Emergency medicine

Rescue Air medical scene response to blunt trauma: effect on early survival Robert A Bartolacci, Blair J Munford, Anna Lee and Patricia A McDougall MJA 1998; 169: 612-616 For editorial comment see Cameron & Zalstein Abstract - Introduction - Methods - Results - Discussion - Conclusions - Acknowledgements - References - Authors' details - - More articles on Emergency medicine Abstract Objective: To assess the impact of on-scene treatment by an experienced critical care physician on prehospital resuscitation, the initial hospital phase and early survival of patients with major blunt trauma. Design, setting and participants: (i) Historical cohort of patients with trauma treated on scene by a helicopter emergency medical service (HEMS), 1986-1994, comparing medical and paramedical treatment and outcomes. (ii) Comparison of a subgroup of 77 patients (injury severity score [ISS] ≥15) treated by the air medical team (AMT) with (a) an ISS-matched group of 308 patients treated by ground paramedics (GPMs) and (b) the Major Trauma Outcome Study cohort. Main outcome measures: Procedural requirements assessed by the Therapeutic Intervention Scoring System (TISS), comparing resuscitation by medical and ambulance personnel; and observed versus expected mortality. Results: (i) Of 445 patients treated on scene, 270 (61%) had sustained trauma, and 215 of these received early management by the AMT. Problems with ventilation or with volume resuscitation were encountered by general duties ambulance personnel (40%) and paramedics (60%) before arrival of the AMT. (ii) Matched patients treated by GPMs required significantly more emergency department interventions on arrival at hospital (P < 0.01), and were possibly more likely to die in the first 48 hours (relative risk of death, 1.43; 95% confidence interval, 0.74-2.78) than patients treated by the AMT. Comparing the AMT-treated patients with the Major Trauma Outcome Study cohort, 9 deaths occurred of the 18 that were predicted -- a 50% reduction in predicted deaths (Z = 3.38; P < 0.001) -- and there were 11 unexpected survivors and one unexpected death. The adjusted "W" statistic was 12.18 (ie, there were 12 more survivors per 100 patients than the Major Trauma Outcome Study prediction, after adjustment for casemix. Conclusions: As part of the air medical team for response to major blunt trauma, a physician can provide significantly improved prehospital stabilisation, especially in airway and ventilatory control. Our results suggest improvement in mortality in AMT-treated patients, probably due to the enhanced procedural capabilities of physicians, despite longer prehospital times. Introduction Helicopter emergency medical services (HEMS) in Australia perform a variety of missions, including search and rescue, scene (or "primary") response to trauma or medical emergencies, and interhospital transport. Critical care physicians are included in the interhospital critical care transport teams, in accordance with specialist medical college policy,1 but staffing for scene responses varies. Some Australian HEMS use only ambulance officers (usually with paramedic certification),2 while others have scene response teams which include an emergency or critical care physician. The value of a physician for scene response is controversial.3-9CareFlight is a medically staffed helicopter service operating from Westmead Hospital, near the demographic centre of Sydney. The air medical team (AMT) comprises a specialist or registrar in anaesthesia, emergency medicine or intensive care, as well as a paramedic and/or aircrewman medical assistant. Since its inception in July 1986, the service has been available for both scene response and interhospital transport. Dispatch for scene response is at the discretion of the New South Wales Ambulance Service and is based on injury severity, entrapment, remote location, or difficult access (including the need for rescue hoist extrication). To assess the value of an experienced critical care physician as a member of scene response teams, we studied a retrospective cohort of patients treated on scene by CareFlight. Our aims were: To analyse the requirement, if any, for resuscitation of major trauma patients on scene and during transport by medically staffed HEMS; To use the Therapeutic Intervention Scoring System (TISS) (Box 1) to compare the hospital interventions required by patients with major blunt trauma after on-scene treatment by either an AMT or by ground ambulance paramedics (GPMs); and To use the Trauma Score - Injury Severity Score (TRISS) to compare early mortality of patients with major blunt trauma treated by an AMT with a matched group of patients treated by GPMs only, as well as with the cohort of the Major Trauma Outcome Study (Box 1). TRISS has been used to evaluate an Australian paramedic-staffed helicopter ambulance,2 but no previous Australasian study has done this for a medically staffed HEMS. Methods Our historical cohort of patients treated on scene by CareFlight was from the period July 1986 - June 1994. A number of groups were analysed (Box 2). CareFlight data Data were collected from CareFlight's clinical database and the Westmead Trauma Registry by one of us (R A B). Mission details from CareFlight's database included dates, patient demographics, nature of the accident, response, turnaround and transport times, injuries, staff on scene, assessment at scene, treatment before the arrival of the AMT, and treatment on scene/in transit by them. This information was supplied by the attending doctor at the completion of the mission. The treatment given by the AMT was in accordance with the principles of early management of severe trauma (EMST).21 On-scene procedures TISS scoring was done by one of us (R A B), and three groups of patients were compared for their resuscitation requirements when (1) AMT first on scene; (2) general duties ambulance officers already on scene; and (3) GPM ambulance officers already on scene. TISS scoring was done for the period from first intervention until arrival at hospital. Patients with major blunt trauma All patients who were transported to Westmead Hospital by the AMT who had major blunt trauma (injury severity score [ISS] ≥15) were identified from the Westmead Trauma Registry. Each of these 77 AMT-treated patients were matched with four randomly chosen patients with equivalent ISS (± 5) treated and transported by GPMs in the same year. Patients who had been treated by GPMs only and who were pronounced dead on arrival at hospital were excluded from this analysis. Other data collected included observations and procedures on arrival in the Emergency Department. TISS scoring was done for procedures performed in the Emergency Department. The predicted mortality of these 77 AMT patients was determined using TRISS and the coefficients derived from the Major Trauma Outcome Study16 (using the 1990 Abbreviated Injury Scale).15,20The revised trauma score (RTS)19 and the ISS14 were calculated from information on injuries sustained recorded in the case notes or the autopsy reports. To calculate the RTS, the Glasgow Coma Scale (GCS) and respiratory rate were obtained from CareFlight's records. The predicted mortality could not be calculated for the ISS-matched GPM group as these data are not recorded by the ambulance service. The comparison between predicted and observed mortality of AMT patients was made at 48 hours after hospital admission. Survival intervals as short as 6-12 hours have been used previously9,22 to measure efficacy of prehospital care, while 48 hours was recommended by Baxt and Moody, who found that all deaths related to prehospital factors occurred within this time.6 Statistical analysis On-scene procedures Kruskall-Wallis ANOVA was used to compare the resuscitation requirements of the three groups with different staff first on scene, as evaluated by TISS. Major blunt trauma patients We compared patient demographics, hospital interventions and outcomes of patients treated by the AMT with these data for patients treated by GPMs using appropriate Student's t tests, Mann-Whitney U tests and chi-squared analysis. Early death was defined as death due to initial injuries or complications of those injuries within 48 hours of hospital admission. The relative risk (RR) of early death and 95% confidence intervals (CI) were estimated to compare outcomes of patients treated by the AMT and GPMs, respectively. Comparisons between predicted and observed mortality of AMT patients were made using the "Z", "W" and "M" statistics.16 Flora's "Z" statistic estimates the deviation of mortality in the study group compared with the Major Trauma Outcome Study benchmark.16 The "W" statistic provides a clinical perspective on a statistically significant "Z" score,19 and calculates the number of survivors more (or less) than the Major Trauma Outcome Study norm per 100 patients analysed.23 The "M" statistic evaluates the match of injury severity between the study group and the entire Major Trauma Outcome Study cohort.16 An adjusted "W" statistic was also estimated using the method of Younge et al,23 which was developed to adjust for the more severely injured patients treated by HEMS. Results Over the study period, the AMT attended 445 patients in scene responses, of whom 270 had trauma (Box 2). This excluded minor injuries where the HEMS was required only for remote access or hoist extrication. Most patients were male (70%). Vehicle-related trauma occurred in 138 patients (51%); 19 patients (7%) were entrapped. The trauma cases included 61 (23%) with spinal injury only, 19 (7%) with head injury only, 81 (30%) with head plus other injuries, and 109 (40%) with other injuries. Only three cases (1%) had penetrating trauma. The median response time for the ATM from initial call to arrival at the patient was 26 minutes (range, 6-624, including several cases requiring prolonged secondary access). The median turnaround time (time from arrival at patient to departure from scene) was 33 minutes (range, 1-400, including entrapments and difficult access). Median transport time (time from scene departure to arrival at tertiary facility) was 18 minutes (range, 3-205). Comparison of on-scene treatment Of 270 patients with trauma, 215 required AMT assistance. The AMT was first on the scene for 31 of these patients (14%); general duties and paramedic ambulance officers were on the scene before the AMT's arrival for 50 (23%) and 125 (58%) patients, respectively. In the remaining nine patients (4%), other health professionals were on the scene. Of the 61 spinal injury patients, 26 (43%) did not require AMT assistance. Conversely, of the 209 remaining patients with head and/or other injuries, only 29 (14%) did not require AMT assistance. No patients died during transport, but 12 died at the scene. Eleven of these were already in traumatic cardiac arrest when the AMT arrived and one was an entrapped motor vehicle accident victim who exsanguinated during release. The on-scene procedures performed by general duties ambulance officers and paramedics, the supplementary patient management by the AMT, and problems identified with treatment given by ambulance officers and paramedics are shown in Box 3. Of the 35 paramedic-treated patients with a low score on the Glasgow Coma Scale (< 9), only 15 (43%) were correctly intubated at the time of the arrival of the AMT. Even in the 16 patients with a score on the Glasgow Coma Scale of 3 or 4, six (37%) were not intubated before AMT arrival. Of the 18 patients with endotracheal tubes placed by paramedics, there were problems in five (28%) cases, including three oesophageal intubations. Intubations by the AMT were all oral, with the aid of muscle relaxants, with no failed or oesophageal intubations. No patient with a low score on the Glasgow Coma Scale (< 9) was transported unintubated. There was a significant difference in median TISS scores between the three patient groups -- AMT first on scene, and general duties ambulance or paramedics first on scene (P = 0.04). There was a significantly higher number of interventions in the paramedic group (median TISS score, 12) than in the AMT (median TISS score, 7) (P = 0.01). Patients with major blunt trauma Hospital interventions and outcome There were no significant differences in patient characteristics between the AMT-treated (n = 77) and matched GPM-treated (n = 308) groups transported to Westmead Hospital (Box 4). Patients in the GPM group required significantly more interventions in the Emergency Department (median TISS score, 3) than those in the AMT group (median TISS score, 2; P < 0.01). In comparing the various resuscitation procedures (Box 4), the AMT group required fewer intravenous line placements and endotracheal intubations and less mechanical ventilation than the GPM-treated group. Patients in the GPM group were 1.43 (95% CI, 0.74-2.78) times more likely to die in the first 48 hours compared with those in the AMT group. Comparison with the Major Trauma Outcome Study The outcomes for the patients in the AMT-treated group using TRISS (1990 coefficients20) are shown in Box 5. The predicted number of deaths for the group analysis was 18. Nine patients actually died within 48 hours, a 50% reduction in expected mortality. The difference in the observed and expected number of survivors was significant (Z = 3.38; P < 0.001). The W statistic was 11.88. The M statistic was 0.52, which is less than the 0.88 acceptable level16 for comparing populations (ie, there was a higher proportion of patients with a low probability of survival in the AMT group compared with the Major Trauma Outcome Study cohort) (Box 6). This required calculation of an adjusted "W" statistic (using the method of Younge et al to compensate for casemix difference), which was 12.18 (95% CI, 5.29-19.07). This suggests that there are 12 more survivors per 100 patients with major blunt trauma than would be predicted by comparing with the Major Trauma Outcome Study, after adjusting for casemix differences but not for late deaths (> 48 hours). Discussion Our study shows the advantages of a medically staffed HEMS, compared with paramedics alone, for prehospital stabilisation of major trauma patients. Of note was the number of patients with low scores on the Glasgow Coma Scale (< 9) who were not able to be intubated by paramedics, reflecting the difference between airway control in patients with cardiac arrest (unmodified oral intubation is usually possible) and those with trauma (likely to require techniques incorporating sedatives and muscle relaxants outside paramedic protocols). Medically treated patients required significantly fewer interventions in their initial hospital phase compared with patients treated by GPMs. Because of hospital proximity, some patients in the paramedic group may have been rapidly transported, thus generating additional interventions and TISS points. However, some interventions (eg, airway control) should be performed as soon as possible regardless of hospital proximity. In AMT-treated patients with severe blunt trauma, there were significantly more early survivors than predicted by TRISS. There were also more survivors compared with the ISS-matched group of GPM-treated and GPM-transported patients, although the 95% confidence interval does not exclude a similar risk of death or even a better chance of survival in the GPM-treated group. The percentage improvement in both comparisons is very similar, suggesting a real improvement over the GPM-treated group. As this occurred despite longer prehospital times, it is presumably due to the enhanced prehospital stabilisation by the AMT. Baxt and Moody were the first to use TRISS to assess the impact of HEMS scene response in trauma. They found a 52% reduction in predicted mortality from blunt trauma in an AMT-treated group versus a non-significant increase in a standard GPM-treated group, despite greater distances and prehospital time in the former.17 Two other studies have found that physicians contributed judgement or procedural skill, or both, in 22%5 to 25%24 of missions. A subsequent US multicentre study showed a 21% reduction in mortality, using the Major Trauma Outcome Study cohort as a benchmark.25 Only four out of seven of these services included a physician in the medical crew. However, this study cannot be directly compared with ours as the non-physician crew were more highly trained and often worked under direct radio control of a critical care or emergency physician, while the physicians were more junior than their Australian equivalents. In Australia, procedures performed by paramedics are limited and on-line medical control is not used. Our study found major differences in resuscitation compared with an earlier Australian HEMS study by Cameron et al with a paramedic crew,2 in which 42% of patients with a low score on the Glasgow Coma Scale (< 9) were transported unintubated (compared with none in our study). This non-intubation rate was almost identical to that before AMT arrival in our study, reflecting the shortcomings of current paramedic protocols as discussed above. Limitations to our study include its small sample size, which may reflect underutilisation of the service, and the fact that it is retrospective. Selection bias cannot be ruled out, and this may have affected the results either way: the AMT may not have been called out for some older patients or those with a poor prognosis; and, conversely, anecdotal evidence suggests that the AMT may be called out by paramedics when a patient's death is imminent. However, we found no difference in demographics between AMT- and GPM-treated patients. The main limitation was that data collection by the NSW Ambulance Service does not include all the variables necessary to calculate the RTS. Hence, TRISS could not be calculated for the matched GPM group, only the ISS. TRISS itself has limitations: the physiological component (RTS) varies with time and therapy. Thus, consistent timing of data collection is logistically impossible in any trauma population, whether this is done prehospital or at admission. Nevertheless, there is a need for better data collection and more outcome studies of all Australian trauma patients. Ideally, TRISS data should be available for all trauma patients to aid in evaluation of trauma care, with calculation of local norms for survival. Only then will it be possible to accurately assess the value of HEMS with and without advanced medical capability. The significance of our study needs to be viewed in the light of the regionalised system of trauma centres, the benefit of which lies in the centralisation of experience and resources available to patients on reaching the trauma centre. The disadvantage is that some patients will now find themselves further from this destination. The need for pretransport stabilisation must be balanced against the need for rapid transport to definitive care. Rotary wing transport can shorten transport times, but may not decrease total prehospital time when used as a secondary response (ie, when called in by emergency services already at the scene). Helicopters, although two to three times faster than road ambulance, must travel twice as far (out and back), plus launch time and time on scene. Consequently, the value of HEMS is limited if the staff are unable to provide a higher level of clinical care on scene and in transit. A study of paramedic-staffed urban HEMS showed no improvement in prehospital time or survival when called in by ground paramedics already on scene.22 This is consistent with the findings of the Australian study by Cameron et al.2 While care must be taken not to unnecessarily prolong scene times, our study showed almost identical scene times to those for Australian paramedics.2 A study of rural HEMS also found that scene times are not prolonged by performance of advanced procedures by physicians.26 Conclusions Our study suggests that an appropriate critical care doctor should be considered, if not routinely incorporated, as part of any air medical scene responses to major blunt trauma. Air medical transport is currently relevant only to those trauma patients who have significant injuries and, because of distance, entrapment, or difficult access, cannot be rapidly transported to an appropriate hospital by conventional ambulance. In these circumstances, prolongation of prehospital time is frequently inevitable despite HEMS. Consequently, more advanced prehospital measures from a critical care medical team may be required aboard the HEMS. The use of HEMS allows an AMT to respond rapidly over a wide area. Acknowledgements We thank Dr P D Middleton, FRACS, formerly Trauma Fellow at Westmead Hospital for his contribution to the pilot study. We also thank Valerie Kuther and Larry Bain from Tri-Analytics Inc for providing unpublished data from the Major Trauma Outcome Study. References Australian and New Zealand College of Anaesthetists/Australasian College of Emergency Medicine. Minimum standards for the transport of the critically ill. Melbourne: Australian and New Zealand College of Anaesthetists/Australasian College of Emergency Medicine, 1992. (Policy Document P23.) Cameron PA, Flett K, Kaan E, et al. Helicopter retrieval of primary trauma patients by a paramedic helicopter service. Aust N Z J Surg 1993; 63: 790-797. Munford BJ, Manning R. Paramedic helicopter retrieval of trauma patients [letter]. Aust N Z J Surg 1994; 64: 640-642. Cameron P. Paramedic helicopter retrieval of trauma patients [letter]. Aust N Z J Surg 1994; 64: 640-642. Rhee KJ, Strozeski M, Burney RE, et al. Is the flight physician needed for helicopter emergency medical services? Ann Emerg Med 1986; 15: 174-177. Baxt WG, Moody P. The impact of a physician as part of the aeromedical prehospital team in patients with blunt trauma. JAMA 1987; 257: 3246-3250. Hamman BL, CuŽ JI, Miller FB, et al. Helicopter transport of trauma victims: does a physician make a difference? J Trauma 1991; 31: 490-494. Burney RE, Passini L, Hubert D, Maio R. Comparison of aeromedical crew performance by patient severity and outcome. Ann Emerg Med 1992; 21: 375-378. Schmidt U, Frame SB, Nerlich ML, et al. On-scene helicopter transport of patients with multiple injuries; comparison of a German and an American system. J Trauma 1992; 33: 548-555. Cullen DJ, Civetta JM, Briggs BA, Ferrara LC. TISS (Therapeutic Intervention Scoring System): a method for quantitative analysis of patient care. Crit Care Med 1974; 2: 57-60. Keene AR, Cullen DJ. Therapeutic intervention scoring system: update 1983. Crit Care Med 1983; 11: 1-3. Rhee KJ, Burney RE, Mackenzie JR, et al. Therapeutic Intervention Scoring as a measure of performance in a helicopter emergency medical services program. Ann Emerg Med 1986; 15: 40-43. Burney RE, Rhee KJ, Cornell RG, et al. Evaluation of hospital-based aeromedical transport programs using therapeutic intervention scoring. Aviat Space Environ Med 1988; 59: 563-566. Baker SP, O'Neil B, Haddon W, Long WB. The Injury Severity Score: a method for describing patients with multiple injuries and evaluating emergency care. J Trauma 1974; 14: 187-196. Champion HR, Copes WS, Sacco WJ, et al. The Major Trauma Outcome Study: establishing national norms for trauma care. J Trauma 1990; 30: 1356-1365. Boyd CR, Tolson MA, Copes WS. Evaluating trauma care: the TRISS method. J Trauma 1987; 27: 370-378. Baxt WG, Moody P. The impact of a rotorcraft aeromedical care service on trauma mortality. JAMA 1983; 249: 3047-3051. Champion HR, Sacco WJ, Carnazzo AJ, et al. Trauma score. Crit Care Med 1981; 9: 672-676. Champion HR, Sacco WJ, Copes WS, et al. A revision of the Trauma Score. J Trauma 1989; 29: 623-629. Champion HR, Sacco WJ, Copes WS. Injury severity scoring again. J Trauma 1995; 38: 94-95. Royal Australasian College of Surgeons, Road Trauma Committee. Early management of severe trauma course manual. Melbourne: RACS, 1989. Schiller WR, Knox R, Zinnecker H, et al. Effect of helicopter transport of trauma victims on survival in an urban trauma centre. J Trauma 1988; 28: 1127-1134. Younge PA, Coats TJ, Gurney D, Kirk CJC. Interpretation of the W s statistic: application to an integrated trauma system. J Trauma 1997; 43: 511-515. Snow N, Hull C, Severns J. Physician presence on a helicopter emergency medical service: necessary or desirable? Aviat Space Environ Med 1986; 57: 1176-1178. Baxt WG, Moody P, Cleveland HC, et al. Hospital based rotorcraft aeromedical emergency care services and trauma mortality: a multicenter study. Ann Emerg Med 1985; 14: 859-864. Anderson TE, Rose WD, Leicht MJ. Physician staffed helicopter scene response from a rural trauma center. Ann Emerg Med 1987; 16: 58-61. (Received 23 Sep 1997, accepted 28 Jul 1998) Authors' detailsNRMA CareFlight, Westmead Hospital, Westmead, NSW. Robert A Bartolacci, MB BS, Provisional Fellow in Anaesthesia. Blair J Munford, MB ChB, FANZCA, Specialist Anaesthetist. Anna Lee, MPH, Honorary Epidemiologist. Department of Surgery, Westmead Hospital, Westmead, NSW. Patricia A McDougall, RN, CNC, Trauma Nurse Coordinator. Reprints: Dr B J Munford, NRMA CareFlight/NSW Medical Retrieval Service, PO Box 159, Westmead, NSW 2145. Email: bmunfordATozemail.com.au Make a comment Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/>

