and the level of out-of-hours cover) may also have contributed to the results. However, to adjust for these would have been more difficult than for the variables studied, which relate directly to the patients at risk and are easily and reliably obtained. Explanation of findings After casemix adjustment, we found reduced rates of both total and index unanticipated ICU/HDU admissions at the MET intervention hospital. There were no differences in the rates of cardiac arrests or deaths. However, at one hospital without the MET, there was a higher rate of non-DNR deaths, the subset of deaths most likely potentially preventable by a MET. The reduction in unanticipated ICU/HDU admissions that was seen in the MET intervention hospital could result from many factors. One possible explanation is that the MET was effective and able to intervene on the wards and prevent further deterioration. Another possible reason may relate to differences in referral practices: perhaps the presence of MET backup engendered a feeling that ICU/HDU referral was not needed. Misclassification of ICU/HDU admissions as anticipated rather than unanticipated was excluded as an explanation of the difference by the finding that the rate of all ICU/HDU admissions was lower at the intervention hospital than one control hospital and trended to lower at the other. The lack of efficacy of the MET to prevent cardiorespiratory arrest and modify death rate may be related to lack of sensitivity of calling criteria, or because pathophysiological processes (eg, shock) become irreversible. Another possible explanation for the lack of effect of the MET on event rates is underutilisation. Based on a previous study,21 up to 706 MET calls could have been expected, and yet only 150 were made. Frequent education is probably also required to ensure the appropriate calling of a MET.22 No special efforts regarding staff education in the study period were made. The clinical staff of the hospital were unaware of the study, to negate any possible Hawthorne effect.23 Finally, organisational changes such as introduction of a MET are difficult to implement in hospitals.24,25 Our results probably reflect the effectiveness of the implementation of the MET system as much as the concept of early intervention. Future directions Our study cannot answer definitively if the MET was the cause of the benefit we observed; it does show that the MET concept is worthy of further study. The study could be likened to a Phase II trial of a drug comparing three hospitals at one point in time. Further studies of the MET system's efficacy are needed, such as a before-after comparison in several hospitals, or a comparison of a larger sample size of intervention and control hospitals. Such studies should be repeated some time after the intervention. Is the benefit observed useful and worth pursuing? If it is possible to reduce unanticipated ICU admissions without increased mortality this may result in cost saving. It has been estimated that the US spends about 1% of its gross national product on intensive care facilities.26 However, any savings in intensive care would be offset by the cost of establishing and maintaining a MET. The MET may also have unexpected costs and benefits on processes such as staff satisfaction with care provided. Again, these need to be quantified. Conclusion In this study, we found that fewer patients were unexpectedly admitted to ICU or HDU at a hospital with the MET system, and this hospital had fewer non-DNR deaths than one of the other hospitals. There was no significant change in the casemix-adjusted rate of arrests or total deaths. This may be an advantage of an early response team, which could have important implications for patient care in hospitals. We believe that the MET concept should be studied further in a larger sample of institutions. Acknowledgements Funding for the study was provided by a Commonwealth Department of Health and Family Services Research and Development Grant (HS338). Associate Professor Robert Gibberd assisted with the statistical analysis. References Brennan TA, Leape LL, Laird N, et al. Incidence of adverse events and negligence in hospitalised patients: results of the Harvard Medical Practice Study I. N Engl J Med 1991; 324: 370-376. Leape LL, Brennan TA, Laird N, et al. Nature of adverse events in hospitalised patients: results of the Harvard Medical Practice Study II. N Engl J Med 1991; 324: 377-384. Wilson R McL, Runciman WB, Gibberd RW, et al. The Quality in Australian Health Care Study. Med J Aust 1995; 163: 458-471. Schein RMH, Hazday N, Pena M, et al. Clinical antecedents to inhospital cardiopulmonary arrest. Chest 1990; 98: 1388-1392. Franklin C, Mathew J. Developing strategies to prevent inhospital cardiac arrest: analyzing responses of physicians and nurses in the hours before the event. Crit Care Med 1994; 22: 246-247. Lundberg JS, Perl TM, Wiblen T, et al. Septic shock: an analysis of outcomes for patients with onset on hospital wards versus intensive care units. Crit Care Med 1998; 26: 1020-1024. Goldhill DR, Sumner A. Outcome of intensive care patients in a group of British intensive care units. Crit Care Med 1998; 26: 1337-1345. McQuillan P, Pilkington S, Allan A, et al. Confidential inquiry into quality of care before admission to intensive care. BMJ 1998; 316: 1853-1858. Lee A, Bishop G, Hillman KM, Daffurn K. The medical emergency team. Anaesth Intensive Care 1995; 23: 183-186. Hourihan F, Bishop G, Hillman KM, et al. The medical emergency team: a new strategy to identify and intervene in high risk patients. Clin Intensive Care 1995; 6: 269-272. Frank ED. A shock team in a general hospital. Anesth Analg 1967; 46: 740-745. Goldhill DR. Introducing the postoperative care team [editorial]. BMJ 1997; 314: 389. Microsoft Access [computer program]. Version 2.0. Redmond, Wa: Microsoft, 1994. SAS for Windows [computer program]. Version 6.12. Cary, NC: SAS Institute Inc, 1997. Stremple JF, Bross DS, Davis CL, McDonald GO. Comparison of postoperative mortality and morbidity in VA and nonfederal hospitals. J Surg Res 1994; 56: 405-416. Hosmer DW, Lemeshow S. Applied logistic regression. New York: John Wiley and Sons, 1989. Iezzoni LI. The risks of risk adjustment. JAMA 1997; 278: 1600-1607. Dubois RW, Rogers WH, Moxley JH, et al. Hospital inpatient mortality. Is it a predictor of quality? N Engl J Med 1987; 317: 1674-1680. Green J, Passman LJ, Wintfield N. Analyzing hospital mortality. The consequences of diversity in patient mix. JAMA 1991; 265: 1849-1853. Iezzoni LI, Shwartz M, Ash A, et al. Severity measurement methods and judging hospital death rates for pneumonia. Med Care 1996; 34: 11-28. Hillman KM, Bishop G, Lee A, et al. Identifying the general ward patient at high risk of cardiac arrest. Clin Int Care 1996; 7: 242-243. Daffurn KD, Lee A, Hillman KM, et al. Do nurses know when to summon emergency assistance? Intensive Crit Care Nurs 1994; 10: 115-120. Grufferman S. Complexity and the Hawthorne effect in community trials [editorial]. Epidemiology 1999; 10: 209-210. Garside P. Organisational context for quality: lessons from the fields of organisational development and change management. Qual Health Care 1998; 7 Suppl: S8-15. Koeck C. Time for organisational development in healthcare organisations [editorial]. BMJ 1998; 317: 1267-1268. Cerra FB. Healthcare reform: the role of coordinated critical care. Crit Care Med 1993; 21: 457-464. (Received 15 Feb, accepted 10 Jul, 2000) Authors' details Liverpool Hospital, Sydney, NSW. Peter J Bristow, MB BS, FRACP, Staff Specialist, Department of Intensive Care; Ken M Hillman, MB BS, FFICANZCA, Professor, University of New South Wales Clinical School; Kathy Daffurn, RN, MAppSc, Co-Director, Division of Critical Care; Sandra L Norman, MN, BAppSc, Clinical Nurse Specialist, Department of Intensive Care; Gillian F Bishop, MB ChB, FFICANZCA, Director, Department of Intensive Care; Tien Chey, BSc, MAppStat, Statistician, Epidemiology Unit. Department of Intensive Care, St George Hospital, Sydney, NSW. Theresa C Jacques, MB BS, FFICANZCA, Director. Department of Intensive Care, Illawarra Regional Hospital, Wollongong, NSW. E Grant Simmons, MB BS, FFICANZCA, Director. Reprints will not be available from the authors. Correspondence: Dr P J Bristow, Intensive Care Offices, Alfred Hospital, Commercial Road, Prahran, VIC 3181. p.bristowATalfred.org.au Make a comment 