Emergency medicine

Access block began to affect hospitals in the Australian Capital Territory during the winter of 2000. Practice was seriously affected first at the Canberra Hospital, a 500-bed mixed adult/paediatric tertiary hospital, in 2000, and then in 2002 at Calvary Hospital (220 beds), the other hospital in the ACT with an emergency department (ED). Access block in the Canberra Hospital averaged 9.1% (Australasian College for Emergency Medicine/Australian Council for Healthcare Standards [ACEM/ACHS] definition: proportion of admissions with total time in the ED longer than eight hours) during 1999. For 14 days between May and September the rate exceeded 20%. During 2000, it averaged 16.3%, with 56 days in excess of 20% between May and September (Box). This trend continued in 2001, when the figures were 22.9% and 79, respectively. The major underlying cause was a reduction in hospital bed capacity from a monthly average of 533 staffed beds in January–August 1999 to 491 in January–August 2000. As a corollary, a marked reduction in access block occurred when additional beds were made available by cancellation of elective surgery during the Sydney Olympics in September 2000. Although access block had a measurable effect on ED waiting time performance in 1999,1 it began to affect overall ED function in the second half of 2000,2 when a significantly lower proportion of presentations achieved their desired ACEM/ACHS waiting time performance. InterventionsThe onset of access block prompted review of ED work practice, leading to some improvement in ED performance in the face of access block during 2000, but little change since. The continued severity of the problem has stimulated ongoing review of all hospital work practice, aiming to reduce the demand on overnight beds through improving overall patient flow, and to improve ED function. The changes have proven to be of variable effectiveness. Interventions to improve patient flowRestructuring and expansion of the Bed Management Unit (May 2001); Revision of admission, discharge and bed management policies (July 2001 to March 2002); Expansion and increased use of hospital in the home and day surgery services (ongoing); Off-site transitional care arrangements for elderly patients (ongoing increase in transitional care beds); Activation of real-time estimated date of departure notification system and daily estimates of occupancy over next 24 hours (May 2001); Containment of elective surgery, particularly during winter (ongoing since 2001); and Opening of a discharge lounge (relatively little effect on time of discharge). Interventions to reduce ED demand for overnight bedsIncreased use of overnight discharge from the ED followed by day surgery for orthopaedic, plastic surgical, and gynaecological presentations; and Improved links with community services to facilitate discharge, particularly of geriatric patients. ED changes to mitigate effects of access blockRearranging medical staff rosters (2001 and 2002); Increasing by one the number of nursing staff on each shift (winter 2001 and ongoing); Drawing additional nursing staff from the hospital pool at times of excessive inpatient care in ED (2002 and ongoing); Establishing formal policies and procedures on prioritisation of ED activity (2001 and 2002); Revising hospital policies on ambulance diversion, although the effect has been limited, as the Canberra Hospital offers the only acute inpatient service in the region for paediatrics, orthopaedics, and most tertiary services; and Providing additional Hospital Assistant and Wardsman staff to assist in the ED (ongoing). Interventions planned for 2002–2003Renovation of the ED to make better use of the available space; Construction of a Clinical Decision Unit/Observation Unit in the ED to manage short-stay patients; and Opening of a short-stay surgical unit close to the operating theatre to better manage short-stay surgical patients. OutcomeAccess block is the major issue facing EDs in the ACT. Despite the above measures, hospitals in the ACT have experienced a continued increase in access block and significant decline in ED waiting time performance. Access block at the Canberra Hospital, January 1999 to September 2002

Drew B Richardson

The Queen Elizabeth Hospital (QEH) is a 340–361-bed acute tertiary referral hospital in the western suburbs of Adelaide. Since 1999, the hospital has had difficulties coping with emergency admissions demand, especially during winter. Over the previous years, there has been a reduction in acute bed numbers from 476 to 361. Also, within the past two years, there has been the loss of 250 residential care facility (RCF) nursing home beds from the western region of Adelaide. At the same time, the activity of the hospital as measured by casemix activity has remained constant. The inpatient occupancy in winter has resulted in the emergency department (ED) requesting to go on ambulance diversion (bypass) almost daily, usually in late afternoon; however, on most occasions, this has not been either approved or possible. Waiting times in the ED for patients to be transferred to a ward are sometimes up to several days and QEH's waiting times in the ED are the longest of South Australian hospitals. Cancellation of elective surgical and medical patients has sometimes been necessary. InterventionsIn a progressive response to reducing access block, the hospital has adopted a range of strategies. In 1996, an Interface Unit based within the Division of Medicine was developed to coordinate and facilitate early discharge from the wards and avoid unnecessary admissions from the ED by initiating treatment/management for patients with conditions that may be managed at home but require additional support. The nurses in this unit "broker" or organise external therapy or services (such as subcutaneous heparin for the treatment of deep venous thrombosis, or home supports for someone who is frail and would otherwise have been admitted to hospital) in association with the patient's general practitioner. With the loss of nursing home beds from the western Adelaide region, a step-down unit was created in the hospital with a lower registered/enrolled nursing skill mix. An active multidisciplinary team facilitates placing patients in RCFs or at home, with additional resources provided through brokered community services or State-based programs, such as the Adelaide Transition Alliance (which provides respite beds in RCFs) or with the Division of Surgery's "Hospital in the Home" program (which provides post-acute home nursing services from within the division's nursing resources). A transit bay of six beds for incoming (ED) and outgoing (discharge) patients has been created. In addition, overcapacity beds (ie, accepting an additional patient into a ward before a patient has been discharged) have been used, and day beds have been used for non-same-day inpatients. Emphasis has been placed on promoting appropriate admission and appropriate day stay, with audits conducted by senior nurses from the Interface Unit based on accepted clinical criteria. Early discharge remains a priority, and is reinforced at medical handover meetings held each morning to review new admissions, facilitate transfer of care, and provide clinical inservice. Home care specialist nurses have also helped prevent admissions (eg, heart failure nurses, home cancer therapy and respiratory care nurses). A "medical flying squad" was established to assess nursing home patients and was clinically effective in reducing transfers from the RCF to the ED, but was too costly to sustain. A GP service located within the ED was unsuccessful because of low numbers of triage category level 4 and 5 patients. A further issue was that it sometimes involved a GP referring to another GP. OutcomeThe impact of these interventions is difficult to measure, as ambulance diversion has sometimes not been allowed in SA. However, without the introduction of the above initiatives, a substantial further reduction in elective activity would have been necessary. One measure of the success of these programs is that in 2001 the hospital had 50 long-stay patients awaiting placement, and this is now down to an average of 25 patients. There have been strategies undertaken to increase the capacity of the ED, but medical and nursing staffing levels have remained an issue. Changes in chronic disease management are required to minimise acute inpatient demand, especially during winter. Strategically reducing elective surgical activity during winter and subsequently increasing it during summer is difficult. The Division of Surgery has trialled weekend surgery, but this has not been widely accepted by the community. The management of long-stay patients remains central to improving patient access. The appropriate allocation of nursing home and respite beds is needed on a regional basis. The failure of nursing home beds to become available through licensing is a major issue that must be addressed at a State and Commonwealth level.

Richard E Ruffin MD, FRACP · Jan K Hooper RN, RM, BNursing

Royal North Shore Hospital (RNSH) is a 550-bed tertiary referral hospital serving a population of about 900 000 in the Northern Sydney Health Area. In 1999, the RNSH executive, to deal with ongoing restricted access (RA = ambulance bypass), decided to implement various changes to the structures, policies and practices of the hospital to alleviate the blockages to patients entering the emergency department (ED) by ambulance. The extent of RA at RNSH is shown in Box 1. As expected, RA was worse during winter, with more than 100 hours per month. InterventionsIn March 1999, the clinical heads of the hospital's divisions implemented a program aimed at improving utilisation of beds in the medical and surgical wards, in the belief that solutions to restricted access lay not within the ED, but within the rest of the hospital. The specific interventions were implemented by committed multidisciplinary teams, underpinned with significant senior medical staff involvement and executive support. Structural changesAdministrative responsibility for the ED was moved to the Division of Medicine so that the problems facing the ED were seen as belonging to the general ward areas. Clinical Supervisors, with responsibility for coordinating bed management, were appointed in the divisions of medicine and surgery, and a Clinical Bed Manager was appointed with responsibility for bed management across the entire hospital. Team-building initiativesDaily meetings with divisional nursing unit managers, the clinical supervisor and the bed manager. These meetings identified patients awaiting discharge, potential delays in treatment requiring attention, delays in consultation, inappropriate admissions, and patients suitable for treatment through ambulatory care or other outpatient services. Friday afternoon meetings with all medical registrars, divisional medical and nursing heads, the clinical supervisor, and the bed manager to ensure that all patients not requiring hospitalisation over weekends had appropriate discharge plans. Provision of data to medical staff regarding clinical practice variation (eg, variation in average length of stay for specific conditions). Clinical initiativesAmbulatory care ward open every day with extended after-hours service, with referrals from all medical teams and directly from the ED. This ward currently treats more than 1400 patients each month, and is available for patients who are well enough to be at home, but require in-hospital treatment as day patients. For example, patients who require blood transfusions, joint aspirations, lumbar punctures, chemotherapy or intravenous antibiotics were all moved from inpatient beds to the ambulatory care service. Similarly, rural patients referred for multiple specialist consultations or investigations are managed in this unit. Early-morning blood collection for patients awaiting results before discharge, with results available by 9: 00 am for discharge by 10: 00 am. Day-only angiography. Fax referral to rehabilitation beds to expedite transfer. Weekend discharge rounds by the divisional medical head and the clinical supervisor. Accommodation initiativesReconfiguration of beds to five-day short-stay to encourage management of elective activity from Monday to Friday. Use of off-site residential accommodation for patients not requiring inpatient beds for investigations. Provision of free transport (taxi vouchers, hospital transport) to patients to facilitate discharge. Nursing home liaison committee to improve communication with local residential care providers and facilitate appropriate transfer from the acute- to the residential-care sector. Leasing of 12 private hospital beds and attached clinical staff from Mater Misericordiae Hospital during winter. Policy initiativesRevision of the restricted access policy. Before activating RA, the ED Staff Specialist must contact inpatient managers to assess whether it is possible to avoid RA by hastening bed movements. Revision of the weekend leave policy. Ward leave greater than eight hours suggests the patient should be treated in the ambulatory centre. Development of an over-census bed policy. Wards to go one patient over census when the ED is considering RA and has no alternatives. This policy only needed implementation on two occasions between March 1999 and October 2000; on both occasions it prevented the hospital going onto RA. OutcomeThe effect of these interventions was dramatic. Within six months of commencing these initiatives, RNSH had effectively eliminated restricted access to the ED (Box 1, 2000), while maintaining elective surgical activity and significantly reducing the number of patients on the waiting list for admission (Box 2). These improvements occurred with bed occupancy rates in excess of 90%. The key contributors to the success of this program appear to be: significant medical leadership through visible operational roles for divisional heads and staff specialists/clinical supervisors in bed management processes; attention to discharge planning for ward patients; centralised bed management with a whole-hospital focus; team-building among senior nursing and medical staff; improved communication between ED and ward areas; engagement of junior medical staff in bed management processes; and a multifaceted implementation program that sought to correct process inefficiencies wherever they were identified. The outcomes of the program support the hypothesis that reducing ED ambulance bypass can be achieved by interventions that address upstream blockages in the hospital rather than specific ED interventions. Maintaining organisational focus on continually questioning the appropriateness of bed management practices is a challenge that must be met to ensure the sustainability of these sorts of improvements. 1: Restricted access (ambulance bypass) at Royal North Shore Hospital, 1997–2000 Interventions to reduce restricted access were implemented from March 1999, and had produced a dramatic decrease in restricted access by the end of 1999. 2: Proportion of patients experiencing a delay to treatment at Royal North Shore Hospital