Robert A Bartolacci · Blair J Munford · Anna Lee · Patricia A McDougall

Letter Removing rectal foreign bodies: is the ventouse gender specific? MJA 1998; 169: 670-671 To the Editor: A man presented in an Australian provincial town with a foreign body in his rectum that would not pass. He stated that he thought it was a bottle top. Arrangements were made for the resident surgeon to retrieve the object by sigmoidoscopy under general anaesthesia. After an uneventful induction of anaesthesia, the surgeon proceeded to try to remove the "bottle top". However, it was soon obvious to him that he was not looking at a bottle top, but rather at the bottom of a glass bottle approximately 5 cm in diameter. Attempts to remove it with fingers, assisted by abdominal pressure, very similar to bimanual pelvic examination of the female pelvis, were unsuccessful. The surgeon was considering proceeding to laparotomy, with the aim of pushing the bottle up into the sigmoid colon and then opening the abdomen and retrieving it. However, the general practitioner anaesthetist, also trained in advanced obstetrics, suggested the possible use of the ventouse. The surgeon agreed, but, having no experience in the use of the ventouse, invited the GP to perform the procedure. The management of the anaesthesia was handed over. A small disposable plastic ventouse cup (Mityvac 0044M) was gently inserted through the already lax anus and manipulated onto the bottle. The rim was checked for trapped rectal mucosa. After three attempts to seal, suction was successfully applied. The rim was then checked again for mucosa and gentle traction applied. The bottle descended easily and delivered per rectum with no obvious trauma to the anus. The surgeon then checked for mucosal tears by sigmoidoscopy. There were none, and the patient was discharged the following day. I describe this case to illustrate two points. Firstly, that general surgeons may find a use for, and possibly adapt, the well-tried ventouse cup for delivery of foreign bodies per rectum. It would be advisable to have some obstetric training to learn how to avoid the dangers of mucosal entrapment. The advantages of the suction cup are that it will mould to the object and that it doesn't increase the diameter of the foreign body. Secondly, that the multiskilled rural GP still has a place in medicine, and can occasionally bring expertise from one area to another to benefit the patient. Richard P G Mackinnon Rural General Practitioner, Crystal Brook, SA 5523 Email: rmackinnATpirie.mtx.net.au Comment: The above tale of clinical cunning is an excellent illustration of the need for lateral thinking in certain situations. The particular clinical problem described has been with us for some time and is seen all over the world. It is relatively common, and requires a sensitive, meticulous and skilfully taken history, a professional physical examination, and diagnostic imaging (usually x-rays, occasionally ultrasound or computed tomography) before a careful plan based on knowledge and experience is formulated. However, a marked degree of modification or even innovation, depending on the particular object to be removed and the clinical circumstances, is often used. Not infrequently, careful trial and error (and luck) are factors in the outcome. A quick scan of the literature confirms the diverse and international nature of the problem and of its solutions. A German report tells of an apple wrapped in cellophane, unable to be retrieved until coagulated intermittently by argon laser. The Indian gastroenterology journal tell us of screwing out carrots, removing needles and whisky bottles.1 A series from Athens reports success with obstetric forceps in 40% of cases, while highlighting the importance of negating the proximal vacuum suction effect caused by traction on the foreign body, especially smooth, round ones like bottles (see Figure 1). This is commonly done by gently passing a well-lubricated Foley-type urinary catheter up past the object to break the air seal.2 An overview of cases from California and London reminds us that, although foreign bodies can be removed in the emergency department in about two out of three cases, some 10% still require a laparotomy and a diverting colostomy to remove the object or to treat bowel perforation. Only one case report (which claimed to be a world's first) described the use of an obstetric vacuum extractor.3 As in the case described above, this report also emphasised the practical issues of ensuring that no mucosa is trapped and the need for follow-up sigmoidoscopy to check for mucosal damage or perforation. The case described above also illustrates the element of surprise when what we are led to expect from the history is nothing like what we really have to deal with (see Figures 2 and 3). As 80% of these events occur for sexual stimulation and 10% involve sexual assault,4 it is understandable that there may be an initial reluctance to tell the truth. At all times, before and after the extraction, extra effort must be made by all staff to show a confidential, sensitive and caring attitude to a patient who is deeply embarrassed and often in great discomfort. Gordian Fulde Director, Emergency Department, St Vincent's Hospital Victoria Street, Darlinghurst, NSW 2010 Vashist MG, Arora AL, Salil. Screwing a carrot out of the rectum [letter]. Ind J Gastroenterol 1997; 16: 120. Kouraklis G, Misiakos E, Dovas N, et al. Management of foreign bodies of the rectum: report of 21 cases. J Roy Coll Surg Edin 1997; 42: 246-247. Johnson SO, Hartranft TH. Nonsurgical removal of a rectal foreign body using a vacuum extractor. Report of a case. Dis Colon Rectum 1996; 39: 935-937. Cohen JS, Sackier JM. Management of colorectal foreign bodies. J Roy Coll Surg Edin 1996; 41: 312-315. Acknowledgment: Figures 2 and 3 were kindly provided by Dr T O'Connor, Colorectal Surgeon, St Vincent's Hospital, Sydney. Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/>