1: Criteria for calling the medical emergency team10 Cardiorespiratory arrest Threatened airway Respiratory rate ≤5 breaths per minute ≥36 breaths per minute Pulse rate ≤40 beats per minute ≥140 beats per minute Systolic blood pressure ≤90mmHg Repeated or prolonged seizures Fall in Glasgow Coma Score >2 points Concern about patient status not detailed above Back to text 2: Variables available for calculation of the various models Sex (binary) Seven age categories (14-24, 25-34, 35-44, 45-54, 55-64, 65-74, ≥75) Same-day admission (binary) (ie, admission and discharge occurred on the same calendar day) Referral from emergency department (binary) Australian born (binary) Casemix categories (16 indicator variables, available from author) Hospital (three indicator variables) Back to text 3: Characteristics of admissions at the three study hospitals from 8 July to 31 December 1996 Hospital* Characteristic 1 2 3 Test of Independence† Number of admissions 18338 13059 19545 Male admissions 44.9% 42.9% 42.8% χ2=21.06‡ (2 df) Same-day admissions 47.7% 47.0% 46.7% χ2=4.35 (2 df) Admission via emergency department 29.6% 36.0% 35.1% χ2=186.53‡ (2 df) Australian born Country of birth not stated 49.3% 6.8% 67.2% 0.5% 50.2% 23.2% Not tested Age distribution 14-24 25-34 35-44 45-54 55-64 65-74 ≥75 9.7% 14.9% 14.3% 12.4% 18.1% 20.5% 10.0% 8.6% 15.2% 9.6% 9.8% 18.5% 22.2% 16.0% 7.8% 13.1% 11.1% 10.4% 14.4% 22.1% 21.1% χ2=1146‡ (12 df) Diagnostic category 1. Cancer 2. Stroke 3. Severe acute heart disease 4. Metabolic and electrolyte disorders 5. Pulmonary disease 6. Ophthalmologic disease 7. Low risk heart disease 8. Gastrointestinal disease 9. Urologic disease 10. Musculoskeletal, connective tissue disease 11. Infectious diseases 12. Symptoms and ill-defined conditions 13. Severe trauma 14. Follow-up care without acute diagnosis 15. Pregnancy, childbirth, puerperium 16. Others 4.4% 1.4% 2.6% 1.3% 3.3% 2.0% 3.5% 6.4% 1.9% 1.8% 1.0% 3.2% 2.9% 34.0% 10.8% 19.5% 4.1% 1.8% 3.0% 1.6% 2.9% 1.2% 2.9% 8.9% 1.7% 3.4% 0.7% 3.0% 2.1% 30.1% 14.1% 18.5% 5.3% 1.6% 3.2% 1.1% 4.2% 0.5% 4.6% 10.2% 1.9% 3.2% 1.0% 6.7% 1.8% 23.4% 11.0% 20.5% χ2=1562‡ (50 df) *Hospital 1 had the medical emergency team. †Test for any difference between the three hospitals. ‡P Back to text 4: Comparisons of total event rates by hospitals Event n Crude rates/10000 Unadjusted ORs Adjusted ORs* Cardiac arrest Hospital 1 Hospital 2 Hospital 3 69 66 99 38 51 51 1.00 1.34 (0.96-1.89) 1.35 (0.99-1.83) 1.00 1.14 (0.81-1.61) 1.00 (0.73-1.37) Death Hospital 1 Hospital 2 Hospital 3 243 240 295 133 184 151 1.00 1.39 (1.16-1.67) 1.14 (0.96-1.35) 1.00 1.08 (0.89-1.30) 0.83 (0.70-1.00) Non-DNR death Hospital 1 Hospital 2 Hospital 3 55 86 88 30 66 45 1.00 2.20 (1.57-3.09) 1.50 (1.07-2.11) 1.00 1.68 (1.19-2.36) 0.94 (0.67-1.33) Unanticipated ICU/HDU admission Hospital 1 Hospital 2 Hospital 3 118 146 234 64 112 120 1.00 1.73 (1.36-2.21) 1.86 (1.49-2.32) 1.00 1.59 (1.24-2.04) 1.73 (1.37-2.16) *Odds ratios (ORs) adjusted for patient characteristics and diagnostic categories. Hospital 1 (which has the medical emergency team) is the reference for the ORs. For shaded ORs, 95% CIs do not cross 1.0. DNR="do not resuscitate" order documented. ICU=intensive care unit. HDU=high dependency unit. Back to text 5: Comparisons of index event rates by hospitals Event n Crude rates/10000 Unadjusted ORs Adjusted ORs* Cardiac arrest Hospital 1 Hospital 2 Hospital 3 60 63 84 33 48 43 1.00 1.48 (1.04-2.10) 1.31 (0.94-1.83) 1.00 1.24 (0.87-1.78) 0.96 (0.69-1.35) Death Hospital 1 Hospital 2 Hospital 3 119 139 191 65 106 98 1.00 1.65 (1.29-2.11) 1.51 (1.20-1.90) 1.00 1.24 (0.97-1.60) 1.05 (0.82-1.33) Unanticipated ICU/HDU admission Hospital 1 Hospital 2 Hospital 3 82 140 222 45 107 114 1.00 2.41 (1.83-3.17) 2.56 (1.98-3.30) 1.00 2.17 (1.65-2.87) 2.35 (1.82-3.04) *Odds ratios (ORs) adjusted for patient characteristics and diagnostic categories. Hospital 1 (which has the medical emergency team) is the reference for the ORs. For shaded ORs, 95% CIs do not cross 1.0. ICU=intensive care unit. HDU=high dependency unit. Back to text 6: An example of how the odds ratios and C statistic changed as variables were added stepwise to the model for total cardiac arrests Odds ratio* (95% CI) Hospital 2 Hospital 3 C statistic Crude odds ratio Admission via emergency department Age ≥75 years Severe acute heart disease Low risk heart disease Infectious disease Pulmonary disease 1.34 (0.96-1.89) 1.16 (0.83-1.63) 1.06 (0.75-1.49) 1.06 (0.75-1.49) 1.07 (0.76-1.50) 1.09 (0.77-1.53) 1.14 (0.81-1.61) 1.35 (0.99-1.83) 1.19 (0.87-1.62) 0.98 (0.72-1.34) 0.99 (0.72-1.35) 0.99 (0.72-1.35) 1.00 (0.73-1.37) 1.00 (0.73-1.37) 0.533 0.755 0.798 0.809 0.826 0.833 0.850 *Hospital 1 is the reference for the odds ratios. Back to text

Peter J Bristow · Ken M Hillman · Tien Chey · Kathy Daffurn · Theresa C Jacques · Sandra L Norman · Gillian F Bishop

Editorial Falls in the elderly: what can be done? We need to streamline referral to falls programs and coordinate services within and outside hospitals MJA 2000; 173: 176-177 Falls are often referred to as one of the "geriatric giants", generating diagnostic and rehabilitative dilemmas for a variety of specialists in a range of settings. In older people, falls are associated with significant mortality and morbidity and frequently lead to a decline in physical and/or psychological function, ultimately encroaching on independence and autonomy. In addition to the costs to the individual and immediate carers, falls consume significant resources in terms of hospital admissions, bed utilisation, and use of other health and allied services. With an ageing population, the problems associated with falls and injury will escalate unless there is a coordinated and effective approach to prevention and intervention. Given that most falls result from a dynamic interaction between intrinsic and extrinsic factors, a multidisciplinary approach to their management -- incorporating medical, functional, and environmental assessment -- is likely to be most rewarding. To date, there is limited evidence to support a population-based preventive strategy -- it thus becomes imperative to focus on high-risk groups with the potential to benefit. For any falls prevention strategy to be effective and of direct clinical relevance, it should: be acceptable and applicable to the affected population (applicability); alter outcome in terms of falls and fall-related injury (efficacy); be cost effective (cost-effectiveness); and be readily applicable to everyday practice (practicability). There is increasing evidence to support intervention in specific populations, although caution is advised when extrapolating results from one setting and population to another. Tinetti and colleagues' seminal article showed the benefits of undertaking risk factor modification in older people in the community with specific risk factors for falls,1 while Campbell et al have shown a reduction in risk of falling after individually tailored home exercise programs for women 80 years or older.2 T'ai chi undertaken in a group setting has also been shown to reduce the risk of recurrent falls.3 More recently, Campbell and colleagues reported a significant reduction in falls after withdrawal of psychotropic medication in older people.4 However, within a month of completion of the study, 47% of their patients had recommenced psychotropic medication, highlighting the need to provide continuing support. The role of the occupational therapist and home environment modification has not been established. A recently published study by Cumming et al showed a reduction in falls in patients having a home environment assessment by an occupational therapist on discharge from hospital.5 Interestingly, the observed reduction was for both indoor and outdoor falls, raising questions as to the mechanism of the observed effect. Perhaps modifying the home environment enhances safety awareness generally. It should be remembered that most people who fall do not sustain any injury and do not present to any medical service,6 despite increasing evidence supporting targeted intervention. Older people presenting to emergency departments are an easily identifiable, high-risk population. Studies have reported that, among older people discharged from emergency departments, up to half show an increase in dependency, usually secondary to trauma.7,8 A two-year follow-up