Rohan J H Hammett MB BS, FRACP · Bruce G Robinson MSc, FRACP

In Queensland, access block was first observed in the peripheral urban hospitals in the Brisbane and Gold Coast area. As the absolute and relative bed capacity of public hospitals declined in the period 1999–2002, access block in Queensland's largest hospitals increased from a barely manageable average of less than 10% (Australasian College for Emergency Medicine/Australian Council on Healthcare Standards definition: proportion of admissions with total time in the emergency department longer than eight hours) to an average of about 14% in financial year 2001–02. Various administrative analyses have shown that the deleterious effects of access block start to become apparent at levels greater than 5%, and that these dysfunctional levels of access block occur when hospital occupancy consistently exceeds 95%. Other observations on Queensland data are that, generally speaking, access block is less of a problem in provincial centres than in metropolitan areas, and that hospitals with the best elective surgery performance tend to have the worst access block performance, and vice versa. The best-performing large hospital in Queensland in relation to access block is the Royal Brisbane Hospital (RBH), which had an average 6.2% in 2001–02. RBH is believed to be one of only two major hospitals in Australia that had no requests for ambulance bypass in 2001–02. This outcome has been achieved through considerable research and innovation and a management view that the RBH cannot go on ambulance bypass, as its emergency department (ED) is the sole department servicing a catchment area population of some 550 000, and because the other EDs in Brisbane do not have the capacity to absorb the additional workload if RBH ED closed its doors, even for a few hours. Over the past decade the hospital has implemented many strategies aimed at optimising the efficiency of the ED, the acute care process and discharge procedures. These are summarised in the Box. All of these strategies are believed to have had some benefit, but the most significant are the ED Short Stay Unit and the Medical Assessment and Planning Unit. It is known that small improvements in bed availability (ie, 5–10 beds) can cumulatively have a very substantial impact on access block, so RBH's current focus is on precision bed management through improved information systems and processes, including geographic information systems (which map the geography of the hospital against variables such as patient numbers, staff numbers, and nurse dependency). The objective is to maximise the identification of the relationships and correlations that exist in separate data sources within the hospital to precisely measure and predict demand and throughput in real time and to communicate that information throughout the organisation. Once this strategy has been exhausted, access block will only be able to be avoided through greater reductions in elective surgical throughput or an increase in system bed capacity, particularly during periods of peak demand. Strategies to improve bed management at Royal Brisbane Hospital, 1992–2002 Emergency department Increased consultants (from two to eight) Admission policy ED Short Stay Unit (18 beds: 24-hour stay for minor head injuries, overdoses, renal colic, etc.) ED Fast Track Zone (for Australasian Triage Scale Category 3 and 4 patients) ED Imaging Unit (computed tomography, ultrasound, picture archiving and communication system/radiology information system) ED Stat Lab Nurse-initiated X-rays (for peripheral skeletal X-rays, according to clinical pathways) Extended Hours Social Work (18 hours/day) ED Primary Care Unit Transit Lounge (a separate lounge for discharged patients awaiting transfer) Acute Mental Health Assessment Unit (6 beds) Inpatient departments Medical Assessment and Planning Unit Medical Day Procedure Unit Increased day-of-surgery admission Increased day-only procedural admission (no overnight stay) Interim Care Unit (inpatient facility for subacute and non-acute patients waiting for nursing home placement) Hospital-in-the-home program

Richard H Ashby

Royal Perth Hospital (RPH) is the largest hospital in Western Australia. The Wellington Street campus has about 600 beds and is located on the edge of the inner city. The emergency department (ED) has an annual census of around 55 000, with an admission rate of 44%. Forty-two per cent of all attendances arrive by ambulance, and data from the ambulance service indicate that RPH receives more priority one ambulances than the other major teaching hospitals combined. From 1996 to 2001, attendances increased by 14% and admissions by 16%. In the same time, inpatient bed numbers have been reduced by about a third. Before 1999, ambulance bypass was extremely rare. In October 2000, four WorkSafe orders were issued because the ED was contravening regulations of the Occupational Safety and Health Act 1984 (WA): employees were not able to move safely within the ED corridors because of obstruction from too many patient trolleys; patient trolleys and other equipment were blocking egress through corridors for evacuation in event of fire or other emergency; employees were exposed to violence hazards; and employees were suffering work-related stress because of excessive work demands. On 12 December 2000, all three major teaching hospitals in Perth were on simultaneous ambulance bypass. As a result, the then Health Minister appointed an Ambulance Bypass Coordinator to prevent this event recurring. On 17 November 2001, the cover story of the West Australian detailed the poor conditions for patients and staff in the ED. As a result, the Department of Health formed an Emergency Services Task Force, with broad representation from the emergency medicine and nursing community. The Box shows the extent of ambulance bypass at RPH from July 1999 to June 2002. Analysis of the first two years indicates that the most common reason for initiating ambulance bypass was entry block (30.4%). Entry block is a result of overwhelming numbers of patients attending the ED in a short period, resulting in a functional block to the entry of the ED and ED overcrowding. This necessitates ambulance bypass, even if there are sufficient inpatient beds available. InterventionsA transit lounge was established in July 1999, allowing ward patients who are being discharged to await discharge medications and collection, thus freeing up their beds earlier. In July 2000, an eight-bed holding bay was opened next to the ED. This is designed for patients who are ready for admission, but for whom the inpatient bed is unavailable, and to relieve the stacking of patients in the ED corridor. Nevertheless, stacking of patients in the corridor still occurs. Within the ED, a transfer coordinator has been appointed since July 2001. This is a senior nurse who readies patients for inpatient admission and organises transfer to the ward. This frees nurses for clinical duties. The transfer coordinator also identifies and coordinates admission of patients to other sites (eg, private hospitals), and can arrange direct admission to the ward, bypassing ED. Bed management within the hospital was changed from a divisional system to a centralised bed management mechanism, allowing for effective crisis management. The hospital now has well-defined criteria for initiating ambulance bypass (involving factors such as excess patient load, environmental, staff or resource issues, excessive number of high-acuity patients, or declared disaster situation). Other options to reduce ED overcrowding include sending trolley patients awaiting admission to wait in the ward corridor. ED medical staffing was increased to address the large patient volume. The ambulance communications room now has a computerised ED patient tracking system (EDIS) installed. EDIS is present in all EDs in Perth. This allows the ambulance service to distribute its workload between sites. Other recommendations of the Emergency Services Task Force that have been implemented are to: increase bed capacity by permanently opening some closed beds if nursing staff can be found (about 40 beds); increase aged care and rehabilitation beds at a regional secondary hospital to allow transfer of inpatients from RPH; increase the availability of care awaiting placement beds; and increase the bed and investigatory capacity of another secondary hospital in the region to allow for greater retention of patients, thus easing the burden on RPH. ED staffing was significantly increased. The above measures have had significant clinical input and are designed to increase the capacity of the system, but the most important outcome has been the recognition at all levels of government that the problem exists and needs to be addressed. The situation is under constant review. Episodes of ambulance bypass at Royal Perth Hospital, July 1999 to June 2002

Daniel M Fatovich MB BS, FACEM

Royal Melbourne Hospital (RMH), a 360–390-bed acute tertiary referral hospital in inner Melbourne, began to experience an acute increase in access block from early 2000. Over the previous few years, there had been a gradual reduction in acute bed numbers and a marked reduction in subacute and nursing home beds in the area serviced by the hospital. At the same time, patient throughput, as measured in weighted inlier equivalent separations (WEIS), had not decreased. The access block was manifest by ambulance bypass of up to 150 hours per month in 2001, worsening access of emergency patients to inpatient beds, and increasing and chaotic theatre cancellations for elective patients. InterventionsDuring 2001, in response to a Victorian government initiative, RMH formed a clinician-led taskforce that developed 51 interventions. These aimed to maximise efficient use of inpatient beds and improve access for elective and emergency patients, and were generally adapted from programs tried at other institutions. The interventions were developed over three months from April to June 2001, and were implemented over the following three months. The more important initiatives were: centralising bed management, introducing a 48-hour short-stay ward, employing care coordinators in the emergency department to improve discharge and avoid inpatient admission,1 monitoring inpatient length of stay, with alerts for patients staying longer than 14 days, and improving access and referral to subacute care. OutcomeFollowing the implementation of the taskforce recommendations, there was a significant improvement in access block indicators, even though hospital bed numbers actually decreased in acute and subacute sectors. The hospital's WEIS remained the same and emergency WEIS increased during the six months from implementation. Ambulance bypass was reduced to fewer than 10 episodes per month, emergency patients waiting more than 12 hours for inpatient beds were reduced by 40%, and same- or prior-day theatre cancellations were reduced to fewer than 10 per month. The elective waiting list remained static during the first six months of implementation. Although the hospital was funded to increase bed numbers, this was not possible because of nursing shortages and rigid workforce rules. Significant components of the success of the interventions appeared to be that clinicians were empowered to drive the changes and the focus was on maximising bed use rather than saving money. Individual interventions that had substantial effects on access block were the 48-hour short-stay ward, care coordination in the emergency department, centralised bed management, day-of-surgery admissions, and monitoring of patients staying as inpatients for more than 14 days. Using a similar strategy, hospitals similar to RMH could function with fewer beds or treat more patients with the same number of beds. It is not possible to determine from our experience whether this would result in cost savings.