Rescue Transport of the critically ill Is there a doctor in the helicopter? MJA 1998; 169: 610-611 In this issue of the Journal, Bartolacci, Munford and coworkers1 present an Australian perspective on major controversies in aeromedical transport. The controversies revolve around two central questions: the benefit of helicopter as opposed to ground transport, and the benefit (or otherwise) of a doctor as part of the transport team. While articles on these aspects of patient transport have been published since the early 1970s, good research is lacking. This largely reflects the difficulty of conducting controlled trials in an extremely complex field with many uncontrolled variables. The article by Bartolacci et al illustrates some of these problems: comparison groups were not randomised and data being compared (eg, admission versus scene data) were not directly comparable. This emphasises the need for a more scientific approach to this form of research. Even the often-quoted landmark studies by Baxt and Moody,2,3 which concluded that medical staffing of a helicopter rescue service significantly improved outcome, had similar drawbacks. They used scene data to calculate trauma scores for the cohort of patients treated by doctors (as part of a helicopter team) and compared outcomes with scores calculated from admission data for the group of patients treated by paramedics. Another study came to the opposite conclusion. Nicholl and colleagues4 found that the London HEMS (Helicopter Emergency Medical Service) made little impact on survival, except perhaps in the most severely injured patients. They used complex statistical manoeuvres in an attempt to artificially separate the effect of the helicopter team's intervention from that of the helicopter transfer and of the major trauma service receiving the patient. Even when the methodological flaws of these studies are overlooked, the conclusions reached are often specific to the system studied, and therefore have little external validity. For example, like Bartolacci et al, Dalton and colleagues concluded that a doctor was of benefit on a HEMS, as he or she could perform procedures that paramedics were not trained to do, such as orotracheal intubation.5 This may apply to the London HEMS, but other systems train non-physician flight staff to perform orotracheal intubation with or without muscle relaxants.6,7 A further concern is that most of the published work to date, like that of Bartolacci et al, focuses on trauma patients, and particularly on scene response. While trauma is important and rapid access of patients to definitive care has been demonstrated to be of benefit, it accounts for only about a third of patient transfers to hospitals (by all modes) for provision of specialised care. Several studies of all forms of interhospital transfer of critically ill non-trauma patients support the view that in such cases not only is it beneficial to have a doctor as part of the transport team, but that the doctor must be highly experienced in the management of critically ill patients -- junior doctors provide no benefit.7-9 While it will not be possible to make valid, universally applicable conclusions until detailed databases are established to act as a basis for integrated transport research, the work conducted to date suggests that the presence of an appropriately trained physician on a helicopter may make a significant impact on the outcome of patients in some circumstances: stable patients with cardiac problems, for example, may not require medical treatment during transport, whereas patients with complex critical illnesses may require an experienced clinician. Despite the limitations and difficulty interpreting studies to date, some aspects of a critical care transport system seem from first principles to be beyond debate. The medical transport system must utilise an integrated approach: it must be clear where patients with given conditions should go, and clinicians and hospitals must identify their role and areas of special expertise within the system. Lines of referral and communication must be clear and established as part of the inherent structure of the system. The process of initiating the transfer should be as simple as possible. A single, 24-hour telephone number which permits rapid communication between the referring doctor, the accepting unit and the transport team permits smooth access to the system. A clinician experienced in critical care should coordinate the process, prioritise transport, facilitate referral and determine which form of transport is most appropriate. Dedicated helicopters must be readily available, with all the equipment necessary for monitoring and safe transport of patients where appropriate. Minimum standards for such transport are detailed in the joint policy document of the Australasian College for Emergency Medicine (ACEM) and the Australian and New Zealand College of Anaesthetists (ANZCA),10 the essential principles being that transport should aim to improve patient care, and that "management during transport should equal or better management at the point of referral". In the debate about the benefit of helicopters as opposed to ground transport, helicopter transport is more expensive, but has the advantage of being able to collect patients from the roadside or referring hospital and deliver them more rapidly to the receiving institution. However, patients less than 30 minutes by road from hospital generally do not benefit from helicopter transport. Similarly, beyond 300 km, or when helicopter flight time exceeds one hour, the question becomes whether the greater air speed of fixed-wing aircraft can overcome the delays inherent in transferring patients between hospitals and airports. The actual point at which the balance favours fixed-wing aircraft probably depends on the conditions, patient needs and the type of aircraft used.11 It is clear that methodologically sound systems research is scarce in the field of critically ill patient transport, but that medical staffing is required for optimal management of some critically ill patients. Peter A Cameron Associate Professor, University of Melbourne; and Director of Emergency Medicine, Royal Melbourne Hospital, Melbourne, VIC Salomon Zalstein Staff Specialist, Department of Emergency Medicine Royal Melbourne Hospital, Melbourne, VIC Bartolacci RA, Munford BJ, Lee A, McDougall PA. Air medical scene response to blunt trauma: effect on early survival. Med J Aust 1998; 169: 612-616. Baxt WG, Moody P. The impact of rotorcraft aeromedical emergency care service on trauma mortality. JAMA 1983; 249: 3047-3051. Baxt WG, Moody P. The impact of a physician as part of the aeromedical prehospital team in patients with blunt trauma. JAMA 1987; 257: 3246-3250. Nicholl JP, Brazier JE, Snooks HA. Effects of London Helicopter Emergency Medical Service on survival after trauma. BMJ 1995; 311: 217-222. Dalton AM, Botha A, Coats T, et al. Helicopter doctors? Injury 1992; 23(4): 249-250. Emergency intubation. Ambulance Service Victoria. Clinical Practice Guidelines. 9th edition. Melbourne: Victorian Department of Human Services, 1997: 137-140. Murphy-Macabobby M, Marshall WJ, Schneider C, Dries D. Neuromuscular blockade in aeromedical airway management. Ann Emerg Med1992; 21: 664-668. Waddell G, Scott PD, Lees NW, Ledingham IM. Effects of ambulance transport in critically ill patients. BMJ 1975; 1; 386-389. Bion JF, Wilson IH, Taylor PA. Transporting critically ill patients by ambulance: audit by sickness scoring. BMJ 1988; 296: 170. Gentleman D, Jennett B. Hazards of inter-hospital transfer of comatose head-injured patients. Lancet 1981; 17: 853-854. Australasian College for Emergency Medicine and Australian and New Zealand College of Anaesthetists. Policy on minimum standards for transport of the critically ill. Emerg Med 1993; 5: 245-324. Schneider C, Gomez M, Lee R. Evaluation of ground ambulance, rotor-wing, and fixed-wing aircraft services. Crit Care Clin 1992; 8: 533-564. Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/>

Peter A Cameron · Salomon Zalstein

Twenty-four hour access to health information and advice An essential component of the healthcare system MJA 1998; 169: 125-126 As the style and funding of healthcare continues to change and evolve, one constant is the need for patients to have access to timely and credible health information. Indeed, it is probable that with the changing nature of the doctor-patient relationship, the doctor's role as the provider of information is becoming more important. Parents, in particular, need information about their children's health,1 and information given in the context of a consultation has been shown to increase patient knowledge,2 decrease anxiety and improve compliance.3 Previously, patients have relied on information and advice being supplied by their healthcare provider, but they now have access to other sources such as the popular media and the Internet.4 However, not all patients have the technical and literacy skills to benefit from written or computer-generated information and, even if they do, it may be difficult for them to extrapolate general information to their own specific problems. Furthermore, because medical problems are often acute and unexpected, it is impossible for patients to predict what information they will need and when they will need it. It is therefore not surprising that the telephone now plays such an important role in healthcare delivery. The provision of around-the-clock telephone advice, especially by hospitals, has been well documented in Australia,5 the United Kingdom6 and North America.7 In this issue of the Journal Fatovich et al8 report the results of their study of telephone advice provided by a hospital emergency department. As well as assessing the usual logistic and demographic data, which can limit the generalisability of findings depending on the particular hospital studied and the community it serves, the authors have attempted to determine the appropriateness of the advice given by hospital staff and the level of patient compliance. The results are not especially striking or surprising, but they raise some important issues for policymakers, hospitals and community-based health providers. There is a huge discrepancy between the amount of attention (and resources) devoted to face-to-face as opposed to telephone consultations. Doctors and nurses undergo extensive supervised training to provide clinical services, there is increasing emphasis on clinical guidelines and evidence-based medicine, good record keeping is considered an important component of quality services -- yet none of these standards has been applied to the provision of telephone advice. Lack of specific funding is also a major issue, especially if, as indicated by the study, emergency departments receive up to 33 phone calls per 100 attendances. The combination of the financial pressure of maintaining a service which is not funded by government, and concern about the medicolegal implications of advice given in an ad hoc manner by relatively junior staff without referring either to medical records or generating any written documentation about the advice given, has led at least one large teaching hospital to discontinue interactive telephone advice and replace it with a recorded information service.9 Presumably general practitioners, community health centres and community nurses also provide telephone advice, although no data are available to estimate the absolute number and proportion of calls relative to the number and proportion received by hospitals. The fact that most calls to hospitals are made after hours may well reflect the unavailability of the patients' usual healthcare provider at this time. Nevertheless, if telephone advice is considered a core part of healthcare services, one might argue that after-hours coverage in the community could be organised in the same way as after-hours locum services. Again, the lack of any remuneration and the potential medicolegal risks are major disincentives. In North America, telephone advice has been accepted as an inevitable part of healthcare services to the extent that individual providers have formally scheduled "call hours", when their patients can call knowing that the doctor or nurse has dedicated this time to the provision of telephone consultations. Furthermore, specific telephone protocols and guidelines have been developed10,11 and evaluated,12 and phone consultation is increasingly becoming part of the training of hospital staff. Twenty-four-hour access to health information and advice has become a service that the community regards as essential. Just as essential is the need for governments and providers to begin to address some of the issues to do with funding, training, quality control and medicolegal responsibility. A possible benefit, which has not been explored systematically, could be the use of hospital telephone advice lines to publicise community-based services and encourage callers to use such services, thus minimising hospital attendances. Furthermore, systematic analyses of calls could provide important information for health promotion efforts and the organisation of health services in a region or community. These are areas that need to be explored if we are serious about developing integrated, cost-effective, "seamless" services and avoiding duplication and fragmentation. Frank Oberklaid Director, Centre for Community Child Health and Ambulatory Paediatrics Royal Children's Hospital, Melbourne, VIC Hall DMB, editor. Health for all children. Oxford: Oxford University Press, 1996. Isaacman DJ, Purvis K, Gyuro J, et al. Standardised instructions: do they improve communication of discharge information from the emergency department? Pediatrics 1992; 89: 1204-1208. Glascoe FP, Oberklaid F, Dworkin PH, Trimm F. Brief approaches to educating patients and parents in primary care. Pediatrics (In press). Vol 101. Also on the American Academy of Pediatrics "web site" <www.pediatrics.org>. Carlile S, Sefton AJ. Healthcare and the information age: implications for medical education. Med J Aust 1998; 168: 340-343. Oberklaid F, Bell J, Duke V. Paediatric telephone consultation -- a neglected area of health service delivery. Aust Paediatr J 1984; 20: 113-114. Crouch R, Patel A, Williams S, Dale J. An analysis of telephone calls to an inner-city accident and emergency department. J Royal Soc Med 1996; 89: 324-328. Perrin EC, Goodman HC. Telephone management of acute pediatric illness. N Engl J Med 1978; 298: 130-135. Fatovich DM, Jacobs IG, McCance JP, et al. Emergency department telephone advice. Med J Aust 1998; 169: 143-146. Royal Children's Hospital, Melbourne. Kid's Health Infoline, 1997. Schmitt BD. Pediatric telephone advice. Boston. Little Brown and Company, 1980. Levy JC, Rosenkrans J, Lamb GA, et al. Developmental and field testing of protocols for the management of pediatric telephone calls: protocol for pediatric telephone calls. Pediatrics 1979; 64: 558-563. Strasser PH, Levy JC, Lamb GA, Rosenkrans J. Controlled clinical trial of pediatric telephone protocols. Pediatrics 1979; 64: 553-557. - Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/>