of patients for whom a geriatric consultation was requested in the emergency department showed 34% had died and 52% were in a long term care facility.9 Falls contribute significantly to the emergency department workload, as highlighted by Bell and colleagues in this issue of the Journal.10 They report data on older people presenting after a fall to an inner-city teaching hospital in Sydney. Their results emphasise the multifactorial nature of falls. A UK inner-city teaching hospital with comparable baseline demographics has produced evidence of the benefits of a structured interdisciplinary assessment of such patients.11 The high rate of injury and admission reported by Bell et al is not surprising and reflects our own experience -- elderly people are four to five times more likely to be admitted to hospital than younger people -- and this must be taken into consideration in the context of demographic projections for the next 25-30 years. The emergency department represents a key interface between the hospital and the community and, as such, affords a unique opportunity for interdisciplinary and multiprofessional cooperation across health and social care sectors. However, assessment in the emergency department focuses largely on injury and limited time is available for investigating underlying causes or implementing preventive strategies. It is neither practical nor feasible for all older people who fall to undergo a detailed assessment in the emergency department, or to be assessed by geriatricians. However, using derived and easily identifiable predictors of risk, it is possible to streamline referrals to a falls program or clinic, which would be in keeping with an attainable level of service commitment. Predictors of future risk, as identified in the emergency department, include a history of one or more falls in the previous year, a fall occurring indoors, inability to get up from the floor after a fall, and polypharmacy (four or more regularly prescribed medications).12 Only through effective liaison with services within and outside hospital can we improve the outcome for older people presenting with falls. The increasing provision of falls programs fulfilling the effective intervention criteria provides the ideal opportunity to bring together existing, but frequently fragmented, services to enhance the care of older people. Jacqueline C T Close Physician Clinical Age Research Unit Department of Health Care of the Elderly King's College School of Medicine and Dentistry London, UK jacqueline.closeATkcl.ac.uk Ed Glucksman Physician, Department of Accident and Emergency Medicine King's College Hospital, London, UK Tinetti ME, Baker DI, McAvay G, et al. A multifactorial intervention to reduce the risk of falling among elderly people living in the community. N Engl J Med 1994; 331: 821-827. Campbell AJ, Robertson MC, Gardner MM, et al. Randomised controlled trial of a general practice programme of home based exercise to prevent falls in elderly women. BMJ 1997; 315: 1065-1069. Wolf SL, Barnhart HX, Kutner NG, et al. Reducing frailty and falls in older persons: an investigation of Tai Chi and computerized balance training. Atlanta FICSIT Group. Frailty and Injuries: Cooperative Studies of Intervention Techniques. J Am Geriatr Soc 1996; 44: 489-497. Campbell AJ, Robertson MC, Gardner MM, et al. Psychotropic medication withdrawal and a home-based exercise program to prevent falls: a randomized, controlled trial. J Am Geriatr Soc 1999; 47: 850-853. Cumming RG, Thomas M, Szonyi G, et al. Home visits by an occupational therapist for assessment and modification of environmental hazards: a randomized trial of falls prevention. J Am Geriatr Soc 1999; 47: 1397-1402. Graham HJ, Firth J. Home accidents in older people: role of primary health care team. BMJ 1992; 305: 30-32. Gerson LW, Rousseau EW, Hogan TM, et al. Multicenter study of case finding in elderly emergency department patients. Acad Emerg Med 1995; 2: 729-734. Khan SA, Miskelly FG, Platt JS, Bhattachryya BK. Missed diagnoses among elderly patients discharged from an accident and emergency department. J Accid Emerg Med 1996; 13: 256-257. Sinoff G, Clarfield AM, Bergman H, Beaudet M. A two-year follow-up of geriatric consults in the emergency department. J Am Geriatr Soc 1998; 46: 716-720. Bell AJ, Talbot-Stern JK, Hennessy A. Characteristics and outcomes of older patients presenting to the emergency department after a fall: a retrospective analysis. Med J Aust 2000; 173: 179-182. Close JCT, Ellis M, Hooper R, et al. Prevention of falls in the elderly trial (PROFET): a randomised controlled trial. Lancet 1999; 353: 93-97. Close JCT, Ellis M, Hooper R, et al. Predictors of falls -- results from Prevention of Falls in the Elderly Trial (PROFET). Age Ageing 1999, 28 Suppl 1: 14. Make a comment

Ed Glucksman

Research Characteristics and outcomes of older patients presenting to the emergency department after a fall: a retrospective analysis Anthony J Bell, Janet K Talbot-Stern and Annemarie Hennessy MJA 2000; 173: 179-182 For editorial comment, see Close & Glucksman Abstract - Methods - Results - Discussion - References - Authors' details - - More articles on Emergency medicine Abstract Objectives: To study older patients presenting to the emergency department after a fall -- factors associated with the fall, injuries sustained and outcome. Design: A retrospective analysis using the Emergency Department Information System (EDIS), the Trauma Registry and the patient information database (CCIS), in addition to the patient's emergency and inpatient medical records. Setting: Emergency department of a major inner city teaching hospital, 1 June - 30 November 1997. Patients: All patients over 65 years presenting to the emergency department (ED) after a fall, for whom complete medical records were available. Results: Of 803 patients over 65 years presenting to the ED after a fall, complete records were available for 733 (91.3%) (283 men and 450 women). Extrinsic (accidental) causes were implicated in more than a third of falls (313 patients [42.7%]). A high proportion of the patients were living at home (520; 70.9%) and walking unaided (389; 53.1%). Although absolute numbers of women increased with age, men were as likely as women to present after a fall. Many patients had fallen before -- 39% of the men (111/283) and 24% of the women (110/450). In 78 patients (10.6%), alcohol misuse may have been a direct cause of the fall. The overall injury rate was 70.5% (517/733 patients), the most common injury being an isolated fracture (269/517 patients; 52.0%). In all, 419 patients (57.2%) were admitted to hospital, 48% (200/419) with a fracture and 52% (219/419) for investigation of the medical cause of the fall. The median length of hospital stay was 6 days (mean, 10.4 days; range, 1-129 days); 35% (146/419) of patients were in hospital for more than 10 days. Conclusion: Older patients presenting to the ED after a fall had high injury rates, high admission rates and often prolonged hospitalisation. About a third had fallen before. Patients at risk can be identified in the ED and referred to falls prevention programs. Census data for 1996 show that 12.1% of Australians are aged 65 years or over.1 This proportion is expected to double in the next 40 years,2 with major implications for healthcare costs. Alone, the cost of falls in patients over 70 years in Australia was estimated to be $398 million in 1989.3In the United States, trauma causes a considerable proportion of presentations (and subsequent hospital admissions) of older patients. Falls account for most of these presentations.4 The annual incidence of all falls increases from 25% at age 70 years to 35% after the age of 75; the risk increases with age and is higher among those living in long-stay institutions.5 Up to 10%-15% of falls result in serious injury, of which at least half are fractures. Even falls not resulting in injury may have serious psychological consequences.5,6 The "postfall anxiety syndrome"7 and fear of falling leads to decreased activity,8 and ultimately an increased risk of future falls.9 Patients have reported continued disability two months after a fall.10 No Australian report has been published specifically about patients in this age group presenting to the emergency department (ED) after falls, although previous studies have looked at older people presenting to the ED.11,12 