Peter A Cameron · Donald A Campbell

The Alfred Hospital, in Melbourne, is a 350–390-bed tertiary referral hospital with acute medical, surgical and psychiatric services. It is one of three hospitals in Bayside Health, a major metropolitan health service, and is one of the two major adult trauma centres in Victoria. The hospital also provides a number of statewide services, including those for heart–lung transplantation, cystic fibrosis and major burns. In 2000 and early 2001, there was a considerable increase in the occasions that the Alfred's emergency department (ED) had to implement ambulance bypass, and there were difficulties in timely access for high priority elective admissions. Several initiatives had already improved access in the hospital, such as hospital-in-the-home, pre-admission and day-of-surgery admission strategies. In addition, an integrated approach to bed management was in place. This involved daily review of priorities for emergency and elective admission, through a centrally coordinated bed assignment process, overseen by senior medical and nursing managers. InterventionsIn financial year 2001–02, the Victorian Department of Human Services funded a number of initiatives under the Hospital Demand Management Strategy, which aimed to improve access for emergency and elective patients. The funded initiatives in the Alfred ED include increased senior medical staff cover after hours and the development of fast-track, an area of the ED where a doctor and a nurse work in partnership to fast-track the patients' care. Other hospital initiatives included a targeted length-of-stay strategy, involving strategies such as additional care coordination for patients admitted to specific clinical units, and the introduction of a weekly ward round by senior medical and nursing staff to facilitate early discharge planning. A third project focused on strategies to avoid patients' presenting to the ED, such as multidisciplinary mobile teams working in concert with nursing homes and general practitioners. Among the more successful strategies were the Medical Ambulatory Day Unit and the Medihotel. These were designed to meet the needs of patients who required inpatient interventions, but who did not need overnight stay in an inpatient bed. These might be rural patients, patients receiving treatment over a series of days, or patients for clinical review or investigation. Previously, there was no alternative but to admit these patients to multiday inpatient beds. The Medical Ambulatory Day Unit (MADU) and Medihotel are next to each other within the main part of the hospital's ward area. The MADU was designed to provide a range of medical interventions and consultation facilities, and patients may attend on consecutive days for their treatment or investigation. The Medihotel provides accommodation to patients of the Alfred who are ambulatory and independent who do not require clinical intervention overnight, but who need to be close to professional expertise if required. OutcomeA review of the outcomes in late 2001 and early 2002 showed a significant reduction in ambulance bypass, from 291 episodes in 2000–01 to 158 episodes in 2001–02. However, similar improvement was not achieved in the number of ED patients waiting for more than 12 hours for an inpatient bed. Hospital-in-the-home substitution rates, which estimate the resulting inpatient capacity, were around 11%, which compared well with similar hospitals. Up to June 2002, there had been more than 3500 occasions of service for patients of the MADU, and more than 1900 patient-nights in the Medihotel. Nearly all clinical units at the Alfred have used the MADU/Medihotel at least once. The ability to plan for elective medical admissions without the risk of cancellation has been well received by staff. The centralised bed allocation and coordination process is extremely effective in maximising access to multiday beds, although this requires a considerable senior medical, nursing and management commitment. Some of the improvements to bed management flows did not require extra resources, as they related to changes in process. An example was the decision to allocate the first five multiday beds that became available each morning to patients awaiting admission in the ED — this had a considerable impact on the ED, without a flow-on disadvantage elsewhere. Other initiatives with high impact on access were increasing the number of senior staff in the ED, care coordination and ED disposition nurses, and weekly ward rounds by clinical bed management staff to identify opportunities for redesign of the processes of discharge and bed management.

Kim N Hill MB BS, MHP, FRACMA

To the Editor: Interpretation of the report describing the first death attributed to the Irukandji syndrome should be tempered by the fact that significant unstated assumptions have been made in attributing the cause of death to a jellyfish.1 While envenomation by a jellyfish remains the likely diagnostic possibility, no evidence is presented that unequivocally confirms a jellyfish as the lethal agent. Several methods could have been used to support or confirm the diagnosis of jellyfish envenomation, including sampling of nematocysts from the victim's skin (before or after death), jellyfish capture, or reports of other similar, but less severe, stings from the same beach around the time the victim was stung. In severe jellyfish envenomation, attempts are often made to harvest nematocysts from patients' skin, most commonly by skin scraping or by sticky tape sampling.2 Recovered nematocysts may help to identify the species, and confirm the diagnosis.3 Although successful nematocyst recovery is uncommon in Irukandji syndrome, it is disappointing that "no attempt was made to sample nematocysts"1 given the relative simplicity of the procedure and the importance of this case. The authors state that "no sting site was clearly delineated",1 but then go on to say that there were, in fact, areas of "skin flushing and intermittent diaphoresis"1 over a significant period of time. Sticky tape sampling of these areas may have yielded nematocysts, allowing positive species identification. Postmortem skin sections have also been employed in Chironex fleckeri fatalities, and have shown nematocyst barbs on the victim's skin.4 Postmortem examination may also have revealed other contributing factors. I am particularly interested in the assertion that almost every Irukandji syndrome patient in the Whitsundays develops a "rise in cardiac troponin levels".1 In fact, the cited article makes no mention of troponin, simply stating that CK-MB (creatine kinase isoenzyme) levels "can be abnormal",5 and that "some severe cases [of Irukandji syndrome] may have a CK-MB [level] well above the normal range".5 Many aspects of the diagnosis and treatment of jellyfish envenoming remain controversial. Accurate reporting of unusual cases is thus of the utmost importance.

Paul M Bailey

To the Editor: In their Notable Case on jellyfish envenomation causing Irukandji syndrome,1 Fenner and Hadok suggest that similar deaths may have occurred in the past, with the relationship to Irukandji syndrome not being recognised. However, their call for urgent research into developing an antivenom needs to be based on a clear understanding about the risk of death. Unfortunately, they have not presented data that clearly establish causation or support their conclusions about treatment and the need for further research. While they reported a history that supports envenomation, there was no confirmation by detection of nematocysts or autopsy to examine for other causes of death. An alternative explanation could be that the patient was overcoagulated and died from complications of an intracerebral haemorrhage. While it is clear that blood pressure must be monitored, to suggest that it must be treated with phentolamine is not supported by this case report. Clearly, supportive management and, in particular, the optimal treatment of cardiovascular complications needs to be defined and may obviate the need for antivenom.

Andrew H Dawson

In reply: While overcoagulation causing intracerebral haemorrhage could have caused the death of the patient we described,1 he was normotensive until developing signs and symptoms of Irukandji syndrome some 20 minutes after being stung. The Irukandji syndrome is, and always has been, a clinical diagnosis only. Biochemical and pathological test results become abnormal later, but are not diagnostic — actual cause and effect have been described only once, with the experiment unlikely to be repeated!2 Nematocyst studies, while established for Chironex fleckeri,3,4 have never identified species associated with Irukandji syndrome, except Carukia barnesi, which appears to occur in the Cairns area only. Other species probably cause the more severe syndrome seen in the Whitsundays and on the Great Barrier Reef, where these deaths occurred.5 One of us (P J F) is possibly the only person to have captured specimens likely responsible for causing Irukandji syndrome from the Whitsundays, and the species remain unidentified, as they are a new species and not described to date. Also, when the moribund patient was admitted, no obvious sting site was visible, and a negative skin scraping would not rule out a jellyfish sting. Phentolamine has previously proved effective for relieving distressing autonomic symptoms,6 and not just for cardiovascular complications, although it appeared ineffective at the lower doses used in our patient. However, nothing appears to prevent toxic cardiac dilatation occasionally occurring later in the syndrome.7 Further research is currently under way. Antivenom development may prevent some (possibly all) major symptoms of Irukandji syndrome. However, production is impossible until sufficient specimens of all species (some six to 10) causing the syndrome are caught and their venom assessed. Such advances are many years away and may never be achieved with current poor levels of funding. Cardiac markers for jellyfish envenomation have previously been identified.5,8 Since 1999 troponin level has replaced creatine kinase isoenzyme (CK-MB) level, and both are invariably raised in patients stung by the Whitsunday jellyfish. Thus, the words "cardiac markers" should have been used in the article and for not doing so I apologise. Despite C. barnesi stings being common at north Cairns beaches, it has taken six years of dragging the beaches, with nets to catch jellyfish of this species. The thought of trying to catch a 12 mm jellyfish that makes erratic and irregular appearances in several hundred square kilometres of ocean around the Whitsunday Islands is totally daunting, but the possibility is being assessed. Such a venture will depend on funding becoming available. Other stings were reported in the area at the time of our patient's death and are well known at the resorts where people who have been stung in surrounding areas are taken for treatment. However, stings remain erratic; they have no predictable patterns of appearance, and unfortunately prophecy is currently impossible.