Frank Oberklaid

Emergency department telephone advice Daniel M Fatovich, Ian G Jacobs, Jill P McCance, Kerry L Sidney and Rod J White MJA 1998; 169: 143-146 For editorial comment, see Oberklaid Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - ©MJA1998 Abstract Objective: To evaluate telephone advice given in an emergency department. Design: Prospective, observational study. Setting: A community-based emergency department in a semi-rural/outer metropolitan setting, between August and November 1995. Participants: All people telephoning the emergency department for medical advice. Methods: Details of all calls, callers and patients were recorded. Within 72 hours, a follow-up call was initiated seeking replies to a series of standardised questions. Main outcome measures: Number, timing and duration of calls; appropriateness of the advice given; compliance with the advice; and callers' satisfaction with the service. Results: Over the four-month period, 1682 calls were received, 58% between 4 pm and midnight. There were 33 telephone calls per 100 emergency department attendances. The mean call duration was 3.9 minutes (range, 0.25-25 minutes); 49% of patients were less than 14 years old, and 72% of callers phoned because of spontaneous illness. The advice given was considered inappropriate in only 1.4% of calls. Follow-up calls were made to 1132 people (67%), revealing a non-compliance rate of only 6.9% and a high level of caller satisfaction, with 99% of callers affirming a need for such a service. Conclusions: The provision of telephone advice by emergency department staff is rated highly by the community and compliance with the advice is strong. Paediatric problems, arising as a result of spontaneous illness, predominate and there is a large bias towards after-hours use of the service. Experienced staff provide better advice. Introduction Emergency department (ED) staff are frequently telephoned by members of the community who seek medical advice. Little is known about who calls and why, how much professional time is required, what problems people call about and the quality of the advice given.1 In particular, caller compliance has seldom been assessed. This study was conducted to provide a detailed analysis of emergency department telephone advice. A prospective, observational study, it was undertaken at Swan District Hospital, which is situated 20 km northeast of the central business district of Perth. The hospital has 148 beds, is community based and over 15 000 patients attend its ED each year. It serves a population of over 142 000 residents in a metropolitan and semi-rural setting. There are approximately 160 general practitioners in the area who provide some after-hours care. The catchment population was more socioeconomically disadvantaged than that of the metropolitan area. Methods Data collection The survey took place from 1 August to 30 November 1995. All telephone calls from people seeking medical advice were answered by an ED registered nurse who was responsible for triage and later reviewed. Details of the call, including the date, time, patient's name, age and sex, caller's name, relationship of the caller to the patient, patient's telephone number, presenting problem and advice given, were recorded on a telephone advice form during the call. Each call was timed using a stopwatch and problems were divided into four categories: spontaneous illness, injury, poisoning, and drug-related. Evaluation of the calls To establish the quality and appropriateness of the telephone advice given, each completed telephone advice form was assessed independently by at least two authors. Disputes were settled by a third author. The authors deemed the advice to be either appropriate or inappropriate and, in cases where the advice was considered to be inappropriate, defined it as potentially life threatening, at risk of causing serious sequelae or not serious. Caller feedback At the completion of each call, permission was sought for a follow-up call to determine the caller's response to the advice given. Where permission was given, a research nurse telephoned the caller within 72 hours of the initial call. The nurse asked each caller how he/she had acted upon the advice, how helpful the advice had been, if the caller had sought advice elsewhere, if he/she had used an ambulance when advised, and his/her overall perception of the telephone advice service. Callers were also encouraged to freely make comments about the service. Statistical analysis Data were analysed using the Statistical Package for Social Sciences (SPSS).2 Ethical approval Approval for the study was obtained from the Ethics Committee of the Swan Area Health Service. Results Number, timing and content of calls During the four-month period 1682 calls were received. The average number of calls per day was 14 (range, 3-32). Given that there were 5127 attendances at the ED during the same period, the ratio of calls to ED attendances was 1:3 (33 calls per 100 attendances). The mean age of the patients was 22 years (range, 1 week-95 years), although 49% were under 14 years (Figure 1). Fifty-five percent of patients were female. Comparison of the age and sex distribution of patients who called the telephone advice service with that of patients who attended the ED showed that callers were more likely to be younger and female (Box). Almost a quarter (24%) of all calls were received on Sunday, 17% were received on Saturday, and Monday was the busiest weekday (Figure 2). Calls between 4 pm and midnight constituted 58% of all calls received (Figure 3). The mean call duration was 3.9 minutes (± 2.5 minutes), with the longest call taking 25 minutes (allowing also for a brief request for a follow-up call). The patient was the caller in 32% of cases. Where the caller was not the patient, 63% and 17% of calls, respectively, were made by a parent or spouse. Eighty-two percent of calls were from the Swan Area Health Service catchment area. The others were from the city of Perth and its surrounds. Spontaneously occurring illness accounted for 72% of calls (1175). The most common problems were fever in children, pain (especially earache in children), and shortness of breath. A further 22% of calls were for injuries. Advice given Advice was considered inappropriate in 23 cases (1.4%). Of these, 11 (48%) were assessed as potentially life threatening (eg, a 42-year-old man with chest pain who had previously had a coronary angioplasty was not advised to attend hospital by ambulance). Four (17%) were considered at possible risk of serious sequelae (eg, an 18-month-old child with a two-week history of lethargy, fever and vomiting was not advised to see a doctor). Staff with less than two years' relevant ED experience were responsible for 78% of the inappropriate advice given (18 of 23 calls) and 100% of potentially life-threatening advice. No advice was given in 97 cases (6%) as the caller rang merely to inform the ED of their impending arrival. Only one call was prompted by an imminently life-threatening situation (a 40-year-old man with insulin-dependent diabetes who could not be roused by the caller). The patient was making a "funny noise breathing" and the caller was unable to give him sugar. The caller was correctly advised to ring for an ambulance. A Dextrostix test performed by ambulance officers indicated a low blood sugar level of 1.4 mmol/L. They administered glucagon intramuscularly, which raised his blood sugar level to 4.2 mmol/L. Caller feedback A total of 1132 patients (67%) consented to follow-up. Of these, 42% had previously used the service and 89% considered the advice to be useful or very useful. Almost a third (30%) had sought advice elsewhere before calling the ED, 43% of these from their general practitioner. The level of compliance with advice was established in 1205 cases (72%). This included 73 cases where the caller later attended the ED and compliance was able to be determined from the medical record. Eighty-three people (6.9%) did not comply with the advice received, including 34 who were advised to call an ambulance but failed to do so. The main reasons for this were the anticipated cost of the ambulance journey, the caller's perception that the problem did not require an ambulance (despite being advised to call one), and the belief that travelling to the ED would be faster by private transport. Other reasons for non-compliance ranged from lack of transport and unwillingness to wait, to simple refusal to follow the advice because the caller believed that they knew better. About a quarter of callers (26%) subsequently attended their general practitioner, and 13% elected to monitor their problem. Five hundred and ninety-nine patients (50%) attended an ED, 92% attending the Swan District Hospital ED. The distribution of problems which warranted attendance was similar to that of the problems which had prompted the original call. Of those attending an ED, 94 patients (16%) were admitted to hospital. Each caller who was followed up was asked to rate the telephone advice service on a scale of one to 10, with 10 being "excellent". The mean score was 8.9, with only 1.5% of respondents giving a score of less than five. There was overwhelming support for a telephone advice service, with 99% of those contacted affirming the need. The majority of respondents (86%) also indicated that they would be disappointed if the telephone advice service were discontinued. Discussion Throughout the world, it is common practice for ED staff to provide telephone advice. This is almost unavoidable because patients require access to health information and medical advice at all times. Health authorities need to consider this when planning health services. The American College of Emergency Physicians3 and the British Association of Emergency Medicine4 have position statements on giving telephone advice, and the British government has announced plans for a 24-hour patient helpline staffed by nurses.5 Pilot schemes have already commenced. We found that the ED in our study received 33 telephone calls for advice per 100 ED attendances. This is consistent with the results of a survey of 130 Australian EDs which reported a national figure of 28 calls per 100 attendances.6 The same study calculated an annual volume of almost 1.2 million ED telephone advice calls (almost two every minute) and found that two-thirds of Australian EDs provide telephone advice, with rural EDs more likely to provide this service than metropolitan EDs. This may reflect rural isolation from medical care. Some metropolitan hospitals have developed specialised advice lines for people with sick children.7 An unavoidable limitation of this study was that a third of callers were lost to follow-up. Seasonal factors may have been another source of bias. Other limitations were that the social desirability of giving an acceptable answer may have contributed to the degree of compliance reported, and that the performance of the nurses giving the advice may have been influenced by the fact that a study was being undertaken (the "Hawthorne effect"). Most Australian households have a telephone and are aware of their nearest public hospital: in our consumer- oriented society, it is little wonder that EDs are frequently telephoned for advice.8 The bias towards after-hours use probably reflects a lack of alternative resources. Previous studies have concluded that ED telephone advice is inexpensive, safe, allows public access to health information and encourages consultation with a doctor as appropriate.9 According to Verdile et al,10 telephone advice should be considered an outreach program of the ED. However, EDs are rarely funded to provide this service. Our finding of a 93.1% compliance rate is high, but consistent with the only other study of compliance. Egleston et al9 found that 99 of 104 callers (95.2%) were compliant with the telephone advice. The commonest scenario in which advice was not followed involved the use of an ambulance. This result should be considered by providers of prehospital care. It was apparent from our study that people telephoned the ED not just for medical advice, but also as a last resort in social crises. These included problems ranging from domestic violence and child abuse to suicide and social isolation. The advice included direction of callers to appropriate community resources, advising medical assessment or simply providing empathy. At times, telephoning the emergency department may be the only option of which the caller is aware. This reflects the ED's function as society's healthcare "safety net" 24 hours a day, seven days a week. Most calls lasting over 15 minutes were in this category. The longest call, which lasted 25 minutes, was from a woman who was anxious about her five-month-old baby being difficult to settle due to "colic" after having been vaccinated the previous day. The call was made during a quiet period in the ED and the nurse who took it took the time to listen and empathise. Nurses have traditionally been, and are described in other reports as, the predominant ED staff members responsible for answering medical advice telephone calls. Often, however, nurse training in this important component of ED work is absent. Protocols for telephone triage have been assessed and found to be effective.11,12 The protocols have checklists which assist the user in gathering essential data from the caller, provide built-in guidelines for patient management and facilitate documentation.10 Such protocols should be standardised as the literature reveals that the quality of medical advice varies and that inappropriate advice can be harmful. Aitken et al13 found the advice to be inadequate in 16 of 36 institutions assessed when given a theoretical case of a 5-week-old infant with a fever of 38.5¡C. When Verdile et al10 surveyed EDs using a scenario that may have been myocardial ischaemia, only 4 of 46 respondents recommended that the patient be brought to the nearest ED by ambulance. Their findings indicate that the telephone advice given by some EDs is inconsistent and may be inadequate to the point of jeopardising the health of those seeking advice. Medicolegal concerns are frequently raised in relation to telephone advice, although an estimate of the exact magnitude of the problem of litigation is difficult to ascertain.10 However, it is possible that hospitals could be held accountable for giving either poor advice or refusing to help. The literature suggests that, although questioning a caller about a problem is acceptable, once any advice is offered over the telephone the ED staff member has assumed a legal obligation to the caller and is responsible for any advice given.14 Hence, it is important to have guidelines and to document all calls. Telephone advice is a difficult skill to perform well but one that is important to master. The consequences of error can be serious, and hence the use of experienced and trained staff who are aware of the limitations and ramifications of providing the service is mandatory. A basic rule is that diagnosis via the telephone is not possible and that the best advice is to recommend a face-to-face consultation. With common sense, the proper use of the telephone can both facilitate patient care and maximise the available human resources. It fulfils a genuine community need and helps promote better community relations. We found that the provision of telephone advice by ED staff is rated highly by the community and that compliance with the advice is strong. Calls regarding children with spontaneous illnesses predominate, and there is a strong bias towards after-hours use of the service. Experienced nursing staff provide better advice. The provision of telephone advice is an under-recognised function of the emergency department of which healthcare planners should be aware. Acknowledgements This study was made possible by a research grant from the Commonwealth Department of Human Services and Health (Ambulatory Care Research and Pilot Program) and the support of the Health Department of Western Australia, Health System Policy Branch. The authors are grateful to all ED staff who participated, especially Sheila Penman, RN. References Knowles PJ, Cummins RO. Emergency department medical advice calls: who calls and why? J Emerg Nurs 1984; 10: 283-286. SPSS Inc, release 6 [computer program]. Chicago,Illinois: SPSS, 1993. American College of Emergency Physicians. Providing telephone advice from the emergency department. Ann Emerg Med 1990; 19: 600. British Association for Emergency Medicine Clinical Services Committee. Guidelines on the handling of telephone enquiries in emergency departments. London: British Association for Emergency Medicine, 1992. Horton R. The realpolitik of a new National Health Service for the UK. Lancet 1998; 351: 76-77. Fatovich DM, Jacobs IG. Emergency department telephone advice: a survey of Australian Emergency Departments. Emerg Medi 1998; 10: 117-121. Best Practice in NSW Health 1994 Sydney. 49-52. Crouch R, Patel A, Williams S, Dale J. An analysis of telephone calls to an inner city accident and emergency department. J R Soc Med 1996; 89: 324-328. Egleston CV, Kelly HC, Cope AR. Use of a telephone advice line in an accident and emergency department. BMJ 1994; 308: 31. Verdile VP, Paris PM, Stewart RD, Verdile LA. Emergency department telephone advice. Ann Emerg Med 1989; 18: 278-282. Levy JC, Rosekrans J, Lamb GA, Friedman M, et al. Development and field testing of protocols for the management of pediatric telephone calls: protocols for pediatric telephone calls. Pediatrics 1979; 64: 558-563. Strasser PH, Levy JC, Lamb GA, Rosekrans J. Controlled clinical trial of pediatric telephone protocols. Pediatrics 1979; 64: 553-557. Aitken ME, Carey MJ, Kool B. Telephone advice about an infant given by after-hours clinics and emergency departments. N Z Med J 1995; 108: 315-317. Dunn JM. Warning: giving telephone advice is hazardous to your professional health. Nursing 1985; 8: 40-41. (Received 7 Oct 1997, accepted 26 Mar 1998) Authors' details Swan District Hospital, Middle Swan, Perth, WA Daniel M Fatovich, MB BS, FACEM, Director of Emergency Medicine; Jill P McCance, RN, Clinical Nurse; Kerry L Sidney, RN, Clinical Nurse Specialist; Rod J White, RN, Clinical Nurse. School of Public Health, Department of Epidemiology & Biostatistics, Curtin University. Ian G Jacobs, PhD, RN, Senior Lecturer. Reprints will not be available from the authors. Correspondence: Dr D M Fatovich, Department of Emergency Medicine, Swan District Hospital, Eveline Road, Middle Swan, WA 6056. E-mail: daniel.fatovichAThealth.wa.gov.au - Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/>