Our aim was therefore to focus on patients over 65 years who presented to our ED as a result of a fall. Several features were of interest: why the patients fell; what, if any, injuries were sustained; what proportion of patients required admission to hospital; and what morbidity and mortality resulted from the fall. Methods Royal Prince Alfred Hospital is a 700-bed tertiary referral centre with 60 000 admissions and 45 000 ED attendances per year. A retrospective review of attendances for the six-month period June - November 1997 was undertaken. All older patients who had fallen were eligible for the study. Patient data Data were obtained from the sources below and thereafter patients remained anonymous. EDIS: Patients eligible for the study were identified by a search of the EDIS (Emergency Department Information System) for "falls" in the age group chosen. EDIS is a computerised database in the ED with demographic information, presenting complaint, diagnosis and disposition for each patient. Medical records: A predetermined dataset was recorded from the medical record for each patient presenting to the ED. This included medical record number, age, sex, type of residence (home, hostel or nursing home), prefall mobility, nature of fall, alcohol misuse, recurrent fall, referral status, triage category, injury score, specific area of the body injured, fracture, admission, specialty, length of stay, mortality, and discharge disposition. Prefall mobility was further defined as unaided versus aided (use of a stick, frame, crutches, assistance by another person) versus unknown. Trauma Registry: Additional data were obtained from the hospital's Trauma Registry. An Injury Severity Score (ISS) is calculated for patients requiring admission after trauma. ISS is the sum of the squares of the highest Abbreviated Injury Scores (an anatomical system classifying injuries by body region on a scale of 1 [minor] to 6 [serious]) for the three most seriously injured body regions. ISS ranges from 1 (minor injury) to 75 (severe injury).13 CCIS: For patients transferred to an affiliated geriatric and rehabilitation hospital, the patient information database (CCIS [Central Sydney Area Health Service Clinical Information System]) was accessed for the length of stay. None of the patients in our study were transferred to non-affiliated geriatric and rehabilitation hospitals. Population data: The Australian Bureau of Statistics supplied population data for the hospital's catchment area.14 Definitions Fall: "Inadvertently coming to rest on the ground or other lower level with or without loss of consciousness."15 Extrinsic (accidental) causes: Environmental factors (eg, rugs, steps, uneven floors). Falls as a result of external trauma, such as motor vehicle accidents and violence, were excluded. Intrinsic (non-accidental) causes: Syncope, dizziness or vertigo, postural drop, central nervous system lesion (haemorrhage or infarct), drop attack, and balance or gait disturbance. Alcohol misuse: A history of alcohol misuse related temporally to the event, a record of alcohol on the breath, or a statement in the ED record about the patient's being intoxicated. Statistical analysis We used Minitab Statistical Software16 for statistical analysis and performed χ2 tests. Analysis was based on age group or sex and compared with a number of variables: presentation as a result of a fall, nature of the fall, outcome of a fracture, and admission status. A multivariate analysis was performed on four aspects of the falls considered to be related to place of residence or mobility: extrinsic cause, recurrent falls, fracture/no fracture and admission. Odds ratios (95% CI) were calculated for each of these groups. Multivariate analysis was also used to calculate odds ratios (95% CI) for whether alcohol use contributed to selected outcomes: admission (yes/no), extrinsic or recurrent falls versus other falls, and age under or over 80 years. Results Patient characteristics Of a total of 22 782 patients presenting to the ED during the six-month study period, 4489 (19.7%) were patients older than 65 years and 803 (17.8%) of these patients presented as a direct consequence of a fall. Of these patients, 733 (91.3%) had medical records available for review at the time of analysis and complete for the purposes of the dataset. Age and sex: The average age was 78.6 years (range, 65-101 years) and the median age was 79 years: 263 patients were aged 65-74 years, 279 were 75-84 years and 191 were 85 years or older. Increasing age of the patients was associated with presenting to the ED as a result of a fall (χ2 test for trend, P < 0.001) (Box 1). There were 283 men and 450 women. However, the number of men and women presenting to the ED after a fall reflected the age and sex distribution within the catchment population (Box 2). Thus, men were as likely as women to present as a result of a fall. Residence: At the time of the fall, 83% (211/253) of the 65-74 year olds, 74% (200/269) of the 75-84 year olds and 57% (109/191) of those over 85 years were living in their own homes. Thus, the proportion of those living in either a hostel or a nursing home increased with advancing age. In 20 patients residence could not be classified. Previous falls: 39% of the men (111/283) and 24% of the women (110/450) had fallen before. Mobility: Patients were classified according to mobility: walking aided or unaided. As expected, as the patients aged the use of a walking aid increased. Cause of fall Extrinsic or intrinsic: Overall, extrinsic causes for the fall accounted for 42.7% of patients presenting to the ED. In the age group 65-74 years extrinsic causes accounted for 49.4% of falls, which is more than expected when compared with the proportion in the older age groups (39.0% and 38.7%, respectively). Intrinsic causes were more likely with advancing age (χ2 test; P = 0.018) and accounted for 50.5% (95% CI, 45%-57%), 60.9% (95% CI, 55%-67%) and 64.2% (95% CI, 54%-68%) of falls in the respective age groups. The breakdown of all causes for falls presenting to the ED is shown in Box 3. Despite extensive review of the medical records we were unable to classify 23% of falls as either extrinsic or intrinsic. Alcohol misuse: This was documented in 78 patients (10.6%): 18% of the 65-74 year olds, 10% of the 75-84 year olds, and was not a factor in those over 85 years (χ2 test; P = 0.001). Sixty-five (83%) of these patients were living in their own homes. Multivariate analysis for alcohol misuse at the time of fall showed it to be significantly associated with an increased risk of both accidental and recurrent falls (Box 4). Outcomes Injury: 517 (70.5%) patients sustained an injury as a result of the fall: 73.3% (379/517) had an ISS of 4 or less (a score of 9 correlated with a femoral fracture); 13 patients had scores between 15 and 25, with all of these patients (except one with spinal cord compression) sustaining intracranial injury. The most common injuries were fractures (36.7%), soft tissue injuries (16%), lacerations and skin tears (14.5%). Fracture: 269 patients (36.7%) sustained a fracture: 36% (98/269) of which were neck-of-femur fractures, 16% fractured wrists, 12% fractured humeral neck and 5% pelvic fractures. The breakdown of fractures in each group is shown in Box 5. Women sustained both neck-of-femur and all fractures more frequently than men (χ2 test; P < 0.001): 64% (63/98) of femoral-neck fractures and 73% (125/171) of all other fractures (95% CI, 66%-80%). Interestingly, in women, the proportion of fractured neck of femur to all fractures was 33.5% (63/188) (95% CI, 27%-40%), whereas in men it was 43% (35/81) (95% CI, 32%-54%). Fracture rate overall was not found to be related to advancing age in either sex. Admission: The total number of patients admitted to hospital was 419, or 57.2% of all older patients with falls (representing 38% of all older patients admitted during the study period). Sixty-three per cent of those 85 years or older were admitted, compared with 60% of the 75-84 year olds and 50% of the 65-74 year olds (χ2 test; P = 0.009). Of the 269 patients with fractures, 200 (74%) were admitted. There was no statistically significant difference in the fracture admission rate across the age groups (χ2 test; P = 0.53). Of the 200 patients admitted, in 49% the cause of the fracture was intrinsic. Patients admitted to hospital after a fall had