Peter J Fenner · John C Hadok

To the Editor: The article by Tan and Fitzgerald1 raises numerous concerns. The authors report that their recommended personal protective equipment (PPE) conforms to standards "in a hospital environment where the chemical vapour concentration will not be high". At the same time, the authors acknowledge data indicating most patients from a disaster will present to the local hospital by private transport (ie, without triage, decontamination, or prehospital care). These two considerations are incompatible and further ignore the possibility of the hospital as a direct terrorist target. The authors' assertion that their three decontamination lines "allow mass casualties, as well as trolleys and equipment, to be decontaminated quickly, efficiently, and in an orderly fashion" is simply not evidence based. Of greater concern, the authors report "major considerations were policies and plans [referring to the hospital External Disaster Committee] and the emergency department response". Although this bottom-up approach to disaster planning is typical, it pays inadequate attention to interdisciplinary issues of proper hazard identification and management, environmental health, syndromic surveillance, and field outbreak investigation. Readers seeking robust emergency department templates are better referred to other sources for guidance.2,3 Of greatest concern, the authors report "our recommendations are similar to systems in the US and Israel, but much less intensive, as the threat of a terrorist attack here is perceived to be much lower". The three references cited for that statement date back to 1994, with none more recent than 1999. Moreover, the logic of the unreferenced threat assertion confuses hazard and risk. Although the absolute probability of a given hazard may be low, the risk attending that hazard encompasses vulnerability of the exposed population. With weapons of mass destruction, the conditional probability of catastrophic public health consequences is high — one event is the only number you will ever need. The current public health context of chemical–biological–radiological (CBR) incident management in Victoria is one of limited experience, performance improvement indicators, and budgetary support from public health authorities. Public health is at risk when authorities report that "faced with dozens of requests each day to attend sites to assess white powder, the stretch capacity did not exist and nor should it".4 As a result, the leading trauma centre in Australia extracts $20 000 from its existing operations budget to discharge its CBR responsibilities. This is not good enough. Nevertheless, the authors deserve credit for their initiative. Until cross-trained and disaster-experienced healthcare authorities reprioritise, this article shows the reader an excellent way to play a very weak hand.

David A Bradt

To the Editor: Tan and Fitzgerald's template for emergency department response to chemical–biological–radiological hazards appears to be based on a dubious assumption of a low level of risk.1 A recent report details exposure of emergency department staff to potentially fatal secondary contamination during a hazardous materials incident, highlighting the need for staff to have the appropriate training and equipment to deal with these events.2 I believe the level of Personal Protective Equipment (PPE) proposed by Tan and Fitzgerald is inadequate. The "facemask with filter" they describe is classified as Level C respiratory protection, and this level only conforms to the Australian Standard (for PPE) when the identity of the chemical and its vapour concentration are known, and when these do not exceed the filtering capacity of the particular filter mask being used.3,4 In the initial confusion of a hazardous materials incident, the identity of the chemical agent and its vapour will not be known. There may even be misinformation: during the 1995 Tokyo sarin attack, for example, initial advice to hospitals by the Tokyo fire service was that the incident was "a gas explosion in the Tokyo subway".5 Emergency department staff must be able to respond before the nature and severity of the chemical hazard can be determined. The only respiratory protection which conforms with the Australian Standard for PPE when the nature and severity of the chemical hazard has not been determined is the supplied gas respirator with full face shield of Level A (an encapsulating suit and self-contained breathing apparatus) or Level B (a non-encapsulating suit with self-contained breathing apparatus or a full face respirator on a gas line).3,4 Confronted with a hazardous materials emergency, potentially involving very toxic chemicals, emergency department staff need to have complete confidence in their own protection. This is only possible with the use of supplied gas respirators (Level A or B PPE), which provide complete respiratory protection. An additional problem with Level C air-purifying respirators is that their performance may be adversely affected by water ingress into the filter, which could occur during the decontamination procedures described in the template. Tan and Fitzgerald also propose having a clerk don PPE and enter the contaminated zone. Any stationery taken into a contaminated area would have to be decontaminated before being taken out to a "clean" area, and it is not clear what a clerk would add to the initial response within a contaminated zone.

Antony Nocera

In reply: We thank Bradt for his interest in our article and acknowledge his expertise in this field, which he has gathered in the United States and other countries. We also thank Nocera for his interest in our article. Our aim was to stimulate interest among the medical community in chemical–biological–radiological (CBR) response. The interdisciplinary issues mentioned by Bradt were mentioned in our article, but not in detail because of space limitations. Our personal protective equipment (PPE) conforms to Australian standards1-3 and the three decontamination lines are in keeping with other institutions. We are not aware of any simple decontamination system which, evidence-based, is superior. The choice of PPE in the ideal situation would be one that would provide adequate protection in all situations with a minimal amount of training, maintenance and expense. Nocera is correct in stating that the respiratory protection in an unidentified chemical hazard is Level A or B. These PPEs are expensive, bulky (which results in poor manual dexterity), and their use requires specialised training. The amount of chemical present on a victim surviving long enough to self-present to an emergency department is significantly less than that involved at the site of the incident. Therefore, the level of protection required for hospital staff would be less than that required by emergency rescue workers. Our PPEs were supplied by the Victorian health authorities. It is more important for staff to be familiar with their PPEs and for hospitals to have a CBR response that is regularly practised than having excessive protection that is limited to personnel who have undergone specialised training. The role of the clerk is to take patient details. These are radioed to staff in the hospital to help identify and correctly label patients, which is very important in mass casualty situations. Recent experience has demonstrated that terrorist acts are a worldwide phenomenon, and Australians are potential targets. This underlines the need for comprehensive training and maintenance of hospitals' CBR response. Since publication of the article, Victorian health authorities have reprioritised, and we therefore feel we have achieved the aims of our article.

Gim A Tan · Mark C B Fitzgerald

To the Editor: I was pleased to read the article on Ross River virus (RRV) disease by Mylonas and colleagues,1 because it included information on the cost of the disease. This makes it much easier to do something practical from a government and health economics perspective about the problem of RRV. The cost of $1018 per patient, including costs of negative tests looking for cases, sums to a total estimated cost to the nation of $5 million per annum (based on the reported average of 5000 cases per year in the study by Harley and colleagues2). Of note, $567 was spent per patient on diagnostic tests (56% of the total cost per patient), while the authors noted that in many cases the condition was self-limiting. I begin to wonder what is the use of spending $567 per patient diagnosed to prove a largely self-limiting condition that is treated symptomatically? Banning RRV testing could save $2.8 million per annum, which would be immediately available for mosquito control measures, and perhaps vaccine research, to reduce the burden of RRV disease. We could model the impact of a vaccination program — vaccine development cost, vaccine unit production cost, vaccine delivery, population target, and savings in disease prevented — to determine whether funding of vaccine research is worthwhile. The point is that without economic data we cannot make sensible "evidence-based" clinical management decisions. We are trapped in a scientific paradigm, and the health system implements unpopular cost–control interventions because it needs to control spiralling costs. We clinicians need to do better. If other researchers would follow the lead of Mylonas and colleagues and explore the economics of their subject, we would be able to make more rational choices about healthcare. It is up to clinicians to understand the economic agenda and suggest interventions that make both economic and clinical sense. We can then begin to make more efficient and rational use of our health dollars, relieving stress on a stressed system.

Ian R Cheong

To the Editor: Dugdale proposed recently in the Journal that people who have a skin reaction to mosquito bites are less likely to be infected by Ross River virus than those who do not.1 As he quotes Kumar, who made a similar comment about malaria infection,2 one could presumably extend his idea to other conditions transmitted by mosquitoes. This accords with my own personal experience of dengue fever acquired in Fiji. While serving there, I had two separate proven infections with dengue virus. As I react very little to mosquito bites, I could not identify the time of infection. Indeed, on the first occasion, I had just returned from a three-month stay in Adelaide and could not recall being bitten by a mosquito at all. In contrast, my wife, who developed large weals whenever bitten, went through at least three epidemics of dengue without being infected. My advice to travellers who consult me is that there is an advantage to reacting badly to mosquitoes, as one is then more likely to take anti-mosquito precautions, whereas the non-reactor is more likely to disregard them. However, Dugdale's suggestion that a local inflammatory reaction may be a factor in defence against infection is intriguing and worth following up. It should be simple to enquire retrospectively about reactions to mosquito bites in those who have had a mosquito-borne disease, as Dugdale has done for Ross River virus infection. This would provide evidence on which to base pathological and immunological studies.

Michael Sorokin

To the Editor: Dugdale recently suggested that people who develop skin reactions to mosquito bites may be protected against Ross River virus (RRV) disease.1 He noted that seven patients with a history of RRV disease all reported no skin reaction to mosquito bites, and 18 patients with no past history of RRV disease reported reacting to such bites. We argue that this correlation is entirely to be expected, as the lack of reaction to mosquito bites illustrates that the individuals have been previously exposed to many bites. At least two studies have shown a clear inverse correlation between mosquito exposure and bite reactions.2,3 Clearly, exposure to a large number of mosquito bites increases the risk of infection.4 Thus, a reaction to mosquito bites probably does not protect against RRV disease, but is simply a marker for low exposure to mosquito bites and therefore low risk of RRV infection. The rationale behind the association of itching bites and protection against RRV infection is also tenuous. Virus is likely to reach the circulation within seconds of introduction by the mosquito, whereas allergic reactions take minutes to develop. It is unlikely that a local reaction will affect viral replication at distant sites. In Dugdale's study, only people with a history of symptomatic RRV disease had undergone RRV serological testing. As about 30% of Queenslanders are seropositive,5 and 60%–75% of RRV infections are thought to be asymptomatic,6 some of the 18 people with no past history of RRV disease might be expected to have had asymptomatic RRV infection. This raises the question, does reaction to mosquito bites correlate with asymptomatic RRV infection?