Daniel M Fatovich · Ian G Jacobs · Jill P McCance · Kerry L Sidney · Rod J White

Facsimile communication between emergency departments and GPs, and patient data confidentiality David McD Taylor, John Chappell-Lawrence and Ian S Graham MJA 1997; 167: 575-578 Abstract - Introduction - Methods - Statistical analysis - Results - Discussion - References - Authors' details - - ©MJA1997 Abstract Objective: To assess general practitioners' perceptions of the effectiveness of facsimile notification of their patients being admitted from the emergency department (ED), and its adequacy in terms of patient confidentiality. Design: Questionnaire survey, before and after the initiation of facsimile notification. Setting: A provincial community of approximately 120 000 residents in Victoria. Main outcome measures: Changes in GPs' ratings of communication with the ED; acceptability of facsimile notification; and concerns about patient confidentiality. Results: 77 of 85 GPs participated; only 44 (57.1%) returned both questionnaires. ED-GP communication ratings of "adequate" or better increased from 48% to 100% ( P < 0.05). The proportion of GPs who were notified of all admissions increased from 0 to 41% ( P < 0.05). The proportion of GPs who preferred facsimile for notification increased from 39% to 68% ( P < 0.05). Most GPs found the initiative acceptable and reservations about confidentiality decreased from 36% to 16% ( P < 0.05). 38 of the 887 patients admitted from the ED (4.3%) refused facsimile notification. Conclusions: Facsimile improves ED-GP communications and may, in turn, improve the quality and continuity of patient care. Informed consent should be obtained from all patients. MJA 1997; 167: 575-578 Introduction With shorter hospital stays and a greater emphasis on same-day surgery and domiciliary or "hospital in the home" services, the involvement of general practitioners in coordinated patient management is increasingly important.1,2 Unfortunately, many GPs report progressive alienation from their community hospitals.1,2 Poor communication between public hospitals and GPs is a major cause of negative effects for both doctors and patients,1,3,4 and has been linked with discontinuity of treatment and patient dissatisfaction with the transition of care between hospitals and primary practice.1,3Anecdotal evidence suggested that there was room for improvement in communications between our hospital (Ballarat Base Hospital) emergency department and local GPs. In particular, a 1995 survey showed that 84.4% of the Ballarat GPs who responded wished to be notified of their patients' admissions (Dr Mark Fitzgerald, Emergency Department Director, St John of God Hospital, personal communication). Ballarat Base Hospital medical officers were required to notify GPs of patient admissions by telephone. However, as 62% of patients are admitted from the emergency department (ED) between 1800 and 0800 (unpublished data) and GPs can be difficult to contact after hours, GPs were often not notified. To rectify this problem, and to improve the relationship between the hospital and GPs, Ballarat Base Hospital and the Ballarat and District Division of General Practice aimed to establish a system of facsimile notification of GPs of patient admissions. Advantages of facsimile transmission of patient information include speed and accuracy of transfer, accessibility, low cost, and the possibility of direct transfer from the computer screen.5-9 However, there are potential problems of misdirection of transmissions and of document security at the transmission destination.10-14 In this study, we aimed, firstly, to examine the perceived success of this initiative in improving communications between the emergency department and GPs, and, secondly, to address potential problems and establish appropriate confidentiality protocols and controls governing the use of facsimile for this purpose. Methods The Ballarat Base Hospital is a community teaching hospital in provincial Victoria serving approximately 120 000 residents in both urban and rural areas. The Ballarat and District Division of General Practice includes all of the 85 GPs who serve this population. All of these GPs regularly refer to the hospital and often contribute to their patients' inpatient and postacute care. Details of our facsimile study were mailed to all these GPs, and they were advised that their participation would involve receiving facsimile admission notification and providing relevant patient information if required. The ED purchased a dedicated facsimile machine with a preprogrammable number dialling facility to ensure that, if an incorrect number were pressed, the facsimile would be sent only to another participating GP. The machine was positioned in a secure area of the ED clerical office where incoming and outgoing facsimiles could not be accessed by unauthorised people. To test the system, a test facsimile was sent to all preprogrammed numbers of participating practices, which were asked to verify the security of their machines and their commitment to the confidentiality of the study by endorsing the test facsimile with the practice stamp and refaxing it to the ED. Specially designed facsimile notification sheets recorded: The GP's name; Patient identification (name, age, date of birth, unit record number, address) and admission details (date, time, diagnosis, ward and inpatient unit); The patient's signature (indicating consent for their GPs to be notified and to provide any relevant medical information by facsimile); and A request from the ED for the GP to provide specific and any other relevant medical information in a space provided (the same facsimile could then be returned). Before each admission, an ED clerk completed the notification sheet, which was checked and signed by the patient. Only the patient, or a parent in the case of a minor, could consent to transmission. Family members were not permitted to sign on behalf of patients. For patients either physically or mentally incapable of consenting, facsimiles were not sent. The completed sheet was then checked and signed by the ED medical officer. If a notification sheet was not sent, the reason was noted in the space provided for the patient's signature. Facsimile notification of patient admission began on 6 June 1996; the study period ended on 31 July 1996. Perceptions of communication between the ED and GPs before and after the establishment of facsimile notification were assessed by two questionnaires, posted to participating GPs in the week before and immediately after the study period. The questionnaires were identical, except for an additional question in the one sent at the end of the study period. For each question, respondents were asked to select the most appropriate response, and were invited to elaborate descriptively. GPs who did not respond were reminded by mail, fax or telephone. Statistical analysis For Questions 1-5, the change in response as a result of the initiation of facsimile notification was used as the variable of interest. The sign test was used to test the null hypothesis ( if the intervention had no effect, the number of positive and negative differences should be similar ). Questions 6-8 required a "yes" or "no" response and the results were analysed using McNemar's test (α = 0.05; df, 1). SPSS 15 was used for all analyses. In all cases, the change from before to after the intervention was considered. Results Seventy-seven GPs (90.6%) agreed to participate in the study. A further seven had no facsimile machine in their surgeries, and one GP elected not to participate. During the study period, 887 patients were admitted from the ED. Facsimile notifications were sent to the GPs of 548 patients (61.8%). A further 74 patients (8.3%) were visitors or transferred from outside the area, 73 (8.2%) were unable to provide informed consent, 47 (5.3%) had GPs with no facsimile machine, 38 (4.3%) refused permission to send notification, 32 (3.6%) had no GP, and 14 (1.6%) had been admitted to the ward before authorising the notification. For the remaining 61 patients (6.9%), no explanation could be found for failure of notification. Usually, no attempt was made to notify GPs if a facsimile was not sent. Of the 77 participating GPs, 44 (51.7%) completed the first, 55 (71.4%) completed the second, and 44 (57.1%) completed both the questionnaires. The demographic characteristics of the 77 GPs, comparing the 44 who completed the study with the 33 who did not, are shown in Box 1. Responses to the questionnaires, before and after the intervention, by the 44 GPs who completed the study are compared in Box 2. After the intervention, there was a significant improvement in GPs' perception of overall communications from the ED (Question 1; P < 0.001). Similarly, GPs reported a significant improvement in the frequency of notification (Question 2; P < 0.001), and in communications (Question 3; P < 0.001) from the ED after one of their patients was admitted. Responses to Question 4 showed a significant change in GPs' preferred mode of communication after the intervention ( P < 0.01). Before the intervention, most preferred a direct telephone call from the admitting officer, while after the intervention most preferred a facsimile. When asked how notification of their patients' admissions from the ED would affect [had affected] their management of those patients (Question 5), most GPs stated, both before and after the intervention, that notification would encourage them to visit their patients in hospital and assist in planning postacute care. After recoding to adjust for the effect of multiple answers (more than one response was allowed), no statistically significant change was found as a result of the intervention. The number of GPs responding that they had recently been aggrieved or inconvenienced as a result of the ED not notifying them of the admission of one of their patients (Question 6) fell significantly after the intervention ( P < 0.001). After the intervention, only two additional GPs responded that prompt notification of a patient's admission was of significant importance to the ongoing management of that patient (Question 7); this was not statistically significant. The number of GPs who had reservations about confidentiality associated with patients' medical records being transmitted by facsimile with their consent (Question 8) fell after the intervention ( P < 0.05). Finally, the question included only in the second questionnaire showed that 43 GPs (97.7%) were prepared to support the continuation of the ED facsimile notification initiative. It also showed that 39 (88.6%) and 40 (90.9%) GPs, respectively, were prepared to support its use in all admissions and discharges at Ballarat Base Hospital. Discussion Our findings clearly show that GPs perceived an improvement in their communications with the ED after the advent of facsimile notification. At the end of the study period, there was a significant increase in the number of GPs who preferred to be notified by facsimile, and a significant reduction in the number of GPs who had reservations about patient confidentiality. Most GPs responded that notification allowed them to visit their patients in hospital, to contribute to inpatient care, to plan their patients' postacute care (e.g., home-help, meals-on-wheels, district nursing and family counselling), and to avoid interruption of the GP-patient relationship. Such continuity of care may affect readmission rates. Objective measurement of whether facsimile notification actually affects GP behaviour and patient outcomes may be worthy of further study. A drawback of our study was its low response rate. Despite encouragement, a considerable number of GPs did not complete both questionnaires. While there were no obvious differences between those who did and did not complete the study, the low response rate may have introduced bias into the results by selecting for more motivated GPs, or those with a special interest in the study. The fact that more GPs responded to the second questionnaire may have indicated some enthusiasm for the project. Lack of confidentiality has been identified as one of the most serious drawbacks of using facsimile machines in clinical practice. The sender loses control once a fax is transmitted, and information can be misdirected as a result of dialling wrong numbers.10,11,13,16,17 None the less, we considered facsimile notification a more appropriate initial step than other accepted methods, such as encrypted electronic data transfer. The infrastructure was easy and relatively cheap to establish. It was also easy for the ED staff to use, with completion and transmission of each notification sheet taking approximately five minutes. Finally, the method allowed the patients to view the notification document before its transmission. The safeguards we used in the facsimile transmission of patient med- ical information (Box 3) have been recommended by other investigators.6,11,12,14,16,17 We contend that, if these safeguards are established, the standard of care for the protection of patient information transmitted by facsimile should be at least as high as that provided by conventional mail. A message reaching a secure facsimile machine is no more susceptible to loss, misdirection or unauthorised access than an opened letter in a doctor's "in-tray". It has been suggested that an authorisation procedure should be in place to facilitate obtaining informed consent for any facsimile transmission of personal information.6,12,14,16,17 We felt that if patients were shown the information that was to be transmitted, its destination and the format in which it was to be sent they could make an informed decision about whether or not GP notification was appropriate. The number of patients who refused consent for facsimile notification (38, or 4.3%) was surprising; our study had not been designed to record the reasons for these refusals and this matter deserves further study. Regardless of the reasons for refusal, patients could suffer distress if medical information was transmitted without consent, and legal action could result from misdirection of unauthorised, non-urgent medical information. Our protocol represented a change in Ballarat Base Hospital's facsimile policy as consent had previously been assumed. In most hospitals, providing the name of the GP at registration or admission is considered implied consent for the hospital to communicate directly with the GP. Letters, discharge summaries and death notifications may be sent by facsimile, electronic transfer or mail. With increasing use of telecommunications and information technology, we contend that it may be appropriate to question some of the practices that are currently undertaken routinely with only the implied consent of patients. Other Australian emergency departments are developing facsimile and electronic data systems for the transfer of patient information. Facsimile remains a "paper-based" technology and is likely to become superseded by electronic data transfer systems. Indeed, the American College of Emergency Physicians believes that, along with facsimile, electronic data facilities should be available to all emergency departments.6 Various electronic data transfer systems have been developed to coordinate the shared care of patients,18 to establish electronic medical records,19 to facilitate communication between hospitals and GPs,20 and to streamline patient referrals.21 While these "paperless" systems may be superior to facsimile, they also raise confidentiality issues. These are being addressed with the use of cryptography,22 digital signatures,20 "need to know" staff clearances,20 and legislation.20,23 Meanwhile, facsimile is accessible and relatively inexpensive, and is likely to remain useful, at least in the near future, until electronic systems become more prevalent. We recommend the use of facsimile transmission for notification of patient admission, provided that adequate safeguards are in place, and that informed consent is obtained before transmitting medical information. Following the success of facsimile notification of admissions from the ED, Ballarat Base Hospital has continued its use and is considering extending it to all hospital admissions and discharges, ED discharge letters and, possibly, to service providers other than GPs. Presently, the hospital is investigating software which will allow computer-generated facsimile transmission and is looking ahead to electronic data transfer. References Bella JI, Jamieson WE. Improving the continuity of care between general practitioners and public hospitals. Med J Aust 1994; 161: 656-659. Freeman G. Continuity of care in general practice: a review and critique. Fam Practitioner 1984; 1: 245-252. Interaction with Fremantle Hospital: final report. Fremantle: Fremantle Regional Division of General Practice, 1994: 1-40. Morrison WG, Pennycook AG, Makower RM, Swann IJ. The general practitioner's use and expectations of an accident and emergency department. J R Soc Med 1990; 83: 237-240. Magennis AW. Fax units in general practice. Aust Fam Physician 1989; 18: 1259-1264. American College of Emergency Physicians. The use of facsimile machines and electronic data transfer in the emergency department [policy statement]. Ann Emerg Med 1993; 22: 266. Spigelman A. Faxed electronic summaries are valued by general practitioners [letter]. BMJ 1995; 311: 746-747. Cole DR, Johnson MS, Heaton CJ, Petti M. Fax/modem board communications decrease preceptor communication costs. Fam Med 1994; 26: 418-420. Yamamoto LG, Wiebe RA. Improving medical communication with facsimile (fax) transmission. Am J Emerg Med 1989; 7: 203-208. Marr P. Maintaining patient confidentiality in an electronic world. Int J Biomed Comput 1994; 35 Suppl: 213-217. Brent N. Facsimile systems revised: focus on confidentiality and privacy. Home Healthcare Nurse 1991; 9: 6-8. Larkin GL, Moskop J, Sanders A, Derse A. The emergency physician and patient confidentiality: a review. Ann Emerg Med 1994; 24: 1161-1167. Carman D, Britten N. Confidentiality of medical records: the patient's perspective. Br J Gen Pract 1995; 45: 485-488. Capen K. Facts about the fax: MDs advised to be cautious. Can Med Assoc J 1995; 153: 1152-1153. SPSS/PC+ statistics [computer program]. Version 4.0. Chicago: SPSS Inc., 1990. Genesen LB, Sharp HM, Genesen MC. Faxing medical records: another threat to confidentiality in medicine [letter]. JAMA 1994; 271: 1401-1402. Grant AE. Legal matters -- facsimile transmissions. Canadian Nurse 1996; 92: 47. Branger P, van't Hooft A, van der Wouden HC. Coordinating shared care using electronic data interchange. Medinfo 1995; 8: 1669-1674. Walker D. Transferring electronic medical records. Aust Family Physician 1997; 26: 48-55. Fisher F, Badge B. Data security and patient confidentiality: the manager's role. Int J Bio-Med Comp 1996; 43: 115-119. Gaudet LA. Electronic referrals and data sharing: can it work for health care and social service providers? J Case Management 1996; 5: 72-77. Biskup J, Bleumer G. Cryptographic protection of health information: cost and benefit. Int J Bio-Med Comp 1996; 43: 61-67. Cassidy SO, Sepulveda MJ. Health information privacy reform. J Occup Environ Med 1995; 37: 605-614. (Received 20 Feb, accepted 23 Jul, 1997) Authors' details Ballarat Base Hospital, Ballarat, VIC. David McD Taylor, MD, FACEM, Former Acting Director of Emergency Medicine (currently, Instructor in Emergency Medicine, University of Pittsburgh Medical Center, Pittsburgh, USA); Ian S Graham, MB BS, FRACMA, Executive Director, Clinical Services. Ballarat and District Division of General Practice, Ballarat, VIC. John Chappell-Lawrence, BBSc(Hons), DipEd, Project Consultant. No reprints will be available. Correspondence: Dr D McD Taylor, A2, 5237 Fifth Avenue, Pittsburgh, PA, 15232, USA. - ©MJA 1997 Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