a mean length of stay of 10.4 days (95% CI, 10.2-10.6) and a median stay of 6 days (range, 1-129 days). Hospitalisation for more than 10 days was necessary in 35% (146/419) of patients. Deaths: Thirty-two patients died in hospital, representing 4.4% of all patients presenting to the ED after a fall: half of those who died were over 85 years of age and half were from nursing homes. In those who died, the cause of the fall was intrinsic rather than extrinsic (27/32), and the most common injury was a fracture of the neck of the femur (10/32). Data analysis: Multivariate analysis of place of residence or mobility and extrinsic cause, recurrent falls, fracture/no fracture and admission showed no significant interaction. Discussion We found that older patients presenting to the ED after a fall had a high injury rate (71%), high admission rates (57%) and often prolonged hospitalisation (> 10 days in about a third of those admitted). Our study complements others performed in Australia and elsewhere on older patients who fall, particularly those who present to an ED.11,12Some studies have found that women in the community fall more frequently than men,17 and others, as we did, found no difference.18 Institutionalised patients have been reported to have higher fall rates than patients living at home,17,19 but most of our patients lived at home and walked unaided. Falls may be caused by an environmental hazard alone or a simple syncopal event, or there may be a complex interaction of environment, physical illness, and type of activity. Changes in vision, vestibular function and proprioception affect physical stability, and musculoskeletal changes affect gait. Postural hypotension from dehydration, drug effects or autonomic dysfunction may be involved. Additionally, acute illness such as respiratory tract infection, arrhythmias, carotid sinus hypersensitivity,20 cardiac failure and neurological problems (eg, Parkinson's disease) may increase the risk of falling. All these intrinsic factors may be compounded by environmental hazards.5,6,17 We found gait disturbance, syncope, central nervous system lesion, postural hypotension and dizziness to be the most common intrinsic causes, and these were statistically more likely to be the underlying reason for a fall as age increased. The proportion of patients with falls in association with alcohol misuse contrasts with the findings of Adams et al.21 They surveyed older patients over an eight-week period for alcohol use, and found a negative relationship between alcohol use and falls. A high proportion of our patients with alcohol misuse lived at home, with perhaps easy access to alcohol. These patients had a greater risk of extrinsic and recurrent falls, a potential relationship that warrants further study. A UK study found that most falls in the community do not result in serious injury.17 We found that patients presenting to the ED after a fall have a high rate of injuries, consistent with previous reports,17,22 but the rate was significantly higher than that found by Tinetti et al.23 We found women to be statistically more likely to suffer a fracture than men. Grisso et al,10 in an older inner-city population in the United States, found that women generally had higher rates of fall injury than men. In addition, they found that injury rates increased with advancing age, a finding that we could not confirm. There were fewer hip fractures in older men than older women in our study, confirming previous findings.24 This is probably related to the higher prevalence of osteoporosis in women. Previous reports have shown that older men with hip fracture have higher mortality rates than age-matched women.23 The high admission rate in our study, which increased in older patients, is only slightly higher than that found by Richardson,11 but this was in patients over 75 years, in whom a higher admission rate is expected. A UK study found admission was needed in only 34% of patients.22 Admission rates for patients with a fracture did not vary significantly across our three age groups, nor were they different according to place of residence or prefall mobility. Length of hospital stay similarly did not depend on place of residence or prefall mobility, differing from the Richardson study, in which a significant relationship was found between accommodation status and outcome at 90 days.11 US studies report that 75% of deaths after a fall occur in patients over 65 years.6 We found that the single most important factor associated with death was hip fracture, a finding similar to that in previous studies.7,11 Modification of the environment and dealing with intrinsic problems such as drug side effects and gait dysfunction can reduce falls,25-27 prevent hospitalisation26 and shorten length of stay.15 If 95% of problems can be identified from the history and physical examination alone, as suggested by Rubenstein et al,15 the emergency physician is well able to identify those patients at risk of further falls. Intrinsic causes can be treated and the patient's general practitioner or specific falls prevention programs can then proceed to modify the risk of recurrence. References Australian Bureau of Statistics. Australia in brief (Census data, 1996). Canberra: ABS, 1998. <www.abs.gov.au> Davis JA. Older Australia: a positive view of ageing. Sydney: Harcourt Brace, 1994. Smith RD, Widiatmoko D. The cost-effectiveness of home assessment and modification to reduce falls in the elderly. Aust N Z J Public Health 1998; 22: 436-440. Spaite DW, Criss EA, Valenzuela TD, et al. Geriatric injury: an analysis of prehospital demographics, mechanisms and patterns. Ann Emerg Med 1990; 19: 1418-1421. Tinetti ME, Speechley M. Prevention of falls among the elderly. N Engl J Med 1989; 320: 1055-1059. Nelson RC, Murlidhar AA. Falls in the elderly. Emerg Med Clin North Am 1990; 8: 309-324. Rubenstein LZ, Josephson KR, Robbins AS. Falls in the nursing home. Ann Intern Med 1994; 121: 442-451. Nevitt MC, Cummings SR, Kidd S, Black D. Risk factors for recurrent nonsyncopal falls: a prospective study. JAMA 1989; 261: 2663-2668. Gostynski M, Ajdacic-Gross V, Gutzwiler F, Michel JP. Epidemiological analysis of accidental falls by the elderly in Zurich and Geneva. Schweiz Med Wochenschr 1999; 129: 270-275. Grisso JA, Schwarz DF, Wishner AR, et al. Injuries in an elderly inner city population. J Am Geriatr Soc 1990; 38: 1326-1331. Richardson DB. Elderly patients in the emergency department: a prospective study of characteristics and outcome. Med J Aust 1992; 157: 234-239. Stathers GM, Delpech V, Raftos JR. Factors influencing the presentation and care of elderly people in the Emergency Department. Med J Aust 1992; 156: 197-200. Baker SP, O'Neill B, Haddon W. The Injury Severity Score. J Trauma 1974; 14: 187. Needs Assessment and Health Outcomes Unit. A demographic profile of the Central Sydney Area Health Service from the 1996 Census. Sydney: Central Sydney Area Health Service, March 1998. Rubenstein LZ, Robbins AS, Josephson KR, Schulman BL. The value of assessing falls in an elderly population: a randomised clinical trial. Ann Intern Med 1990, 113: 308-316. Minitab Statistical Software [computer program], version 12. State College, Pa: Minitab Inc, 1998. Blake AJ. Falls in the elderly. Br J Hosp Med 1992; 47: 268-272. Campbell AJ, Borrie MJ, Spears GF, et al. Circumstances and consequences of falls experienced by a community population 70 years and over in a prospective trial. Age Ageing 1990; 19: 136-141. Cummings SR, Nevitt MC. Falls [editorial]. N Engl J Med 1993; 331: 872-873. Ward CR, McIntosh S, Kenny RA. Carotid sinus hyersensitivity -- a modifiable risk factor for fractured neck of femur. Age Ageing 1999; 28: 127-133. Adams WL, Magruder-Habib K, Trued S, Broome HL. Alcohol abuse in elderly Emergency Department patients. J Am Geriatr Soc 1992; 40: 1236-1240. Davies AJ, Kenny RA. Falls presenting to the Accident and Emergency Department: types of presentation and risk factor profile. Age Ageing 1996; 25: 362-366. Tinetti ME, Speechley M, Ginter SF. Risk factors for falls among elderly persons living in the community. N Engl J Med 1988; 319: 1701-1707. Diamond TH, Thornley SW, Sekel R, Smerdely P. Hip fracture in elderly men: prognostic factors and outcomes. Med J Aust 1997; 167: 412-414. Province MA, Hadley EC, Hornbrook MC, Lipsitz LA. The effects of exercise on falls in elderly patients: a