Peter A Ryan · Jillann F Farmer · Brian H Kay · Andreas Suhrbier

Interest in envenoming syndromes caused by Australian jellyfish has been intense since the deaths in early 2002 of two tourists in Queensland, attributed to the Irukandji syndrome. We review current knowledge of these envenoming syndromes, mechanisms of venom action and therapy, focusing on the deadly box jellyfish, Chironex fleckeri, and the array of jellyfish thought to cause the Irukandji syndrome. Current understanding of jellyfish venom activity is very limited, and many treatments are unproven and based on anecdote. Worldwide media attention recently focused on Australia following the first two known human fatalities attributed to the Irukandji syndrome in Queensland in 2002.1 Jellyfish envenoming represents a major cost to northern Australian communities in terms of public health, leisure and tourism. Management of these syndromes depends on improved understanding of venom action and critical analysis of current therapy. We review the current state of knowledge of envenoming syndromes caused by Australian jellyfish, the mechanisms of venom action and management. We focus on the deadly box jellyfish, Chironex fleckeri, and the array of jellyfish thought to cause the Irukandji syndrome. Information was obtained from a search of MEDLINE, EMBASE and SciFinder Scholar for articles published in English over the period 1966–2002, using the keywords jellyfish, venom, Chironex fleckeri, Irukandji, Carukia barnesi, antivenom, pressure immobilisation bandaging, verapamil and therapy. Chironex fleckeriThe box jellyfish, C. fleckeri, is found in tropical waters of Australia's north, from Gladstone in Queensland to Broome in Western Australia (Box 1 and Box 2). It is most prevalent in summer, although stings have been reported year-round.1 The jellyfish has a transparent box-shaped bell measuring up to 20 cm by 30 cm and weighing up to 6 kg, while the total length of tentacles may exceed 60 m.3 Skin contact with C. fleckeri tentacles can result in dermonecrosis, pain and death, occasionally with alarming speed. Some patients also develop delayed cutaneous hypersensitivity reactions at the sting site.4 There have been 67 human deaths attributed to C. fleckeri, the most recent a six-year-old boy at Yarrabah, near Cairns in Queensland, in 1999.1 However, despite this jellyfish's reputation as the "world's most venomous animal",5 the vast majority of human stings are of little consequence.4 Most are managed with no analgesia, local ice packs or oral analgesia only, and rarely require hospital admission. The mechanism of action of C. fleckeri venom in severe envenoming remains unclear, but the key events appear to be cardiac or respiratory failure, or both.6,7 Some patients with severe C. fleckeri envenoming have been successfully treated by expired-air resuscitation alone,8,9 but fatalities have also occurred due to cardiac toxicity in mechanically ventilated patients.10 The Irukandji syndromeA number of jellyfish can cause the Irukandji syndrome,11 although only Carukia barnesi is conclusively known to do so. C. barnesi is a small carybdeid jellyfish with a transparent bell 1.5–2.5 cm in diameter. The infrequency of sightings or capture of C. barnesi and other small jellyfish that may cause the Irukandji syndrome makes precise knowledge of its geographic distribution problematic. Cases of Irukandji syndrome have occurred from Rockhampton in Queensland to Broome, although prevalence is greatest in the Cairns region. Recently, an Irukandji-like syndrome was reported in Hawaii.12 The Irukandji syndrome most commonly presents with generalised pain, hypertension (often severe), nausea, vomiting, and distress. The similarity of many of these symptoms to decompression sickness can provide a diagnostic challenge in scuba divers. Most patients presenting to emergency departments are treated with opiate analgesia, and about half require admission. A small number require advanced life support, usually because of cardiac failure.13 Catecholamine excess has long been proposed as a significant underlying mechanism in severe Irukandji syndrome.1,3,21 Victims develop symptoms mimicking medical conditions associated with endogenous catecholamine excess, such as phaeochromocytoma. Experiments in ventilated piglets showed a 200-fold increase in serum noradrenalin levels and a 100-fold increase in serum adrenalin levels after injection with crude extract of C. barnesi.22 These experiments quantified for the first time a relationship between experimental envenoming by C. barnesi and a hypercatecholaminergic state. However, there is no evidence of further deterioration in patients with cardiac dysfunction associated with severe Irukandji syndrome treated with adrenalin infusions.11 The mechanism of the cardiac dysfunction is yet to be elucidated. A review of 11 cases of pulmonary oedema developing in patients with Irukandji syndrome suggested that these patients had features of myocarditis.23 In a review of 116 patients with Irukandji syndrome presenting to Cairns Base Hospital in the summer of 2001–2002, 25 had raised serum levels of troponin I.24 Eighteen of these 25 patients had echocardiography, with six showing echocardiographic evidence of cardiac dysfunction. Significantly, no patients developed clinical cardiac failure. It is unclear whether the cardiac dysfunction is caused by a myotoxin or the hypercatecholaminergic state, or a combination. Venom delivery and actionJellyfish venom is delivered into prey or victims by millions of microscopic stinging cells, known as nematocysts. Light microscopy examination of nematocysts recovered from victims' skin is used to identify the envenoming jellyfish, particularly in Chironex stings. Two techniques are used to harvest nematocysts — scalpel-blade scraping of the sting site, and sticky-tape sampling. These tests generally demonstrate good specificity (ie, positive nematocyst identification correlates well with observed clinical syndromes).14 Both methods also appear to have similar efficacy in terms of nematocyst retrieval, although, given the low nematocyst identification rates in the Irukandji syndrome, their sensitivity remains unknown. The rapid onset of systemic symptoms after major jellyfish envenoming by C. fleckeri suggests that venom is "most probably introduced directly into blood vessels".15 Postmortem evidence from the last C. fleckeri fatality demonstrated nematocyst barbs penetrating the vascular dermis.16 C. fleckeri venom has haemolytic, lethal, myotoxic and dermonecrotic effects.17 Current evidence suggests that the venom toxins are proteinaceous and target specific organs. Monoclonal antibodies capable of neutralising C. fleckeri-induced haemolysis did not protect against the lethal effects of venom.18 Several myotoxins, with molecular weights of about 600 kDa and 150 kDa, have been reported in C fleckeri venom.19,20 These toxins showed significant lethality in a mouse model of envenomation and may play a role in human cardiotoxicity.3 We speculate that these and other, as yet unidentified, proteins cause ion flux and transmitter release through altering cell membrane permeability, either through specific interactions with ion-channels or receptors or through non-specific interactions with cell membranes. Treatment of jellyfish envenomingPrevention and first aidThe only reliable preventive measure is to avoid any contact with sea water. Other measures include wearing "stinger suits" or swimming inside "stinger nets" (Box 1), although these do not appear to protect against Irukandji syndrome.13 First aid measures include retrieval of the patient from the water, activation of the emergency medical system, and cardiopulmonary resuscitation, if appropriate. Acetic acid irreversibly inhibits firing of previously undischarged C. fleckeri nematocysts,25 and has greatest acceptance for beachside treatment of jellyfish stings; large amounts of vinegar are placed in prominent positions along swimming beaches in jellyfish-endemic areas. Pressure immobilisation bandagingPressure immobilisation bandaging (PIB) is advocated by Queensland26,27 and national28 authorities for first aid in jellyfish stings, but not by Northern Territory authorities.29 It was first proposed because of its effectiveness in treating elapid snakebite,30 but the link between treatments for snakebite and jellyfish stings is tenuous. Animal models demonstrate that PIB slows entry of snake venom to the circulation by halting lymphatic flow from the venom depot.31 However, in jellyfish stings, nematocysts may be widely distributed on victims' skin, and there is evidence that venom enters the victim's bloodstream directly rather than via lymphatics.16 No animal studies have been performed to demonstrate a beneficial effect of PIB in jellyfish stings, and a recent review found no scientific evidence to support the ongoing use of PIB in this setting.16 Furthermore, a significant amount of venom may remain in discharged nematocysts adherent to the patient's skin.32 An in-vitro model of nematocyst discharge showed that pressure equivalent to PIB caused further venom liberation from previously electrically discharged nematocysts from Chiropsalmus spp.32 Similarly, pressure equivalent to PIB caused additional venom release from naturally discharged C. fleckeri nematocysts exposed to vinegar, in amount similar to the initial firing.33 PIB in jellyfish envenoming thus remains at best unproven, and at worst potentially dangerous. More evidence is required to delineate its role in human jellyfish envenoming. The Australian Resuscitation Council has recently announced a change in advice to a more neutral position.34 Treatment of Chironex fleckeri envenomingAntivenomC. fleckeri antivenom is produced using "milked" venom, obtained by electrical stimulation of C. fleckeri tentacles. The antivenom neutralises the lethal, haemolytic, dermo-necrotic and pain-inducing effects of milked venom and whole-tentacle extracts in experimental animal models.3,5,6,35,36 However, it is less effective in neutralising crude nematocyst venom (obtained by mechanical rupture of nematocysts) compared with milked venom in a mouse model,5 creating doubt as to whether the milked venom used in its production contains all the lethal factors present in native venom. Evidence supporting the efficacy of C. fleckeri antivenom in human envenoming is anecdotal, with several reports of successful use.9,30,37 However, there is also a report of survival in major envenoming in the absence of antivenom.8 C. fleckeri antivenom appears safe to use. It is widely available in C. fleckeri-endemic areas, and is carried routinely by Queensland paramedics. As most patients who are envenomed by C. fleckeri have minimal symptoms, we believe that antivenom should be used only in those with cardiorespiratory instability, including cardiac arrest, or severe pain unrelieved by opiate analgesia (Box 3). VerapamilVerapamil was initially advocated to treat C. fleckeri envenoming on the basis of isolated organ experiments showing that C. fleckeri venom causes arterial constriction, reduced coronary blood flow and bradycardia.38,39 There is experimental evidence that these effects may be due to increased intracellular calcium concentrations in the affected organs.6,40 Two studies reported that verapamil significantly delayed death in experimental C. fleckeri envenoming, perhaps buying time for more definitive therapy.41,42 However, verapamil was associated with increased morbidity and mortality in a pig model of envenoming.6 There are theoretical reasons to be cautious in using verapamil for the potentially unstable patient, as it may potentiate hypotension and induce cardiac dysrhythmias. At best, it can be considered appropriate as experimental treatment for the patient in extremis. Clearly, more evidence is required to determine its role. Treatment of dermonecrosis and delayed cutaneous hypersensitivity reactionsDermonecrosis is a frequent acute complication of serious C. fleckeri stings. While indomethacin and methysergide have been shown to reduce C. fleckeri-induced capillary leakage,43 no animal or human clinical data have identified any agent that reduces long-term scarring. There are case reports of improvement in both acute and long-term cutaneous damage when C. fleckeri antivenom is used,30 but it should be noted that the acute skin changes of C. fleckeri envenoming often resolve spontaneously. At present, acute dermonecrosis is treated as a burn, with specific attention to avoiding secondary bacterial infection.7 Delayed hypersensitivity reactions are a common late complication of C. fleckeri stings, occurring in about 50% of cases, and are usually minor.4 Corticosteroid cream and oral antihistamines are the mainstay of treatment. Treatment of Irukandji syndromeEvidence as to the best treatment for Irukandji syndrome is anecdotal. The relative infrequency of patients with severe illness makes the prospect of high quality evidence unlikely. AnalgesiaNarcotic analgesia is routinely required, but no single agent has met with universal approval. There are several theoretical reasons to avoid pethidine, including potential for norpethidine toxicity and myocardial depression. Antihypertensive agentsPatients are often hypertensive at presentation, although it is unclear if this is due to pain or catecholamine-like effect. Phentolamine has been used to treat hypertension,44 but is rarely used in emergency departments and may not be available in some centres. An agent with a shorter half-life may be more advisable given the potential for cardiovascular collapse. Glyceryl trinitrate has been used15 and may be the first-line agent for hypertension. As cases of echocardiographically proven cardiac dysfunction have occurred, caution should be exercised in avoiding life-threatening hypotension. Treatment of pulmonary oedemaPulmonary oedema is treated in the usual manner, with supplemental oxygen, inotropic support with dopamine and adrenalin, and positive-pressure ventilation. The underlying cause appears to be significant cardiac dysfunction which returns to normal within three to four days. ConclusionsFundamental knowledge of the biology, venomology and toxidromes of medically important jellyfish is severely lacking. Many therapies currently used for jellyfish envenoming are based on anecdote and may be harmful. Formal understanding of the functional components of jellyfish venom may reveal a mechanism of action that is reversible with currently available pharmaceuticals. Alternatively, novel treatments for envenomed humans may also be developed, based on a more thorough knowledge of the mechanism of action of the venom components. 1: "Stinger net" at Palm Cove, Cairns Of all the beaches around Cairns, Palm Cove has the highest incidence of Irukandji syndrome. Stinger nets offer no protection against the tiny causative jellyfish, Carukia barnesi. 2: Distribution of Chironex fleckeri stings and Irukandji syndrome Sites of recent fatalities attributed to Irukandji syndrome (Hamilton Island, Jan 2002; Port Douglas, Apr 2002), and to C. fleckeri envenomation (Yarrabah, 1999). 3: Characteristics of Chironex fleckeri antivenom Derived from sheep serum Carries risk of anaphylaxis, although rare Indications: Cardiorespiratory instability Cardiac arrest Severe pain unrelieved by narcotics Dose: Initial dose is three ampoules, diluted 1 in 10 with normal saline If cardiac arrest, give up to six ampoules as an intravenous bolus Has been given safely as an intramuscular dose by ambulance staff before reaching hospital