John Chappell-Lawrence · Ian S Graham

Medical log: forward command Thredbo Roger D Harris A first-hand account of the medical response to the disaster MJA 1997; 167: 627-629 Introduction - Postscript - Acknowledgements - Authors' details - - - ©MJA1997 Introduction At 2340 on Wednesday, 30 July 1997, a landslide hit the ski resort village of Thredbo, in New South Wales. Two ski lodges were destroyed, with the loss of 18 lives. There was only one survivor, rescued about 66 hours after the disaster struck. More than 30 doctors were directly involved in the rescue effort and many more covered for their absent colleagues. The NSW Ambulance Service responded with 183 officers, and hundreds of fire brigade personnel, police, State Emergency Service and volunteer rescue association personnel participated in the rescue effort. Here is a brief account taken from the "doctors' log", a medical record compiled at the site by the attending physicians during the first few days of the disaster. Entries were made in the log every few hours to assist in monitoring the medical progress of the disaster and to serve as a record for later audit. Wednesday 30 July 2340: Disaster strikes A landslide completely destroys two ski lodges within a matter of seconds. Fortunately, the first lodge has only one occupant (as it is midweek and snowfalls are light), but, tragically, the second lodge is the staff accommodation for the resort employees and as many as 20 to 30 people are feared trapped or dead. As local rescuers arrive on the scene, there are reports of cries for help from people trapped within the wreckage. A rapid assessment of the site by the Thredbo fire brigade and police reveals that it is dangerously unstable and there is a strong smell of gas and diesel fuel. The police decide to clear the site until it is declared safe enough to allow further rescue attempts. Two general practitioners who practise in Thredbo and several other doctors holidaying there are on stand-by at the disaster site, but are unable to get to people trapped within the wreckage. Thursday 31 July0030: Medical support is mobilised A regional disaster is declared (see Box below). Goulburn (in southern NSW, approximately 300 km from Thredbo) is established as the regional disaster coordination centre, but as it is feared that regional resources may be overwhelmed Sydney coordination is also notified. Teams of doctors and nurses are sent from Cooma to Thredbo and from Canberra to Jindabyne (a triage point), and a four-person specialist medical team (an emergency physician, surgeon, anaesthetist and a medical retrieval specialist) is flown to Thredbo from St George Hospital in south-eastern Sydney. (Medical retrieval specialists in NSW are either emergency physicians or anaesthetists who work for the medical retrieval unit at St George Hospital.) The medical specialist team is sent from Sydney so as not to drain the supply of medical specialists from local areas, including Canberra. At this point, it was feared that there would be mass casualties that would need to be transferred to regional hospitals. The medical retrieval unit conducts a disaster bed count and locates 25 potential intensive care beds in the State. The Thredbo landslide: a regional disaster A "disaster" is an event that overwhelms the capacity of the local resources to deal with the situation. The level of the disaster is graded according to the size of the response necessary. A disaster may involve mobilising only the resources of a single institution such as a hospital, or it may extend to involve the region, the State or the entire nation. The Thredbo landslide was classified as a regional disaster, although it did extend to involve many resources drawn from throughout New South Wales. 0730: Forward medical command post established The medical command post, along with the other emergency services, is set up in a lodge 50 m from the disaster site. The forward medical command post is responsible for coordinating the on-site medical rescue and liaising with medical command posts in Goulburn and Sydney. Telephone and fax lines, desks, chairs, stationery and white boards are organised. After consultation with the fire brigade, it is decided that the police will take overall charge of the site and coordinate all emergency personnel. The medical team from St George Hospital relieves the Thredbo and Cooma doctors, who have manned the site overnight. Their initial task is to establish a line of communication with both Goulburn and Sydney coordination centres. The Thredbo medical centre is chosen as the primary casualty treatment area because it already has the infrastructure and equipment (e.g., lighting, heating, handbasins, x-ray machines, oxygen, suction) necessary to stabilise patients before transport. A comprehensive inventory is taken of all the medical equipment and is sent to Sydney and Goulburn to help with planning of additional supplies. A temporary mortuary is set up in the Thredbo fire brigade station as it is close to both the disaster site and the medical centre. People are evacuated from homes adjacent to the landslide as there is real concern that these buildings may also slip, and also so as not to hamper the rescue. Arrangements are made for the medical team to review all evacuees to ensure that they have no special medical requirements. A second specialist medical team from Sydney is activated (from the Royal North Shore Hospital) and accommodation is organised for the medical staff in Thredbo. 1030: Medical team inspects the disaster site By mid morning, the initial tasks involved in establishing the disaster medical command are complete. Geological engineers and mine rescue experts examine the disaster site and consider it very unstable. The first inspection of the site by a medical officer is carried out. The medical team realise that they need to be prepared to treat possible mass casualties among the rescue workers, and identify several occupational health issues: Irritated eyes/throat. Rescuers to wear goggles and face masks while clearing dusty plasterboard and fibreglass insulation bats. Minor injuries, such as foreign bodies in the eye and lacerations. Medical supplies are organised from Goulburn. Exhaustion and hypothermia among the rescuers. All rescue personnel are alerted to the relevant signs and symptoms and told to report any concerns to their superiors and the medical staff. The medical team decides to inspect the disaster site every four to six hours to deal with these problems and others as they develop. Rescue shifts are limited to between four and eight hours, with adequate breaks during the shift for food and drink. The Salvation Army provides hot food and drinks around the clock and the rescuers warm themselves by fires burning in 44-gallon drums around the site. 1620: The first body is recovered As the bodies of victims are found, the medical team works with the police disaster victim identification squad. The medical officers pronounce the person deceased and tag them with a preliminary identification number. The police take video recordings and photographs of the victims both at the spot where they are found and at the temporary mortuary. This information will be submitted to the coronial investigation into the disaster. Finally, bodies are taken to Sydney for further examination and formal identification. After consultation with coronial medical officers, the police insist that no bodies are to be viewed at the scene by significant others. The coronial medical officers state that viewing the body in this setting can be more traumatic and that identification at this point is frequently wrong, leading to more confusion, delays and further trauma. 1830: Second medical specialist team arrives The St George doctors are relieved by the Royal North Shore team and are exhausted as they have not slept in 36 hours. The temperature in Thredbo drops to -14oC overnight. Friday 1 August0800: St George medical team return to Sydney It is decided that two medical teams are not necessary at the forward command post as the medical personnel at both Cooma and Canberra can be mobilised at short notice. Each medical team at the forward command post will be replaced every 24 hours by a new team from Sydney. At the forward command post, teams will divide into two groups of two and work six-hour shifts to provide 24-hour cover. The NSW Premier and the Police Commissioner are to visit the disaster site, and the medical commander is asked to attend a briefing and site inspection with them. Several public health and environmental issues arise during the day: Water and sewerage is cut off to the site and surrounding village. Some rescue personnel are staying in lodges without running water, and toilets are not flushing. One rescue worker develops abdominal pain, vomiting and diarrhoea. As there is concern about the possible cause as well as contamination of other rescuers, the patient is interviewed and returned to Sydney. Water, vomitus and stool samples are sent to Sydney. A directive is issued to drink only bottled water or cooled boiled water. Exposure by the rescue workers to decomposing bodies and body effluent. The principles of universal precautions are re-emphasised to the rescuers, decontamination posts are established at all exit points from the disaster site, and protective suits are brought in for those in direct contact with bodies. Diesel fuel seeps continuously into Thredbo creek. The leak is largely contained by the fire brigade using booms and siphons, but some oil escapes downstream. The Public Health Office, Environmental Protection Agency and Snowy Mountains Shire are all notified and asked to review the situation. 1500: Meeting the relatives The doctors meet the relatives of those still missing. The relatives, understandably distraught and angry that the rescue effort appears to be going so slowly, interpret the cautious pace of the rescue as indicating that the medical team has lost all hope of finding any survivors. The meetings are very emotional and extremely draining on the already tired doctors. 1800: The third night begins The rescue effort will continue through the night. Special helium balloons containing a light source are suspended over the rescue area to provide a very bright light with minimal shadowing. Saturday 2 August 0530: A possible survivor is located. The medical team is notified by the ambulance paramedics at the site that a survivor has been found. The patient is believed to be a male with minimal injuries. The initial action is to ensure that the relatives are given the known facts about the survivor before possibly misleading media reports filter through to them. A rescue helicopter is activated from Sydney and is to stand-by in Thredbo ready to transfer the patient to a tertiary hospital. The information from the site is that the survivor is trapped in a confined space surrounded by concrete slabs and underneath two further slabs. The only access to him is through a small hole and it is estimated that extrication will take eight to 12 hours. Attempting intravenous access is not feasible, but an oxygen mask is passed down to him by paramedics. The medical team discusses the clinical problems likely to be affecting the survivor: dehydration, hypothermia, rhabdomyolysis and possibly vascular instability if he is moved or sat up. A doctor goes down to the site and crawls under the concrete slabs to assess the patient as best he can. He can only talk to him and see his hand reaching up through the hole, but cannot reach it. As extrication will take some time and he appears in relatively good health (from his own reports), it is decided a trial of warm oral fluids should be tried. Glucose 25 g is added to normal saline 1000 mL, and the fluid warmed with a small Biegler fluid warmer (ATOM, Austria) plugged into a fire brigade power supply. A giving set is lowered to him through the hole and he sips 20 mL every 20 minutes to see if he can tolerate it. Surprisingly, he states that the warm saline tastes fine and even "compliments the chef". A Warm Touch air warmer (Mallinckrodt, USA) is modified by connecting a domestic vacuum cleaner hose to the outlet pipe in order to extend its length. The hosing is insulated by wrapping multiple foil sheets around the tubing. The warmer is plugged into the power source at the site and generates a steady flow of slightly warm air through the end of the long hose. The hose is fed down to the patient, who uses the warm air to dry his soaking wet jumper and shorts. During this time, a lengthened pulse oximeter probe from a Criticare oximeter (Criticare Systems, Inc., Waukesha, Wisconsin, USA) is applied by the patient to monitor pulse rate and oxygen saturation. 1700: The survivor is rescued The access hole to the patient is enlarged significantly. An ambulance paramedic goes down inside the hole with the patient and a doctor leans into it to perform a saphenous-vein cutdown by torchlight to establish intravenous access. Two litres of warmed Hartmann's solution to which has been added 100 mEq of sodium bicarbonate is infused. A cardiac rhythm strip shows slow atrial fibrillation, but there are no QRS, ST or T-wave changes to suggest hyperkalaemia. The patient is slowly removed from the hole and all efforts are made to maintain him in a horizontal position, as prolonged hypothermia and immobilisation might impair his ability to autoregulate his blood pressure, and sudden movements might cause his blood pressure to fall precipitately. He is taken to the Thredbo medical centre, where a "trauma team" conducts a primary survey (airway, breathing, circulation) and secondary survey (full head-to-toe examination) and initial resuscitation before transferring him by helicopter to Canberra 50 minutes later. Amazingly, he has minimal injuries other than extensive frostbite to both feet. A relief medical team arrives from Westmead Hospital, in Sydney, and, after aiding with resucitation, proceed to the forward command post and disaster site. More specialists arrive from the Prince of Wales Hospital and St Vincent's Hospital in Sydney. Victim identification, monitoring of occupational health and public health problems and general medical cover continue for another three days. Tragically, no other survivors are found. Postscript From a medical perspective, the Thredbo disaster was unusual in that there were no mass casualties. However, there was a considerable workload for the doctors, who, in addition to carrying out medical duties, had to cope with exhaustion, certifications of death and dealing with grieving relatives, as well as exposing themselves to danger while attending to a patient who was still trapped. The biggest stressor was probably the environment itself. At night the disaster site was lit with floodlights and helium light balloons. Anyone approaching the site had to pass through two checkpoints. The first, "perimeter", checkpoint was manned by the State Emergency Service, and the second, "central", checkpoint was manned by the police. At each checkpoint (and at other positions around the site), fires burned in 44-gallon drums for the rescuers to warm themselves by. The lights, the fires, the checkpoints and the devastation of the hillside created an atmosphere similar to a war zone. One medical officer commented: "It's like being in a Mad Max movie!". Acknowledgements On behalf of the medical team that attended the disaster site, acknowledgement should be given to the leadership shown by Dr Ronald Manning (Emergency Physician). Credit should also be given to those who "held the fort" while their colleagues were in Thredbo. Photography: Dr Roger Harris, Trevor Lee (NSW Ambulance Service), and Dr Michael King. Authors' details Department of Emergency Medicine, Royal North Shore Hospital, St Leonards, NSW. Roger D Harris, MB BS, FACEM, Research Fellow in Emergency Medicine. Reprints: Dr R D Harris, Department of Emergency Medicine, Royal North Shore Hospital, St Leonards, NSW 2065. - ©MJA 1997 Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

Roger D Harris

Sydney 2000: guarding against disasters Planning for the unexpected and practising responses is the critical task now MJA 1997; 166: 517-518 Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au/>". - ©MJA1997 In this issue of the Journal, Nocera describes the consequences of a grenade explosion in a munitions factory that injured four women, two of them critically. The report is a reminder of the ingenious creativity of the human race in weapons and war, with its impetus to do as much harm as possible -- but it might also remind us that some major advances in care for trauma patients have been spawned by wars, particularly methods to decrease the time from injury to first aid and advanced resuscitation techniques. In the incident described by Nocera, the prompt response by emergency services was the key to the survival of the injured. The first ambulance arrived five minutes after the explosion, followed by two more in the next six minutes. As part of the controlled response, a helicopter was put on stand-by nine minutes after the accident and took off five minutes later, carrying universal donor (O Rh-negative) blood, a paramedic and an emergency medicine doctor. The obvious cooperation between all personnel involved -- including police, fire, ambulance officers and helicopter staff -- enabled appropriate deployment of resources, prompt triage and transportation (making allowances for peak hour traffic and matching the capabilities of the hospitals in the area with the patients' conditions). "it is too late to plan a response once a disaster occurs" On a more general note, the article prompts us to review our preparations for disasters in general. Sydney is hosting the Olympics and many other mass gatherings in 2000. What if something happens: explosion, fire or mass transport accident . . . ? Are we prepared? A disaster may be defined as "Any incident, involving large numbers of casualties, which overwhelms the capacity of available resources to cope with it."1 A disaster is, obviously, unexpected, but we might expect Murphy's Law to operate. The recent history of the Olympics includes the tragedies of Munich (1972) and Atlanta (1996). Disaster preparedness was part of our successful bid for the Games in 2000. The response plan was based on DISPLAN/MEDPLAN. MEDPLAN has now been superseded by HEALTHPLAN,2 which defines the command structure and standard operating procedures to be followed in a disaster by the New South Wales health services (ambulance, medical, mental health and public health). These disaster-response plans have been tested and refined through the challenges of bushfires, the Newcastle earthquake, bus crashes and mass gatherings such as visits by two Popes, Royalty and United States Presidents, at rock concerts,3 City to Surf runs and many other occasions. The New South Wales State Emergency and Rescue Management Act 1989 has required increased disaster planning and preparedness at local government, district, area health and State levels. Training and certification of selected health professionals and practical texts4 are now readily available. A glimpse of the complexity of the overall picture of disaster response is provided by the table of contents (10 pages) of the Commonwealth's Australian emergency manual: disaster medicine,5 which covers all aspects of disasters through to recovery. Both this manual and the New South Wales HealthPlan2 have been revised for 1997. Disaster planning brings forth apathy, denial, squabbles about resources, turf battles and many committees representing various disciplines creating camels,* as well as serious professionals trying to plan for "What if . . . ?". The Olympic Health and Medical Working Committee, with senior representatives from the Sydney Olympic Games Organising Committee, the NSW Department of Health and other agencies, is setting up the framework for events in 2000. There are several established principles in disaster planning: In disasters, do the greatest good for the greatest number (a reversal of the usual clinical emphasis on quality of care for the individual). This explains why any disaster scene has to be declared safe by fire officers, why police are in charge overall, why systems are set up to evacuate "walking wounded" before attention is given to the mortally injured. Both military and civilian experience has confirmed that in a disaster a rigid chain of command is essential (doctors, with their individualistic training and professional independence, are poor at this), and that personnel should perform tasks similar to their normal duties (e.g., that surgeons should continue in surgery and not be called upon to organise transport). Overall service command must be led by a controller off site . Each service must have liaison officers from all other major agencies involved. The biggest problem is always communication: this must be organised by those agencies with the relevant expertise and equipment. Emergency physicians are the appropriate controllers of the medical response to a disaster: ". . . they are familiar with the system and personnel providing care before hospitalization; they are practiced in rapid assessment, basic treatment, and triage; and they have a good working rapport with other specialists needed during the response."6 As Waeckerle states in an article on disaster planning, it is too late to plan a response once a disaster occurs.6 Disaster response will always be a team collaborative effort which must be planned and practised. As everybody's time and resources are short, we have to use tabletop exercises, mass gatherings and even expensive exercises with moulaged victims to practise to get it right well before 2000. Gordian W O Fulde Director, Emergency Department St Vincent's Hospital, Sydney A Senior Commander, NSW Healthplan . * "A camel is a horse designed by a committee and an elephant is a mouse built to military specifications" -- Caxton C Foster Ambrose G. Disaster medical planning. In: Fulde GWO, editor. Emergency medicine: the principles of practice. 2nd ed. Sydney: Maclennan and Petty, 1992: 13-19. NSW Healthplan . Functional area supporting plan to the NSW State Disaster Plan (NSW DISPLAN). Sydney: Department of Health, 1997. Fulde GW, Forster SL, Preisz P. Open air rock concert: an organised disaster. Med J Aust 1992; 157: 820-822. Hodgetts TJ, Mackway-Jones K, editors. Major incident medical management and support. The practical approach. London: BMJ Publishing, 1995. Australian emergency manual: disaster medicine. Canberra: Commonwealth Department of Human Services and Health, 1995. Waeckerle J. Disaster planning and response. N Engl J Med 1991; 324: 815-821. ©MJA 1997 <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