preplanned meta-analysis of the FICSIT trials. JAMA 1995; 273: 1341-1347. Close J, Ellis M, Hooper R, Glucksman E. Prevention of falls in the elderly trial (PROFET): a randomised controlled trial. Lancet 1999; 353: 93-97. Tinetti ME, Baker DI, McAvay G, Claus EB. A multifactorial intervention to reduce the risk of falling among elderly people living in the community. N Engl J Med 1994; 331: 821-827. (Received 10 Aug 1999, accepted 29 May 2000) Authors' details Department of Emergency Medicine, Royal Prince Alfred Hospital, Sydney, NSW. Anthony J Bell, MB BS, Emergency Medicine Registrar. Janet K Talbot-Stern, MD, FACEM, FACEP, Director, Emergency Department; and Clinical Senior Lecturer, Department of Surgery, University of Sydney. Department of Medicine, University of Sydney, Sydney, NSW. Annemarie Hennessy, MB BS, PhD, Senior Lecturer. Reprints will not be available from the authors. Correspondence: Dr A J Bell, Department of Emergency Medicine, Royal Prince Alfred Hospital, Missenden Road, Camperdown, NSW 2050. Make a comment 1: Patients presenting to the emergency department, by age group, June - November, 1997 65-74 years (n=2060) 75-84 years (n=1672) ≥85 years (n=757) Total (n=4489) Presentation after a fall Other presentations 295 (14.3%) 1765 317 (19.0%) 1355 191 (25.2%) 566 803 (17.9%) 3686 χ2 test for age trend (P<0.001). Back to text 2: Age and sex distribution of patients presenting to the emergency department after a fall compared with the catchment population 65-74 years 75-84 years ≥85 years Men Presentation after a fall Proportion of catchment population 124/263 (47%) 15415/32185 (47.9%) 107/279 (38%) 7251/18448 (39.3%) 52/191 (27%) 1650/6038 (27.3%) Women Presentation after a fall Proportion of catchment population 139/263 (53%) 15770/32185 (49.0%) 172/279 (62%) 11187/18448 (60.6%) 139/191 (73%) 4388/6038 (72.7%) Back to text Back to text 4: Multivariate analysis (logistic regression) of alcohol misuse and selected variables in older patients presenting to the emergency department after a fall Variable Alcohol misuse odds ratio (95% CI) Age at presentation 5.5 (2.8-10.6) Extrinsic cause of fall 1.72 (1.05-2.83) Recurrent falls 2.24 (1.35-3.72) Back to text 5: Fractures in older patients presenting to the emergency department after a fall, by age group (years) Fracture 65-74 (n=263) 74-85 (n=279) >85 (n=191) Total (n=733) Neck of femur 28 (11%) 37 (13%) 33 (17%) 98 (13.4%) Other 74 (28%) 59 (21%) 38 (20%) 171 (23.3%) No fracture 161 (61%) 183 (66%) 120 (63%) 464 (63.3%) Back to text

Anthony J Bell · Janet K Talbot-Stern · Annemarie Hennessy

For Debate The hospitalist: a third alternative The role of hospitalist is already evolving in Australia, being filled by Career Medical Officers John M Egan, Mary G T Webber, Michael R D King, Michael Boyd, Gabrielle du Preez-Wilkinson and David Brock MJA 2000; 172: 335-338 The need for the "hospitalist" - The role of the hospitalist - Who best fills this role? - References - Authors' details - - More articles on Administration and health services - More articles on General medicine - More articles on Emergency medicine The hospitalist debate began in the Journal in April 1999, when we published an article by Hillman on how acute-care hospitals are changing. In September 1999, Scott and Phillips suggested that general physicians should take on the role of hospitalist. The start of the debate1 . . . in some countries [there has been] the emergence of a "hospitalist" who has a wide range of expertise, but concentrating more on acute hospital medicine -- more like a general physician, but specialising in acute and serious illness rather than chronic and mainly ambulant medicine. The hospitalist also has advanced resuscitation and procedural skills. They are familiar with the medical comorbidities increasingly associated with surgical patients and understand how different organs fail and interact in acute illness. They are a move back to the generalist physician. The equivalent in Australia is probably the intensive care or emergency physician. The hospitalist also understands about continuity and coordination of patient care, managing the patient's inpatient course and arranging a seamless transition to a community setting. . . . A hospitalist could enable community-based specialists to devote more time to what they do best, rather than being continuously confronted by the dilemma of maintaining a busy professional practice with tight appointment schedules and having seriously ill in-hospital patients who might require their attention day or night in an unpredictable way. Having skilled clinical cover 24 hours a day would also help guarantee patient safety. . . . Australia could explore other ways of achieving the same standards. (Hillman K. MJA 1999; 170: 325-328) The general physician as hospitalist2 . . . patients are more likely to be assured of continuous, integrated and efficient care for a multiplicity of concurrent problems if attended to by general physicians from the time of admission via emergency departments right through to the time of discharge and beyond into ambulatory care. Adequate resourcing of general medical units, greater involvement of general physicians in emergency and intensive care settings, ready access to specialised medical, nursing and allied health expertise as needed . . . (Scott IA, Phillips PA. MJA 1999; 171: 312-314) THERE HAS BEEN AN ONGOING DEBATE in the Journal1-6 on the changing role of the acute-care hospital and, associated with this change, the desirability of a new type of doctor, the hospitalist. It is argued that in the hospital of the near future there will be fewer patients, who will, generally, be more seriously ill than at present.7,8 Leaving aside discussion of the likelihood of this scenario,9 we believe there needs to be a change in the role and experience of doctors who work in this hospital setting: the hospitalist is one suggestion for this change. We argue here that this role is already evolving and currently functioning in a variety of clinical situations in the Australian healthcare system.10The doctor delivering those aspects of seniority, experience and permanence relevant to a hospital generalist is a Career Medical Officer (CMO) (see Box). There are two interrelated parts to this debate: What problems are there with current medical staffing of acute care hospitals? What solutions are available? The need for the "hospitalist" The present model of a Visiting Medical Officer (VMO) who has overall responsibility for the patient and who delegates this responsibility to more junior medical staff in a hierarchical manner (registrars, Resident Medical Officers [RMOs]) while out of the hospital, has a long tradition in medicine. This model, while having some excellent features, may have outlived its usefulness at the beginning of the 21st century. There is increasing evidence of major inadequacies in the functioning of our hospitals.11 This may reflect the way we educate and organise our medical staff. An analysis of the causes of adverse events reported in the Quality in Australian Health Care Study12 showed that human error was involved in 82% of adverse events and that the most common causes were failure in technical performance and cognitive failure: failure to act on available information, failure to consult or investigate, and failure to attend or provide adequate attention. A recent study of critical events (ie, cardiac arrest or unplanned admission to ICU) in an Australian metropolitan teaching hospital13 found that these episodes are frequently preceded by documented clinical instability of the patient and multiple medical review before admission to ICU or cardiac arrest ensued. The authors commented that the patients in their study (generally those with complex medical and surgical conditions) were usually managed initially by the most junior member on the ward (intern or resident). We do not suggest that junior medical officers should not be involved in direct care of the very sick, but there appear to be problems with current hospital practice: the major deficiencies appear to us to be the understandable lack of experience of the junior medical staff and their rapid turnover. This outdated way of organising medical staffing has long caused problems with our nursing colleagues14-16 and others, who assist the overworked and inexperienced medical officers organise their