Paul M Bailey FACEM · Mark Little FACEM, MPHTM · George A Jelinek MD, FACEM · Jacqueline A Wilce BSc, PhD

Objectives: (1) To identify the causative jellyfish species by examining skin scrapings in patients presenting to Cairns Base Hospital with marine stings, and (2) to describe clinical outcomes of those with Irukandji syndrome and those in whom nematocysts were identified from skin scrapings.Design and setting: (1) A retrospective case series of 128 patients, identified from Cairns Base Hospital emergency department records with discharge diagnoses of marine stings between 1 July 2001 and 30 June 2002. (2) A prospective study of skin scrapings from 50 patients presenting with marine stings from the same period.Main outcome measures: Number of patients with Irukandji syndrome, their opioid requirements and cardiac findings (where available); identification of causative species from nematocysts isolated from skin scrapings.Results: 116 patients retrospectively identified with marine stings had Irukandji syndrome. Of 50 patients who had skin scrapings, 39 had nematocysts consistent with Carukia barnesi. Symptoms experienced ranged from local pain alone to severe Irukandji syndrome with elevated troponin I levels, changes on electrocardiogram, cardiac dysfunction on echocardiography, and high opioid dose requirements. One patient had an unidentified cnidome on his skin scraping. He developed severe Irukandji syndrome and subsequently died from its complications.Conclusion: This is the first published report of Carukia barnesi being successfully identified from skin scrapings. Most patients with identifiable cnidomes experiencing Irukandji syndrome were stung by Carukia barnesi, which we show causes a wide range of illness, including cardiac dysfunction. Our finding of a cnidome not consistent with Carukia barnesi in the setting of Irukandji syndrome makes it possible that other species of jellyfish may also cause this syndrome.

Truc T Huynh MB BS · Peter Pereira FACEM · Richard Mulcahy FACEM · Paul Cullen FACEM · Jamie Seymour PhD · Teresa Carrette BSc · Mark Little FACEM