The St Marys fragmentation grenade explosion Antony Nocera The accidental explosion of a fragmentation grenade in a munitions factory at St Marys injured four workers, two critically. The prompt response by ambulances and physician-staffed helicopter emergency medical service prevented deaths, but the incident suggests lessons for the future handling of urban explosions. (MJA 1997; 166: 545-548) For editorial comment see Fulde Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au/>". Introduction - Patient records - What makes a grenade - Discussion - Acknowledgement - References - Authors' details Make a comment - Register to be notified of new articles by e-mail - Current contents list - ©MJA1997 Introduction On 14 November 1995 an F1 fragmentation hand grenade exploded in a grenade testing facility in a munitions factory on a 1600 hectare site at St Marys, NSW. Seven employees were in the room. The grenade exploded at 8:36 am on a work bench and injured four workers around the bench (Figure 1). None were wearing body armour and there were no blast shields in the work area. Figure 1: Immediate area of the explosion. Patient C was sitting in the chair in the foreground, with Patient A in the chair immediately behind, while Patient B was standing behind the two. Patient D was sitting on the other side of the bench, opposite Patient C. The pallet to the left carried 1000 live grenades and was 1.85 m from the grenade burst point. Forty-eight grenades were damaged in the explosion and represented an explosive hazard during recovery operations. Photograph courtesy of the New South Wales Police. The first ambulances arrived at 8:41, 8:44 and 8:47. The four injured workers were extricated from the factory building to an adjacent courtyard by other employees and ambulance personnel. NRMA CareFlight, a Bell 412 HP helicopter emergency medical service (HEMS) with a physician on board, was placed on standby at 8:45 and dispatched at 8:50, landing at the site at 9:06. Two patients were transported by air to a trauma centre with full cardiothoracic facilities about 24 km (10 minutes' flying time) from the factory. Access to this centre by road would have encountered peak hour traffic flowing into Sydney via the major western arterial road routes. Two patients were transported by road to a local trauma centre (10 minutes' travelling time) which has limited cardiothoracic surgical facilities. Patient records Patient A Patient A was a 44-year-old woman sitting 0.25 m from the grenade burst point. On arrival of the HEMS, she had a Glasgow coma score of 12-13 and no recordable blood pressure. Only carotid pulses were palpable after an infusion of 1.5 L of polygeline by ambulance personnel; an additional 500 mL polygeline and 500 mL normal saline were infused. The patient's conscious state began to fluctuate, and a rapid sequence induction and endotracheal intubation were performed before transport by helicopter. The patient received a further two units of O negative blood during transport. On arrival at hospital, Patient A had a heart rate of 100/min, systolic blood pressure, 118 mmHg; haemoglobin level, 79 g/L (normal range, 115-165 g/L); pH, 7.29 (normal range, 7.35-7.45); PO2, 518 mmHg (normal range, 75-100 mmHg); PCO2, 30 mmHg (normal range, 35-45 mmHg); HCO3, 14 mmol/L (normal range, 22-26 mmol/L); and serum lactate, 3.04 mmol/L (normal range, 0.63-2.44 mmol/L). She was taken to theatre for thoracotomy and laparotomy, enucleation of left orbit, amputation of right ring and little fingers, debridement of right forearm and thigh, with internal fixation of her right forearm fractures. By the end of her first theatre session she had received (in addition to her prehospital fluids) 6.5 L of polygeline, 4 L of crystalloid, 24 units of packed red blood cells, 8 units of frozen plasma and 6 units of platelets. Patient A's injuries were: Multiple puncture wounds to the face, neck, chest and abdomen Singed hair and eyebrows Grenade fragments in the right maxillary antrum and right side of the nasopharynx Multiple puncture wounds to the left eye Bilateral perforated tympanic membranes Multiple fractured teeth Subtotal traumatic mastectomies (Figure 2a) Bilateral haemothoraces, with contusions of the right middle lobe and both lower lobes of the lungs Perforation of the right ventricle and apex of the heart, with a 250 mL pericardial haematoma Perforations of the stomach, left lobe of the liver, and splenic flexure of the colon Haematomas of the head of the pancreas, lesser omentum and left perinephric region Comminuted compound fracture of the right radius and ulna, with major soft tissue disruption to the dorsal surface of the right forearm (Figure 2b) Subtotal amputation of the right ring and little fingers A large skin and muscle defect to the anterior aspect of the right thigh (Figure 2c). After her initial surgery, Patient A required mechanically assisted ventilation for 11 days and underwent five additional operative procedures during her initial 39 days in hospital. In the next year she underwent another five operative procedures, with a further five reconstructive procedures scheduled for the following year. Patient B Patient B was a 45-year-old woman standing behind and to the left of Patient A, about 0.6 m from the grenade burst point. On arrival of the HEMS, she was in severe respiratory distress, with a heart rate of 105/min, systolic blood pressure of 60 mmHg, and Glasgow coma score of 10. Patient B was treated by ambulance personnel with 1.7 L of polygeline and transported to hospital by road. On arrival at hospital, Patient B had a heart rate of 88/min; systolic blood pressure, 140 mmHg; Glasgow coma score, 15; haemoglobin level, 83 g/L; pH, 7.30; PO2, 331 mmHg; PCO2, 36.6 mmHg; HCO3, 17.8 mmol/L; and base excess, - 7.2 (normal range, - 3 to 3). Patient B was taken to theatre for laparotomy and cholecystectomy. Her injuries were: Multiple puncture wounds to the face, neck, thorax and abdomen Forehead laceration and fractured nose Grenade fragments in the ethmoid and sphenoid sinuses, plus a fragment in the occipital lobe of the brain. Contusion of the lower lobe of the left lung Multiple perforations of the liver and gallbladder Lacerated right kidney and retroperitoneal haematoma Fragments adjacent to the abdominal aorta and the right L3 nerve root Delayed third-nerve palsy. She was discharged from intensive care after 1.5 days and discharged home after 18 days. She underwent six subsequent day procedures to repair soft tissue injuries and extract fragments. Patient C Patient C was a 54-year-old woman sitting to the right of patient A, 1.3 m from the burst point. On arrival of the HEMS, she had a heart rate of 80/min, systolic blood pressure of 130 mmHg and Glasgow coma score of 14. She was treated with 1 L of Hartmann's solution and 250 mL of polygeline and transported by air. On arrival at hospital, Patient C's heart rate was 83/min; systolic blood pressure, 151 mmHg; Glasgow coma score, 14; and haemoglobin level, 125 g/L. Her injuries were: Multiple small puncture wounds to the left upper limb and left side of the thorax A chin laceration and left periorbital haematoma; there were no perforations of the tympanic membranes A closed fracture of the left ulna A small left retinal tear and preretinal haematoma A fragment in the medial rectus of the left orbit. Patient C was discharged home after two days. Patient D Patient D was a 50-year-old woman sitting diagonally opposite Patient A about 1.6 m from the grenade burst point. On arrival of the HEMS, she had a heart rate of 105/min, systolic blood pressure of 70 mmHg and Glasgow coma score of 11. She was treated with 1 L of polygeline and transported by road. On arrival at hospital, Patient D had a heart rate of 90/min; systolic blood pressure, 150 mmHg; Glasgow coma score, 15; and haemoglobin level, 108 g/L. Her injuries were: Multiple fragment wounds to the right side of the face, neck, thorax and upper limb, including an intracapsular fragment in the right shoulder joint and a 4 cm scalp laceration Bilateral perforations of the tympanic membranes Right pneumothorax requiring drainage with an intercostal catheter, plus pulmonary contusions of the right mid and lower zones. She was discharged after seven days and subsequently underwent two outpatient procedures to extract fragments. Discussion The injuries of the four accident victims demonstrate the capability of military weapons to inflict serious physical injury -- but the potential psychological impact of these weapons extends well beyond their injury radius. The grenade exploded on a bench top, which directed most of the blast and fragments onto the upper torso of the victims, but it also blew a hole in the bench top, producing the wound to the right thigh of patient A. Any bomb or blast scene should always be considered dangerous until declared safe from the risk of secondary explosion by appropriate technical personnel. Specialist bomb disposal personnel were not part of the initial response to the St Marys incident, which contributed to the delayed recognition of a potential secondary explosion hazard from 48 damaged grenades at the site. The size and shape of modern military weapons often belie their wounding potential. Explosive devices may contain fuse mechanisms that detonate in response to stimuli other than that of direct impact. The bodies of victims may conceivably hold unexploded devices that pose a threat to rescue, medical and mortuary personnel.11,12 Major injuries and deaths occurred during the Gulf War among medical and service personnel handling souvenired battlefield ordnance.13 Injury from military weapons is uncommon in Australia. Army ammunition technical officers can provide expert advice on the composition and function of a particular device. This information is vital in the assessment of individuals wearing body armour, or who have been potentially exposed to either radiolucent fragments or items of ordnance which have become airborne.11,12 Early on-site specialist technical advice is critical to safe operations at the scene of an urban explosion. Helicopter emergency medical services have been used in the primary and secondary transport of blast victims.14,15 In this incident the HEMS rapidly provided a doctor on-site to assist in trauma triage. This allowed patients to be referred immediately for specialist surgical care, while dispersing casualties over a wider network of receiving hospitals (thus Patient A and Patient B were sent to different hospitals so that both could receive immediate surgical treatment; this would not have occurred under ambulance protocols). In addition, on-site medical care went beyond the scope of paramedic protocols16 (e.g., in performing a relaxant-assisted intubation and giving a blood transfusion). The NSW Ambulance Service Disaster Plan (December 1995) precludes the immediate dispatch of physician-staffed helicopter emergency medical services to potential multicasualty incidents. This may introduce avoidable delays in delivering seriously injured patients to definitive surgical care, especially in incidents geographically removed from designated trauma centres. Acknowledgement I thank Mr Mike Etzel for generously providing some of the background material. References Owen J. Infantry weapons of the world 1979. London: Brassey's 1979. Hogg IV. The illustrated encyclopaedia of ammunition. Sydney: Colporteur Press, 1985. Gander TJ, editor. Jane's infantry weapons. 22nd ed. 1996-97. London; Jane's Information Group, 1995. Rawlins JSP. Physical and pathophysiological effects of blast. Injury 1978; 9: 313-320. Huller T, Yaacov B. Blast injuries of the chest and abdomen. Arch Surg 1970; 100: 24-30. Cooper GJ, Maynard RL, Cross NL, Hill JF. Casualties from terrorist bombings. J Trauma 1983; 23: 955-967. Bellamy RF. The medical effects of conventional weapons. World J Surg 1992; 16: 888-892. Mellor SG. The relationship of blast loading to death and injury from explosion. World J Surg 1992; 16: 893-898. Handbook on weaponry. 2nd ed. DŸsseldorf: Rheinmetall GmbH, 1992. Courtney-Green PR. Ammunition for the land battle. London: Brassey's 1991. Clark MA. A fatal wound from an unusual military projectile: potential dangers of live military ordnance to the autopsy pathologist. J Forensic Sci 1987; 32: 793-797. Spencer JD. Accidental death by light anti-tank weapon: a dangerous autopsy? J Forensic Sci 1979; 24: 479-482. Thomson JD, Lisecki EJ. Injuries and deaths from collecting war souvenirs in Operation Desert Storm. Mil Med 1993; 158: 505-507. Brown MG, Marshall SG. The Enniskillen bomb: A disaster plan. BMJ 1988; 297: 1113-1116. Merriman M. Emergency medical response teams react swiftly to the Philips Plant tragedy. Occup Health Saf 1990; 59: 32-37. NSW Ambulance Service protocols, procedures and pharmacology. Sydney: NSW Ambulance Service, 1993. (Received 17 Jul 1996, accepted 18 Feb 1997) Authors' details NRMA CareFlight, Westmead, NSW. Antony Nocera, MB BS, Emergency Medicine Registrar. No reprints will be available. Correspondence: Dr Antony Nocera, NRMA CareFlight, PO Box 159, Westmead, NSW 2145. E-mail: tonynoceATozemail.com.au <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