time and energies to most effectively care for and investigate sick patients -- and then repeat this education once again with the next rotation. Is it right to give increasing responsibility to our junior doctors, but leave them at times relatively unsupervised, unsupported and responsible for major medical decisions when their level of training may be inadequate for the task? The Postgraduate Medical Councils in the various states provide increasingly good-quality support for first- and second-year graduates, but this is in a logistical and educational role rather than a directly supportive clinical role. The role of the hospitalist We argue that hospital wards may run more smoothly and there may be greater satisfaction by patients, nursing staff, consultant medical staff and, importantly, junior medical staff if there is rapid access at all times to an onsite experienced medical officer. This senior doctor would be conversant with the dynamics of the ward, have good relationships with and an appreciation of the role of ancillary staff, and have a relatively long-term commitment to the hospital. These attributes would enable him or her to deal with evolving clinical situations before they became major problems. An additional benefit would be the provision of extra educational opportunities for interns and RMOs during their "apprenticeship" years. Hillman1 and Scott and Phillips2 appear to be attempting to address the problems by placing another specialist physician into the increasingly fragmented world of hospital medicine. There are examples of this in the United States,17-19 where the hospitalist is usually (but not always20) a specialist in internal medicine who works predominantly in the hospital setting. Physicians who work outside of the hospital relinquish their responsibility for the patient at the hospital entrance and take it up again on discharge. The unstated but underlying expectation is that the hospitalist would usurp the primary role and responsibility of the attending doctor. We believe this vision of a hospitalist to be fundamentally flawed. On the one hand, it sidelines doctors who should be intimately involved in the inpatient care of patients (including specialist physicians, general practitioners and paediatricians) whose main area of practice remains office based; on the other, it may miss out on providing a "new deal" of care for many patients who are in hospital and whose particular problems might not necessarily fall within the expertise of the intensivist/physician (eg, falls in hospital, paediatric problems, or dementia). Our contention is that this role demands not the narrow focus of the specialist but the broad-based knowledge of the generalist -- someone who can be a "jack of all trades". The preceding contributions to this debate1,2 appear to have as their central vision a hospital filled with medical patients or seriously ill surgical patients who would be better managed by a physician. Most hospitals have, and will continue to have, a much wider range of patients and conditions, including all the major and minor acute problems that one finds in paediatric, gynaecological, obstetric and psychiatric wards. We believe the role calls for a "middle management" doctor who has a breadth of knowledge and experience gained from working in hospitals and who is proficient in as many branches of hospital medicine as possible. The optimal solution is to have someone who is conversant with and experienced in treating seriously ill patients expeditiously, who is quite at home in managing the multiple minor problems that beset hospital patients, and who is used to consulting with a wide range of medical and surgical specialties as needed. The role of hospitalist should be complementary to, not in confrontation with, the established Australian model of inpatient care. That is, it seems to us better to have an experienced doctor "on site" to organise -- not take over -- the management of the hospital inpatient. There is some evidence that hospitalists who have complete control of inpatient care increase, rather than decrease, the length of stay in hospital.21 In the model we propose, the consultant physician, surgeon, paediatrician, gynaecologist, or, increasingly, general practitioner would retain primary responsibility for the patient's management, but would be actively supported by someone who had worked in the hospital system for many years and could competently manage most problems that may arise, at least in the short term. This doctor should also have the trust of, and rapid access to, the consultant staff, and good working relationships with the nursing and paramedical staff (mutual respect of each other's role and abilities) as well as a good understanding of the "mechanics" (eg, layout, routine, and regular practices) of the hospital. Who best fills this role? We believe that Scott and Phillips2 are right in having major reservations about intensivists being responsible for general ward patients. The prevention of a slow deterioration of a general medical or surgical patient to serious illness does not require the considerable skills of an intensivist -- most doctors with experience and education, alerted by protocols that highlight dangerous trends, can quite adequately look after these cases and refer to the intensive care or cardiac care unit if appropriate. The opposite and far more common scenario, that of a relatively minor problem, may well lead to the over-investigation and treatment of a condition that could have been easily handled by a broadly experienced medical officer. Although the general physician may have a better claim to this role (especially rural physicians, who are, by necessity, well-rounded generalists), there is still the problem of a doctor who may be overeducated for some aspects of the work, and undereducated for others. Many of the problems outlined above have in the past been handled by registrars, RMOs and interns. Senior registrars are usually quite able to manage patients without the direct supervision of the VMO; however, this is not necessarily the case with more junior registrars and RMOs. Again, frequent rotation takes well-performing doctors out of the loop just as they attain a level of familiarity and experience with a particular group of patients. Although doctors who performed similar roles had been in the health systems throughout Australia for many years, CMOs were initially brought into service in New South Wales in the early 1980s to maintain experienced medical practitioners in the public hospital system. These doctors were working in posts as unaccredited medical registrars or emergency medical officers, particularly in suburban and rural hospitals. The New South Wales Department of Health10 noted in 1989 that there had been a positive response to the introduction of CMOs: it had increased retention rates of hospital doctors, improved middle grade medical staffing in peripheral hospitals, and addressed the service needs of these hospitals, and the individuals were able to undertake more clinical responsibilities and required less supervision. Many CMOs have now been working in these positions for well over 12 years, and have developed considerable expertise in their area of practice. A recent study in Queensland,22 addressing the training needs and career paths of this cohort of doctors, noted their wide range of practice -- predominantly in emergency medicine ("they make up the majority of the senior emergency work force in Queensland"22), but also in orthopaedics, sexual health, community health, and other areas. The report also pointed out the experience of those who worked in emergency medicine: 73% had worked for more than three years full-time since their third postgraduate year, and 25% had worked for 10 or more years in this capacity. Furthermore, a large proportion (69%) of CMOs had postgraduate qualifications. The study also commented on a major flaw in the Australian Medical Workforce Advisory Committee report The Emergency Medicine Workforce in Australia,23 which totally ignored the role played by CMOs in the staffing of emergency departments. This omission seems to be symptomatic of a "blind spot" by some in the profession to the valuable service provided by these doctors. Many modern private hospitals are turning to CMOs to fill a demand in the medical care of hospitalised patients. In the