"Operation Bali Assist" was the name given to the Australian Defence Force (ADF) evacuation of injured Australians and foreign nationals after the Bali terrorist bombing on 12 October 2002. The operation involved the triage, stabilisation and evacuation of 66 critically ill patients from Bali to Darwin over 21 hours. Subsequently, the patients were stabilised in Royal Darwin Hospital (RDH) and then, under direction of Emergency Management Australia (EMA), transferred to various centres in Australia. The Royal Australian Air Force (RAAF) transported 35 patients in four separate missions and the operation involved 50 medical staff. Deployment ADF reservists sent in a Hercules C-130 13 October 2002, 0700 EST: The RAAF was tasked by Headquarters Air Command to send a Hercules C-130 transport aircraft to Bali for medical evacuation of Australians injured in an explosion the previous night. The initial information suggested that up to five patients might be seriously injured, possibly more. The medical team assembled at the RAAF's No. 3 Combat Support Hospital at Richmond Air Force Base, NSW, and prepared equipment to be loaded on the aircraft. This included equipment to transport two intubated and ventilated patients, 20 NATO litters (canvas stretchers in a standard size to fit any aircraft) for other patients, four units of locally sourced blood, and other items essential for an aeromedical evacuation (AME) in a military aircraft. 13 October 2002, 1530 CST: The aircraft arrived in Darwin and the AME team, which included one medical officer, three critical care nurses and three medical assistants, was advised that in Bali there were 15 very seriously injured and 20 seriously injured patients. The team was joined by two Army Reserve specialists (a surgeon and intensivist from RDH), another Air Force medical officer and nurse from RAAF Darwin, and extra equipment to allow the surgeon to perform operations as required. By this stage, a second aircraft was en route to Darwin from Richmond Air Force Base to assist in the evacuation. Phase 1: AME Bali to Darwin, 1930 13 October 2002 to 1400 14 October 2002Denpasar Airport, 13 October 2002, 1930 CST: The first RAAF aircraft arrived in Bali. The initial plan was to assess patients waiting at the airport and load these for the return flight. However, on landing we were informed that five casualties had just left on a private Learjet to Perth and that the most seriously injured people were at Sanglah Hospital (more than 40 minutes away by road). The medical team then split, leaving a medical officer and two medical assistants to prepare an Aeromedical Staging Facility (ASF), while the remainder went to Sanglah Hospital to manage the triage, resuscitation and movement of patients to the ASF. Three satellite phones were distributed to the medical officers to allow communication on the ground and to relay medical information and casualty estimates to Headquarters Air Command in Australia. Denpasar Aeromedical Staging Facility The ASF was situated in the airfield fire section in a hangar housing fire trucks and appliances. This provided shelter, light, electricity, places to hang IV lines, vehicle access, and direct access to the tarmac where RAAF Hercules C-130 aircraft would unload supplies and load patients. What greeted the medical team at Sanglah Hospital was something they will never forget. The hospital was overwhelmed with injured Australians with severe burn, blast and shrapnel wounds. There were two critical patients: one was a man with 80%–90% burns who was being ventilated by an Australian paramedic from Darwin on holiday; the other had extensive burns and had had a laparotomy for shrapnel wounds to the abdomen. Denpasar Airport, 13 October 2002, 2230 CST: The first aircraft had to leave for Darwin because of aircrew duty limits (the crew's duty time had already been extended twice). On board the RAAF Hercules C-130 were 15 patients: two critical and 13 relatively stable. One and a half hours into the flight, one critical patient died, despite aggressive attempts at resuscitation. The others thankfully remained stable and on arrival in Darwin were transferred to RDH. Denpasar Airport, 14 October 2002, 0130: At the ASF in Bali, casualties were pouring in, with up to 30 patients on the hangar floor being stabilised and operated on by medical staff and volunteers. The patients were mostly young, quiet and stoical. There were no complaints or unreasonable demands; on the contrary, most were concerned for their mates. Casualty management at Denpasar Denpasar Airport, 14 October 2002, 0430 CST: The second C-130 departed for Darwin with 22 patients on board (two in intensive care and ventilated, six in a serious condition). Denpasar Airport, 14 October 2002, 0600 CST: A third C-130 arrived with three anaesthetists, extra nursing staff and supplies. It was closely followed by a fourth C-130 carrying an AME team and two anaesthetists. The newly arrived staff were most welcome, and increased the capacity to stabilise patients before flight. Soon after, a fifth C-130 arrived with four more AME members and further supplies. Airway and circulation assessments, femoral lines, venous cutdowns — a gritty but surreal scene on the floor of a concrete fire hangar in tropical heat, ringed by anxious friends, relatives and interested Balinese emergency service personnel. Denpasar Airport, 14 October 2002, 0830 CST: The third aircraft was loaded with 16 patients (most critical patients last on – first off) and departed. The fourth C-130 was not far behind, carrying 11 patients and all remaining medical personnel who had been on the ground since the beginning of the evacuation. Left behind were 11 medical personnel, but no patients. The team resupplied and cleaned the ASF and consulate, and two medical personnel left the airport to check that no injured Australian or foreign national had been left behind in the hospitals or hotels. In the Denpasar Airport civilian terminal, large numbers of tourists evacuated by Qantas were checked for injuries requiring potential AME. Over the next few hours, only two more patients arrived at the ASF (one with three surfboards!). Denpasar Airport, 14 October 2002, 1400 CST: The fifth C-130 departed with all medical personnel, two patients and a small number of uninjured Australians (and three surfboards). Sixty-six patients were evacuated out of Bali in 21 hours using five Hercules C-130 aircraft and 34 Australian permanent and reserve military medical staff. An ASF was established to allow for stabilisation, resuscitation and field surgery to the injured people awaiting transport on military aircraft. Importantly, the medical staff were able to communicate through satellite phone to military headquarters to allow appropriate medical staff and supplies to be brought to the ASF and to coordinate the evacuation. Civilian retrieval companies, including Qantas, complemented the evacuation. Phase 2: AME Darwin to various major burns units, 2400 13 October 2002 to 1700 15 October 2002 Sydney: awaiting the arrival of patients from Darwin. The strategic AME component of Operation Bali Assist began while the first phase was ending. Civilian retrieval organisations (Royal Flying Doctor Service, Medical Emergency Adult Retrieval Service, CareFlight, and Retrieval Team Royal Adelaide Hospital) had flown to Darwin and began to transport ventilated patients to various hospitals throughout the country. This activity continued into the night of Monday. We focus on the ADF activities. Darwin, 14 October 2002, 1300 CST: The initial directive from Air Command was that there would be two strategic AMEs: one to Perth and the other to Brisbane, then Sydney and Melbourne. However, this soon changed, with the news that RDH and EMA had requested four strategic AMEs that evening: to Perth; to Adelaide then Melbourne; to Brisbane; and to Sydney. These were to be conducted in quick succession and would require a high level of logistical and personnel support. Darwin, 14 October 2002, 1600 CST: The first meeting was held with the staff from the RDH to determine the numbers of patients to be transferred to each of the capital cities, the priority of the patients, and how these patients were to be transported. A difficulty at this meeting was that patient priorities were still changing because of ongoing resuscitation and initial surgery. However, it was resolved that only the AME to Perth would transport ventilated patients; the other AME would not do so unless necessary. At the meeting, a rough patient manifest was determined for the AME to Perth. This included 12 patients, with burn surface areas between 5% and 40% and with varying degrees of blast and shrapnel injury. Two of the 12 patients were intubated and ventilated. It was decided that the most efficient means of transferring patients from RDH to the C-130 Hercules was by the RAAF ambulance bus. This bus is capable of carrying patients on NATO stretchers and can allow for transfer of a large number of patients. Volunteer crews from RAAF Darwin were responsible for loading and unloading the bus and aircraft under the direction of medical personnel. Darwin, 15 October 2002, 0150 CST: The first of the AMEs departed Darwin. The six-hour flight to Perth was uneventful until two hours out from Perth, when a ventilated patient suffered a cardiac arrest. Resuscitation efforts by the staff on board were successful. All patients were eventually transferred to Royal Perth Hospital. Darwin, 15 October 2002, 0305 CST: The second AME departed for Adelaide. On this flight were six patients with burn areas ranging from 15% to 50%, two patients with shrapnel injury, and two family members. None of the patients had been previously intubated and ventilated, but there was concern that one patient might have needed ventilatory support during flight. Also on this flight were three members of the Royal Adelaide Hospital retrieval team who had been working for the previous 24 hours. All patients were transferred to their destination medical facilities without incident. Darwin, 15 October 2002, 0530 CST: The third AME (seven patients with various blast, burn and shrapnel injuries) departed for Brisbane. By that stage of the operation, medical supplies and medications were beginning to run low and equipment issues began to appear. A late request from RDH to transfer a ventilated patient was accommodated; however, when reviewed, the patient was deemed to be too unstable for the four-hour mission to Brisbane. The medical staff on this flight consisted of two RAAF Specialist Reserve anaesthetists, one Navy Reserve anaesthetist and one Army Reserve anaesthetist, all proceeding home following the first phase of the operation. Without these Reserve personnel, the mission would not have been conducted. All members of the team remaining in Darwin were beginning to show obvious signs of fatigue by the time the third AME departed. The fourth AME was delayed while patients were prepared, and did not depart Darwin until about 1100 CST on Tuesday. On board the final flight were the bulk of the initial crew from RAAF Base Richmond who had mobilised initially, additional Reserve specialists and a CareFlight member who had been stranded in Darwin. Eight patients with various areas of burns and two family members were transferred on this flight. In all, 35 patients were transferred to the four capital cities over 16 hours on Tuesday, 15 October 2002. Crews that had been pushed to the limits of fatigue, having been working for an average of 34 hours with only broken sleep, undertook this feat and continued to provide optimal care for their patients until the work was completed. The second phase of Operation Bali Assist enabled the load to be shared among burns units across Australia. It ensured that most patients would be treated in their home State and it allowed the RDH the ability to cope with the numbers of injured patients for the time necessary to conduct vital resuscitation before resources became stretched. DiscussionA terrorist act causing large numbers of critically injured Australians in a country where the provision of medical services differs from our own provided unprecedented challenges. This tragedy required a response not previously conducted by Australia. Burns required prompt resuscitation and expert surgical management. It was recognised that the best response for these victims was to bring them safely to Australia and then to specialist burns units around the country. Military and civilian agencies, their planners and operators worked seamlessly to meet this challenge. No single agency could have conducted the whole operation. The tragedy focused the resources of the nation to give the best outcome for injured Australians. The AME had unique problems. There were large numbers of critically injured patients, necessitating large numbers of Specialist Reserve support, significant quantities of oxygen, IV fluids, blood products, drugs (morphine, ketamine, midazolam, muscle relaxants, antibiotics and Tet Tox) and critical care equipment (oxylog, Propaq monitors, etc). In the short response time, these were sourced from ADF facilities in Sydney and Darwin, and local hospitals in Sydney, Darwin and Adelaide. Each C-130 aircraft arriving in Bali brought more supplies, until the surplus allowed some excess fluids to be sent to Sanglah Hospital on our departure from Denpasar. The prompt response and support of ADF Specialist Reserve allowed expert medical care to be projected with this operation. As always, they provided experienced clinical judgement, procedural skills and support to the permanent medical force. The RAAF has identified areas for future improvement to maximise the capability we can project. These mainly focus around critical care equipment update, and training and alliances with civilian critical care services. Operation Bali Assist was successful because of the united and dedicated response of all people involved. So often in tragedy, individuals and organisations exceed normal expectations; this was no different. The ADF, EMA, the Department of Foreign Affairs and Trade, RDH, burns units around Australia and the Australian public were all crucial to the best outcomes for the victims of terrorism in Bali. With this operation comes the responsibility to ensure Australia's capability to react to such tragedies is enhanced. The possibility of future acts of terrorism ensures its maintenance.