Sydney area the Hills, Kareena and the Sydney Adventist private hospitals have significant CMO staffing (Dr Stephen Delprado, Deputy Director, Emergency Department, Hills Private Hospital, personal communication), and seven private hospitals in Queensland have CMO cover.22 Most CMOs report that they are quite happy to continue to work in these roles (J M E and M R D K, unpublished survey of 32 rural CMOs in NSW, presented to Directors of Clinical Training meeting, Postgraduate Medical Council, Sydney, May 1996). Recently, some have formed themselves into organised subgroups of the medical workforce. The largest of these (the Career Medical Officers Association) is now taking responsibility for initiating educational and industrial policies for CMOs. Examples of these are the provision of continuing medical education (in association with the Royal College of Pathologists of Australasia); discussions with universities and others about more formal training, qualifications and accreditation; and representations on various committees, including the Hospital Medical Officer Subcommittee of the Medical Training Review Panel. We believe that this broad-based experience and commitment is what makes the CMO the ideal person to take on the role of the hospitalist. Furthermore, the changes necessary to do this are relatively minor and merely a continuation of recent trends in medical workforce utilisation in the modern Australian hospital. In our opinion, CMOs are well able to fulfil such future requirements and do it in the most efficient and cost-effective way. We note the invitation by Scott and Phillips to put the respective views of hospitalist practice to the test in a randomised trial comparing the intensivist or internal medicine models of hospitalist.2 Although we have some misgivings about the applicability of this methodology, we firmly believe that any rigorous evaluation of the various hospitalist models on offer would be incomplete without the inclusion of CMOs. References Hillman K. The changing role of acute-care hospitals. Med J Aust 1999; 170: 325-328. Scott IA, Phillips PA. Hospitals and hospitalists: an alternative view. Med J Aust 1999; 171: 312-314. Denaro CP, Bennett CJ. The changing role of acute-care hospitals [letter]. Med J Aust 1999; 171: 224. Hillman K. Hospitals and hospitalists: an alternative view [letter]. Med J Aust 2000; 172: 299. Sartain JB. Hospitals and hospitalists: an alternative view [letter]. Med J Aust 2000; 172: 299. Phillips PA, Scott IA. Hospitals and hospitalists: an alternative view [letter]. Med J Aust 2000; 172: 299. Komesaroff PA, Clunie GJA, Duckett SJ. What is the future of the hospital system? Med J Aust 1997; 166: 17-22. Braithwaite J. The 21st-century hospital [editorial]. Med J Aust 1997; 166: 6. Braithwaite J, Hindle D. Research and the acute-care hospital of the future. Med J Aust 1999; 170: 292-293. Career Medical Officers (CMOs). Circular no. 89/156. Sydney: NSW Health, 1989. Wilson RMcL, Runciman WB, Gibberd RW, et al. The Quality in Australian Health Care Study. Med J Aust 1995; 163: 458-471. Wilson RMcL, Harrison BT, Gibberd RW, Hamilton JD. An analysis of the causes of adverse events from the Quality in Australian Health Care Study. Med J Aust 1999; 170: 411-415. Buist MD, Jarmolowski E, Burton PR, et al. Recognising clinical instability in hospital patients before cardiac arrest or unplanned admission to intensive care. A pilot study in a tertiary-care hospital. Med J Aust 1999; 171: 22-25. Lublin J, Gething L. RNs as teachers of junior doctors. Aust J Advanced Nursing 1992; 10(2): 3-9. Agnew T. Just rewards on the wards. Nursing Times. 1995; 91(34): 19. Junior doctors turn to nurses for help. Nursing Standard 1999; 13(47): 8. Wachter RM. An introduction to the hospitalist model. Ann Intern Med 1999; 130: 338-342. Sox HC. The hospitalist model: perspectives of the patient, the internist, and internal medicine. Ann Intern Med 1999; 130: 368-372. Schroeder SA, Schapiro R. The hospitalist: new boon for internal medicine or retreat from primary care? Ann Intern Med 1999; 130: 382-387. NAIP affiliates with the American College of Physicians. <http://www.naipon line.org/hist.htm>. Accessed 2 March 2000. Jackson JL. The international experience with hospitalists. The Hospitalist 1997; Summer. Available at <http://www.naiponline.org/archives/guest.htm>. Accessed 2 March 2000. Bricknall B, Daly M, Catchpole M. The career paths, training needs and future role of non-specialist senior medical officers in the Queensland public health care system. An exploratory study. Brisbane: Health Advisory Unit, Queensland Health, 1999. Australian Medical Workforce Advisory Committee. The Emergency Medicine Workforce in Australia. Sydney: AMWAC, 1997. Summary available at <http://amwac.health.nsw.gov.au/corporate-services/amwac/emerg.htm>. Accessed 2 March 2000. Authors' details Goulburn Base Hospital, Goulburn, NSW. John M Egan, MB BS, Career Medical Officer, Emergency Department. Kareen Private Hospital, Sydney, NSW. Mary G T Webber, MB BS, Career Medical Officer, Emergency Department, and President Career Medical Officers Association. Coffs Harbour Base Hospital, Coffs Harbour, NSW. Michael R D King, FRACGP, FACRRM, Director of Emergency Services. Camden Hospital, Sydney, NSW. Michael Boyd, MB BS, Co-ordinator of Emergency Department. Prince Charles Hospital, Brisbane, QLD. Gabrielle du Preez-Wilkinson, FRACMA, AFCHSE, Medical Officer, Emergency Department. Tweed Heads Hospital, Tweed Heads, NSW. David Brock, MB BS, Career Medical Officer, Emergency Department. Reprints: Dr J M Egan, PO Box 131, Goulburn, NSW 2580. eganjATinteract.net.au Make a comment What is a Career Medical Officer? Officially, a Career Medical Officer (CMO) is a grade of medical officer employed by the New South Wales Department of Health. Unofficially, and more accurately, CMOs are: "middle management" doctors who increasingly perform in responsible and demanding clinical roles; doctors beyond the second postgraduate year and working in clinical medicine; not general practitioners (although some work in both roles), nor specialists, nor in training for these roles; a distinct subgroup within the wider medical community, with their own aspirations, experience and educational needs. In different parts of Australia doctors in this role have different designations: Senior Medical Officer (SMO: Qld, WA, SA, NT); Hospital Medical Officer (HMO: Vic); Career Medical Officer (CMO: NSW, but this title also known and occasionally used in other states). In practice, awards for these medical officers range from registrar to staff specialist range. How many CMOs are there? No accurate numbers are available. Recent medical workforce surveys show 652 "other hospital career" doctors in NSW. In Queensland, there are 149 funded SMO positions. These figures are almost certainly an underestimate as they do not take into account community CMOs who may be labelled as GPs or specialists, and self-reporting of some hospital CMOs as registrars or staff-specialists. Likely "ball-park" figures are 1000 in NSW, and 2000 Australia-wide, but there may be significantly more. Where do CMOs work? About 60%-70% of CMOs work in emergency departments in rural, suburban and private hospitals. CMOs also work in psychiatry, sexual health, women's health, police forensic, intensive care, neonatal, orthopaedics, and other areas. In rural Queensland and NSW, CMOs are the predominant senior doctors in emergency departments. What education do CMOs have? No formal qualifications are required at present, but at least half have postgraduate qualifications. Many (especially in emergency departments) have early management of severe trauma (EMST), emergency life support (ELS), or advanced paediatric life support (APLS) qualifications. Discussions are in progress with the University of Newcastle regarding more formal postgraduate qualifications for CMOs. The Postgraduate Medical Councils may have an advisory or other role in CMO education and training. The Career Medical Officers Association (CMOA) website <http://www.cmoa.ican.net.au/> has details of current interest for CMOs and others. The information in this Box comes from many sources, including the NSW Medical Labour Force Annual Survey 1998, the CMOA website, the CMOA database, Bricknall et al22 and discussions with CMOs. Back to text

John M Egan · Michael Boyd · David Brock