Gregory V Hampson MB BS · Steven P Cook MB BS · Steven R Frederiksen MB BS

Several Australian medical practitioners were holidaying in Bali at the time of the nightclub bombing on 12 October 2002. On learning of the disaster, they went to Sanglah Hospital to assist. With the very limited resources of the hospital, they helped in providing emergency treatment, stabilising patients, and preparing Australian patients for evacuation. (MJA 2002; 177: 624-626) Bali is a common holiday destination for Australians — within easy reach, with a wonderful climate, a range of costs to suit all budgets, and friendly Balinese people. So it was that some medical practitioners from Australia happened to be in Bali near Kuta on the evening of 12 October 2002 when bombs exploded in a local nightclub, killing more than 100 people and injuring many more. On Sunday morning, we made our way to Sanglah Hospital to help the injured (Box). The hospital and patientsThere are several hospitals in Bali. The main one is Sanglah Hospital, laid out in extensive grounds with long, open corridor wards fed by a maze of partly covered walkways. Directories are not easy to read or follow. The scene at the hospital was like a movie set gone wrong, with many people milling around the walkways and in the wards. One of us was confronted with a multitude of patients (mostly Australian) with relatively minor injuries — lacerations, shrapnel and other foreign body wounds, and minor burns. These patients were given basic treatment and advised to fly back to Australia as soon as possible. The more seriously injured patients had been admitted to wards. An early decision was made to try and locate the non-Indonesian patients into ward 6, which we called "Australia Ward". This allowed us to focus our resources, but created logistical problems, as the beds were old, heavy and not on wheels. Moving them involved placing a hydraulic hoist arrangement under the bed, manually pumping it up to raise the bed, and then slowly and precariously wheeling the bed to Australia Ward. Almost all ward patients had serious, full-thickness burns (ranging from about 25% to 85%) and many had shrapnel wounds or intra-abdominal injuries. One patient had a torn right brachial artery, one a crushed left foot and right leg (both requiring amputation), another a fractured cervical vertebra and fractured pelvis and intra-abdominal wounds with damaged bowel. Two intensive care units held several ventilated patients with severe injuries, including major burns and abdominal trauma. One of these patients was a young unidentified girl who had a severe head injury and inhalation burns and was on escalating doses of inotropic drugs. She was looked after initially by an Indonesian neurosurgeon. It was evident her death was imminent. A difficult decision was made to transfer her to Australia in the hope that she would survive the trip and die on home soil. Our initial aims were to: resuscitate; treat emergency situations as they developed; stabilise the patients as much as possible; coordinate the evacuation in conjunction with the Australian consulate and the Australian military attaché; triage patients for evacuation (most severe and stable out first); and transport patients to the airport for stretcher flights to Australia as soon as practicable. Ambulance transport was available, with at least nine ambulances ready to shuttle patients — one patient per ambulance. Limited resourcesWard work was very arduous with the limited equipment available. Vital resources such as monitoring equipment, oxygen, large-bore cannulas and central venous lines were in extremely short supply. All patients required intravenous fluids, with several needing central lines, but we could find only four to use. Intravenous cannulas were small-bore and, as the burns commonly involved all limbs, insertion was often not easy. As luck would have it, our wonderful anaesthetic registrar made it look easy. The "rule of nines" was used to estimate the percentage total body surface area (%TBSA) and the Parkland formula (4 mL/kg/%TBSA burn in the first 24 hours) was used to calculate each patient's fluid requirement. The required amounts were written on patients' bed sheets or fluid balance charts and instructions given to the volunteers monitoring individual patients to ensure that each patient received the required fluid. As only 500 mL saline flasks were available, we needed to pump in the fluids. The small-bore cannulas often blocked or slowed. At least 40 urinary catheters were inserted and urinary outputs were monitored closely. Hourly urine volumes were measured, and specific gravity was estimated by the urine's colour. Medical records, including fluid balance charts, were kept as accurately as circumstances allowed. Our aim was to send the charts with the patients on evacuation — we felt communication to our Australian colleagues for ongoing care was very important. Cephalosporin antibiotics were available and given to all patients intravenously. Pain medication was in limited supply; some IV flasks were already made up with pethidine/saline and these were infused, titrating against pain. We split the limited available ampoules of pethidine and tramadol between us and administered and charted them according to pain levels. One of us well remembers an Australian man whose face was totally burnt, who could hardly open his eyes and, like many, could not hear well because of blast injury deafness. When offered pain relief he said, "No thank you doc, but go and see someone who needs it more than me". Unfortunately, despite his return to Australia, he did not survive. His unselfishness will live on. Burns were dressed as much as possible with the limited dressings available. Silver sulfadiazine started to become available late Sunday afternoon, but only in small tubes and limited supply. We had a dressing trolley with small amounts of gauze but no true bandages, and limited "semi-sterile" open bottles of antiseptic. We ran out of disposable gloves — no sterile gloves could be found. The water was not to be trusted for washing. Routine blood tests were not available and we had limited blood for transfusion. Four units were sent to us from the Royal Australian Air Force (RAAF) (2 O Rh– and 2 O Rh+) and yet many patients needed transfusing. We had no cross-matching facilities and were afraid to give Rh+ blood to young women. As time went by, limb swelling and peripheral ischaemia developed in many patients. About 20 escharotomies and fasciotomies were performed using limited equipment (eg, a blade without a handle). In most instances, these were performed without anaesthesia and analgesia because of the severe lack of resources. The patients understood the need for these operations and showed great courage in withstanding the severe pain. StaffWe would like to pay tribute to the few, overworked Australian nursing staff who aided us greatly. We had a smaller room in which we placed two very sick patients — one with more than 80% body burn and intra-abdominal wounds and one with a severed brachial artery which our Indonesian colleagues had repaired with a saphenous vein graft. In this quasi "high dependency unit" was a lovely New Zealand nurse who was very attentive. We are sure there were other medical staff who ably assisted the injured and we apologise that we cannot name them all. We hope that this record does them justice. A strong part of our team were the many volunteers who gave so much of their time and energy. With no training, just goodwill, they stayed for hours beside a fellow human being following our instructions — taking pulses, measuring urine outputs, checking IV fluid rates. Other volunteers spent hours manually fanning patients, as the ward had no air-conditioning. Evacuation The Australian embassy staff were excellent and very active in liaising with the Indonesian authorities, the hospital, the RAAF and the airport authorities. Initially we were told that aircraft would be arriving in the early evening of Sunday, 13 October, but this was delayed by a few hours. The first plane was a private jet, which took five seriously ill patients to Perth. The other planes were RAAF Hercules C-130 aircraft, each capable of transporting 28 stretcher patients and with a medical crew on board. They would transport patients to Darwin, where the patients would be reassessed at the Royal Darwin Hospital and then transferred to burns units around Australia (see page 620). The "walking wounded" from smaller peripheral hospitals and the Sanglah Hospital were evacuated to Sydney and Perth on a Qantas airliner and a privately owned jet. As the time to evacuate patients arrived, we listed the patients in the ward, grading them according to seriousness of injury, stability for travel, and need to get urgent multidisciplinary treatment in a better-equipped environment. As soon as the evacuations cleared Australia Ward, other patients from nearby wards were moved in. Eventually only eight or so Indonesian burns patients remained; these patients were treated no differently from those evacuated, except we were instructed that they were to remain. We found it difficult to leave these patients behind in the ward at this time (about 3:30 am, Monday, 14 October 2002), but we had learned of eight non-Indonesian patients in other hospitals. Leaving the Indonesian patients to Indonesian medical staff, we divided ourselves into three groups with three ambulances each and an Australian Embassy staff member to travel to each hospital and escort the patients to the airport for evacuation. On arrival at the airport we were impressed by the marvellous job the RAAF had done in setting up a triage hospital. The RAAF medical teams continued with the care of patients. We were required to perform two more fasciotomies at the airport, but as the last plane arrived we all headed back to our hotels, weary and drained from the experience. AftermathWe are indebted to our Indonesian colleagues for their care, without which we feel sure that many more lives would have been lost. We have attempted to convey the enormity of the situation, which is hard to appreciate without having been there. It is difficult to imagine an Australian hospital, despite its access to resources, coping with such a dramatic onslaught of casualties with so much carnage. Nevertheless, Bali is an underdeveloped country with matching facilities and this made it all the more difficult to attain the goals we set. It made us all very proud to know that the last of the RAAF aircraft took off from Denpasar Airport within about 30 hours of the explosion, taking the last of the 66 seriously injured patients back to Australia. We had performed as a team, used inner strengths none of us could ever imagine, brought people together and amassed a powerful human spirit that would leave all physically, mentally and emotionally drained. It is important to learn from this Bali bomb disaster, as, although we all pray for the day that all humans can live in peace, we all know that there will remain an element among us intent on repeating such atrocities. As doctors we must always be available to assist the injured. The disaster also brings home to us the powerful message of how fortunate we are to have trained so well in our profession in Australia. Although nothing could have prepared us for this situation, we feel that our Australian medical training was second to none. In the following days we would all suffer the problems of having been so intimately involved in a disaster — feelings that interfere with our daily lives. Physical and mental tiredness, emotional feelings that interfere with eating and sleep. Some of us have had stress reactions; however, experienced counselling has been invaluable as a preventive therapy. We are all now back to a near-normal life. Hannie Rayson, the renowned Australian playwright, wrote on "Courage" for one of us to read at a State memorial service for the victims of the Bali bombing. It epitomises how we, as doctors, felt: In the middle of this outrage, I was delivered an unexpected privilege — I experienced the force of the human spirit. I saw how courageous and selfless men and women can be, when the chasm opens beneath them. Tony Pethick, a general practitioner from Perth, had just returned to his hotel near the Sari Club when there was an initial "pop" noise followed by a much larger explosion. This almost blew him off his feet and shattered all his room's windows. He ran onto the street to see a massive orange mushroom cloud rising nearby and people staggering, running, and screaming. A man was clutching his abdominal viscera, hanging from an abdominal wound; there were lots of people with minor burns. Cars on fire were slewed across the road; in one the driver was slumped over the door, and closer inspection revealed he had been decapitated. After initial "numbness", Tony picked up a seriously burnt person from the roadway, and covered some of the burns with t-shirts from a nearby shop window. He then placed the patient into a small van and took him to a nearby clinic. More than 30 injured people were in the clinic, lying 2–3 per bed or on the floor. There was virtually no equipment. Tony comforted several patients, and they were slowly transferred to Sanglah Hospital. He accompanied one young girl with severe burns who was conscious until she was taken to the operating theatre. Holding her hand, he told her he would see her later. Some hours later, he found out that she had died — he telephoned her mother to explain. After several hours' sleep, he joined the other doctors at Sanglah Hospital. Priya Thalayasingam, an advanced trainee in anaesthetics, and Vijith Vijayasekaran, an advanced trainee in plastic surgery, are a couple from Perth. They arrived in Kuta on Saturday, 12 October, for a week's holiday. That night, as they returned to their hotel, they witnessed an explosion in the distance. At that stage, they were unable to find out what had happened, but early on Sunday morning their parents phoned, and they learned that many Australians had been injured in an explosion at the Sari nightclub. After several attempts, they contacted the Sanglah Hospital and Australian Consulate staff and proceeded to the hospital. John Hogg, a general surgeon from Wollongong, had arrived in Bali with his wife Linda, on the afternoon of the bombing. They were woken early the next morning by a call from their daughter in Australia, telling them of the blast. They immediately took a taxi, asking the driver to take them to the main hospital. John became involved in patient care, while Linda spent the next 20 hours trying to locate the missing, often in the morgue. Graeme Southwick, a plastic surgeon from Melbourne, had been a guest lecturer in Kuta and was spending three days after the conference with his wife at a resort. In the early hours of Sunday morning, his son phoned to say that a bomb had exploded in Kuta. Television reports initially suggested only a few casualties, but soon the full extent of the disaster became apparent. Phone calls to two hospitals on three occasions offering help were rejected. A few hours later a plastic surgeon in Jakarta (who had attended the conference) phoned to request help (agreed to by the Indonesian Minister of Health), and this opened the door to the hospitals. → See also "Operation Bali Assist. The Australian Defence Force response to the Bali bombing"

Graeme J Southwick FRACS, FACS · Anthony J Pethick MB BS · Priya Thalayasingam MB BS · Vijith S Vijayasekaran MB BS · John HW Hogg FRACS, FRCS(Engl)

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

Bart Currie · Melita McKinnon · Bernie Whelan · Philip Alderslade

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

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

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

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

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

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

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

Drew B Richardson FACEM