Anthony Nocera

Serious injuries in jet skiers Elizabeth E L Swinburn Personal motorised watercraft (often referred to as jet skis) are an enjoyable leisure activity on the nation's waterways. However, there have been several serious accidents, and licensing requirements are deficient. Inconsistent reporting of accidents has hindered investigations into the causes. We describe six recent cases and the factors that may have contributed to accidents, and suggest ways to reduce the hazards associated with the sport. MJA 1996; 165: 606 Readers may print a single copy for personal use. No further reproduction or distribution of the articles in whole or in part should proceed without the permission of the publisher. For copyright permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au/>". Introduction - Discussion - Conclusions - Acknowledgement - References - Author's details - ©MJA1996 Introduction Motorised personal watercraft (MPWC), colloquially referred to as jet skis, are a popular recreational device and are the fastest growing section of the Australian boat market (sales have increased by 10%-15% per year for the last four years). 1 MPWCs are defined by the Waterways Authority (NSW) (formerly, the Maritime Services Board) as a vessel of no more than 3.5 m in length with a fully enclosed hull, which is power driven and designed to be operated by a person standing, sitting astride or kneeling on the craft, but the driver is not sealed inside the vessel. They are distinct from non-motorised personal watercraft (e.g., surf skis, surfboards, canoes and kayaks) and are capable of speeds of up to 72 kt (125 km/h). They are also being trialled as rescue craft by Surf Life Saving Australia Limited. There are many regulations controlling their use which are governed by the Waterways Authority (see Box 1). There are 4300 registered MPWC owners in NSW. 4 During a recent campaign to assess irresponsible use of MPWCs, 1466 MPWCs were stopped and 68 infringement notices were issued. Of these, 55% related to licensing and registration and 21% concerned safety issues. 4 We report six patients who presented to the Royal North Shore Hospital (RNSH) Emergency Department in Sydney over a four-year period (1992-1996) with serious or fatal injuries sustained while riding an MPWC. Four patients were identified by a search of hospital medical records from 1990 to 1995 and another from a search of the trauma database. Another patient was identified after an analysis of Waterways Authority data. The St John Ambulance Service (NSW), Water Police, Surf Life Saving Australia Limited and the Australian Institute of Health and Welfare National Injury Surveillance Unit did not have data on MPWC injuries. Four patients gave permission to publish their case histories, one declined, and the other was unable to be contacted. Case 1 Case 2 Case 3 Case 4 Discussion MPWCs are generally perceived by the public to be a fun (albeit noisy) way to enjoy many of the nation's coastal and inland waterways. There are many hire outlets, especially in holiday areas, and they may advertise that no licence is required. One establishment stated: "If you can sit on a chair when you're drunk, then you can ride a jetski when you're sober." The six patients who presented to our emergency department show that MPWCs can cause accidents that may result in injury or even death. In total, these patients accounted for over 130 hospital-days (18 in the intensive care unit). At time of writing, two patients are still in hospital and there has been one death. Their average age was 31 years, which is similar to that of the 25 cases of MPWC incidents reported to the Waterways Authority (Box 2). Unofficial data collected by the Surfriders Foundation Australia suggest there have been three fatalities in NSW (J Bradley, officer in charge of MPWCs, personal communication). The first report of MPWC injury was in 1989, and involved 13 people injured over the previous three-year period, including two fatalities.5 Three other overseas studies reported injuries to 134 people caused by MPWCs.6-8 None of these studies reported fatalities. The only Australian study pertaining to MPWCs was a case report of a full-thickness vaginal laceration extending to the peritoneal cavity. 9 Although six of the eight drivers involved in serious accidents reported to the Waterways Authority were licensed, it is of concern that the cause of the collision was poor judgement, excess speed or failure to keep a proper lookout in five of these accidents. This suggests that the licensing requirements may be inadequate. Currently, a boat driver's licence is required to operate an MPWC. However, the knowledge pertaining to driving a boat may not be sufficient to drive an MPWC in a safe manner, in the same way that the knowledge and/or skills required to drive a motor vehicle and a motor bike are different and they therefore require separate licences. Of the six cases that presented to our hospital, three riders were licensed and very experienced and two were not licensed. It is not known if the remaining rider was licensed. All that is needed to obtain a boat driver's licence in NSW is to pass a written test set by the Waterways Authority, and the person must be at least 16 years of age. There are no restrictions on MPWC engine capacity; recent models are 1100 cc and weigh over 250 kg without passengers. 10 New licensees can immediately drive any size machine at any speed, whereas (in NSW and some other States) newly licensed motorbike riders are restricted to machines of engine capacity of no greater than 250 cc. Another area of concern is the lack of reporting of MPWC incidents. A requirement of having a boating licence is that when an accident results in death or injury to a person, or damage to property, a written report must be forwarded to the Waterways Authority within 24 hours. 2 Only three of the six cases presenting to our hospital were reported to the Waterways Authority. The United States Coast Guard estimated that only 10% of non-fatal watersports accidents were reported.8 Case 4 was not reported, despite aninvestigation by the NSW Police Service at the time. Anecdotal reports suggest that there is a high incidence of personal injury to MPWC drivers (particularly inexperienced drivers), with bruising to the groin region the most common injury. However, MPWC drivers are often reluctant to report incidents because they fear that this will lead to increased regulation of their sport. All holders of a boat driver's licence are restricted to a blood alcohol level of less than 0.05% (or 5 g/100 mL). Under the Marine (Boating Safety -- Alcohol and Drugs) Act 1991 (NSW), people who present to a hospital after an injury incurred while in charge of a boat or MPWC must have blood taken for blood alcohol testing. Five of the six people who presented to our hospital were not tested for blood alcohol levels (one tested negative). No data are available on whether alcohol was involved in any of the incidents reported to the Waterways Authority. United States data suggest that more than half of boating deaths are associated with alcohol.11 An Australian review of alcohol and accidental drowning reported that, of 29 male victims of moving water-transport accidents, 10 had postmortem blood alcohol concentrations of over 15 g/100 mL.12 The Australasian Jet Sports Boating Association (AJSBA) conducts races in Australia and New Zealand each week and has strict safety regulations. Competitors must wear helmets and many also wear leg protectors and back protectors. Some form of medical coverage is provided at all competitions, and all competitors are covered by insurance. In 10 years of competition there have been no fatalities and no serious injuries. The average age of racers is 30 years. The AJSBA is assisting some States to formulate regulations (M DeBie, General Manager, AJSBA, personal communication). Conclusions The public needs to be educated about the potential dangers involved with riding MPWCs and of the necessity for a boating licence. The Waterways Authority should consider implementing a practical examination for those wishing to drive an MPWC, and possibly also introducing a speed or engine- capacity limit for new licensees. Present deficiencies in the reporting of MPWC accidents need to be addressed. The Waterways Authority accepts reports from anyone involved, not just the licensee. Alerting ambulance and police officers, lifesavers and hospital emergency department staff of the need for reporting incidents would be an effective approach. Emergency department staff also need to be aware that blood must be taken after MPWC accidents to determine blood alcohol concentrations. A simple preaddressed form (similar to the adverse drug reaction report form used by the Australian Drug Evaluation Committee) could be made available to emergency services and hospitals and also to registered MPWC owners and holders of boating licences. A comprehensive reporting system would assist in further research into the incidence, severity and causes of MPWC accidents. Acknowledgement Photos courtesy of the Waterways Authority (NSW). References Lewis D. It's war on the water: a blitz on jetskiers. Sydney Morning Herald 1996 Mar 23; Sect 1: 4. Waterways Authority. NSW safe boating handbook. Sydney: Waterways Authority, May 1995. The Royal Life Saving Society - Australia. Swimming and lifesaving. 3rd ed. Sydney: Mosby Lifeline, 1995. New South Wales Department of Public Works and Services. Media Release. 1996; May 19. Vernberg D, Fine EG, Jagger J. Personal water craft injuries [letter]. JAMA 1989; 261: 1883. Francis RA, Vize R. Personal water craft injuries: experience at a community hospital. Missouri Med 1994; 91: 241-243. Jeffery RS, Caiach S. Waterbike injuries. Br J Sports Med 1991; 25: 232-234. Hamman BL, Miller FB, Fallat ME, Richardson JD. Injuries resulting from motorized personal watercraft. J Pediatr Surg 1993; 28: 920-922. Wein P, Thompson DJ. Vaginal perforation due to jet ski accident. Aust N Z J Obstet Gynaecol 1990; 30: 384-385. Personal watercraft buyers guide. In: King M, editor. Jet Action; 1996 May-June: 54. Bradley J. Growing public menace caused by ineffective control of motorised personal watercraft in the surf. Proceedings of the Local Governments Authority Fourth Annual NSW Coastal Council Conference; 1994 Oct 18-20; Terrigal, NSW. Plueckhahn VD. Alcohol and accidental drowning. Med J Aust 1984; 141: 22-25. (Received 11 June, accepted 30 Sep 1996) Author's details Emergency Department, Royal North Shore Hospital, St Leonards, NSW. Elizabeth E L Swinburn, MB BS. No reprints will be available. Correspondence: Dr E E L Swinburn, Emergency Department, Royal North Shore Hospital, St Leonards, NSW 2065. - To top of article - ©MJA 1996 <URL: http://www.mja.com.au/> © 1996 Medical Journal of Australia.

Worldwide deaths and severe envenomation from jellyfish stingsPeter J Fenner and John A Williamson From our database of fatal and serious human envenomations, we report several cases, look at the distribution of these events, and discuss treatment. MJA 1996; 165: 658 Readers may print a single copy for personal use. No further reproduction or distribution of the articles in whole or in part should proceed without the permission of the publisher. For copyright permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au/>". Introduction - Distribution of jellyfish and reported envenomations - Sting seasons - Reflections on treatment - Applying vinegar - Removing adherent tentacles - The role of steroid therapy - Chironex fleckeri antivenom - Conclusions - Acknowledgments - References - Authors' details - ©MJA1996 Introduction We have collected worldwide information about jellyfish and their stings since 1990, through personal communication with members of the International Consortium of Jellyfish Stings (ICJS), 1 investigating reports of serious jellyfish stings heard on the "grapevine", and travelling in areas of chirodropid (multitentacled "box" jellyfish) distribution. Annual reports of our data have been published from 1991 to 1993. 2 Our database now records over 1100 individual cases of stings (some severe and fatal), as well as some 1000 monthly reports of jellyfish numbers and stings, from surf life saving clubs in Queensland over the past six years. Our data are only the "tip of the iceberg" and probably an inadequate indication of the extent of the problem worldwide. However, we continue to seek information, now also by internet and e-mail. Our data include information on envenomation by Physalia , the Portu guese man-o'-war or bluebottle. Although not a true jellyfish (actually a siphonophore, or hydroid colony), it stings like one, is popularly regarded as one, and we treat it as one in this article. A brief description of the mechanism of a jellyfish sting is provided in Box 1. While many suspected deaths from envenomation, and the jellyfish species involved, remain inadequately authenticated, documented deaths from jellyfish stings usually involve species of chirodropid, 5,6 described and shown in Box 2. In this article we examine the distribution of serious and fatal jellyfish envenomations (illustrated in the Map), the animals involved and aspects of treatment, and we describe some previously unreported cases (Table). Distribution of jellyfish and reported envenomations Australia In Australia, particularly on the east coast, up to 10 000 stings occur each summer from the bluebottle (Physalia spp.) alone, with others also from the "hair jellyfish" (Cyanea) and "blubber" (Catostylus). More bluebottle stings occur in South Australia and Western Australia, as well as stings from a single-tentacled box jellyfish, the "jimble" (Carybdea rastoni) (personal data) . The chirodropid Chironex fleckeri 3,4,8 is known to be the most lethal jellyfish in the world, 3 and has caused at least 63 recorded deaths in tropical Australian waters off Queensland and the Northern Territory since 1884. 3 Indo-Pacific region The presence of chirodropids has now been confirmed in the tropical Indo-Pa cific ocean from the Maldive Islands 9-12 in the west, eastwards to the Philippines, north to Amani Island, Japan (see below), and south to tropical Australia; this includes Brunei, Sarawak, Sabah (L Marsh, Curator of Marine Invertebrates, West Australian Museum, 1993, personal communication), Papua New Guinea, the Malaysian archipelago, Gulf of Thailand, 8 Java and southern India. 12 Deaths have previously been reported from Penang (Malaysia), the Philippines, Bougainville Island, the Solomon Islands, "North Borneo" (now Sarawak, Brunei, Sabah), and Papua New Guinea (d'Entrecasteaux Islands). 8 Medical officers at the Labuan District Hospital (in Malaysia) have been quoted as saying that there are two to three deaths there each year from jellyfish stings and another one or two victims who survive, but require intensive care and commonly remain unconscious for 12-24 hours. 13 Chirodropid jellyfish are well known in the Philippines, and an estimated annual death rate from jellyfish stings there of 20-40 does not seem excessive (P J F, 1987, personal experience). More recently, Dr Paul Cornelius, of the British Museum of Natural History, has made a similar estimate of fatalities (unpublished observations, April 1994). As a death certificate is not necessary for burial in the Philippines, these estimates cannot be verified. World map showing human fatalities from chirodropid and other jellyfish stings, and presently confirmed and probable chirodropid distribution. The Americas Chirodropids have been described in waters along the eastern coast of the Americas between the Tropics, including the waters around many Caribbean islands. 11,14 Serious stings from these chirodropids have also been reported from beaches in Puerto Rico during the summer months (B Cutress, Associate Investigator, Marine Biology Department, Puerto Rico University, 1992, personal communication). In 1990, a 4-year-old boy at Galveston Island, in the Gulf of Mexico, was stung and died within 20 minutes, despite cardiopulmonary resuscitation. 6 Stinging cells were identified as being from a chirodropid previously described in that region. 14 Three fatal envenomations from Physalia physalis have been reported from Florida and North Carolina, in the United States. 15,16 Serious envenomations have also been reported from both sides of the Atlantic. 17-19 China Apart from Physalia species and chirodropids, the only other jellyfish presently known to cause deaths in humans are large specimens (up to 1 m diameter) of Stomolophus nomurai (Mingliang, Research Assistant, Qingdao Hospital, 1991, personal communication), a jellyfish found in the Yellow Sea between China and South Korea. Reports of eight deaths have now been published, five in detail. 20,21 Victims die with acute pulmonary oedema some 2-24 hours after the initial envenomation. Africa A chirodropid occurs in the tropical oceans of west Africa, 22,23 but we know of no published reports of deaths or serious stings. Although chirodropids have not been reported to occur on the eastern tropical coastline of Africa, they must be expected in these waters. South India and Sri Lanka Serious jellyfish envenomations occur in the Indian region, with peripheral ischaemia reported in at least two victims. 24,25 Although the jellyfish is frequently unidentified, chirodropids, Sanderia and Physalia species occur in this region. Two fatalities were reported recently on the eastern side of the Indian Ocean, on Langkawi Island, a tourist resort in Kedah, a northern state of Malaysia. From the rapid demise of the victims, and appearance of sting marks, they probably died of chirodropid envenomation (Dr Iekhsan Othman, Malaysia, personal communication). 12 Sting seasons In the Southern Hemisphere, chirodropid stings occur mainly in the summer months (December-May), 3 but over a longer season in areas closer to the Equator. In the Northern Territory stings have occurred in every month, with deaths in all months except July. 3,4,8 Chirodropids may occur only in December and January at the southern extreme of their recorded range (just north of Bundaberg, Queensland). 3 In the northern area of Borneo (Northern Hemisphere), stings usually occur in the dry hot season, from March to July, when seas are calm. Reflections on treatment Applying vinegar Two to 10 per cent acetic acid in water was recommended as a first-aid treatment for Chironex fleckeri nematocyst inhibition by Hartwick et al. in 1980. 26 Household vinegar has been a traditional treatment for box jellyfish stings in the Philippines since the turn of the century, although other "traditional" treatments were also used. Fishermen in Kukup also describe stings from cubozoan jellyfish in Malaysia as being treated with vinegar (P J F, personal observation, 1987). We do not know how long this remedy has been used. In two cases recorded on our database ( Table, Cases 3 and 7), victims seemed to stop breathing after vinegar was poured on the envenomed area. Whether this was a cause-related effect is not known; further research is needed. Removing adherent tentacles In another of our cases ( Table, Case 5), removal of the adherent tentacle material was accompanied by impairment of consciousness. Our advice has been for the rescuers to remove the tentacles physically with fingers, if vinegar is unavailable, before applying any compression bandages. 3 While this single report scarcely invalidates such advice, further case studies and research are awaited. The issue of removing adherent tentacle material in any jellyfish (especially serious chirodropid) stinging is complex. Fully extended tentacle material presents most of the nematocysts to the victim's skin, 27 and most will have discharged by the time adherent tentacles on the skin are being dealt with by the first-aiders. However, even partial contraction of tentacle material protects some nematocysts from discharge upon contact, 27 and the response of chirodropid tentacles to sudden entanglement with a human victim seems likely to involve at least some immediate tentacular contraction. Consequently, it seems probable that some nematocysts in adherent tentacle material will remain undischarged, and inappropriate stimulation could result in additional venom being injected into an already seriously envenomed person. If tentacles have not been inactivated with vinegar, 26 it would seem prudent to carefully, but promptly, "pick them off" the patient's skin with minimal handling, and no rubbing, before applying either compression bandages (in the case of serious chirodropid stings) or analgesic cold packs (for use in chirodropid or other cnidarian stings). Applying compression bandages directly over untreated adherent tentacle material cannot be recommended. However, once tentacles have been doused with vinegar for a minimum of 30 seconds, no time should be lost in removing them before applying bandages. 3 One of our cases (Table, Case 3) describes papilloedema after a chirodropid sting. This is the first such observation published, although Heazlewood (personal communication, 1992) reports a case of cerebral oedema in a 4-year-old in Cairns in 1980, after an "irukandji" (the carybdeid Carukia barnesi ) sting. The role of steroid therapy Steroid creams may be useful for mild itching in the immediate healing period after a cubozoan sting, 27 although Burnett 3 now doubts their efficacy. Systemic steroids should be used for severe cases of delayed hypersensitivity, given as prednisone (0.5-1 mg/kg body weight, daily), until the symptoms are fully controlled -- usually just a few days. After such a short course, it is unnecessary to taper the dose. Chironex fleckeri antivenom The exact mechanism of action of Chironex fleckeri venom and antivenom remains incompletely understood, despite several studies. 28,29 The efficacy of Chironex fleckeri antivenom in stings from the Australian chirodropid named Chiropsalmus quadrigatus is also unclear -- as is the exact identification of this species. 3 An early study showed in-vitro neutralisation of the dermatonecrotic, haemolytic and lethal factors of the venom of this Australian species when Chironex antivenom was used. However, although passive immunisation of mice with the antivenom reduced dermato necrosis, it did not protect against the lethal effects of Chiropsalmus quadrigatus venom. 30 Another study, using rabbit antisera prepared against Chironex fleckeri venom, showed no in-vitro cross- protection against the venom of Chiropsalmus quadrigatus . 31 However, the Commonwealth Serum Laboratories (CSL) currently recommends the use of Chironex antivenom for severe envenomation from the Australian " Chiro psalmus quadrigatus ". The possible benefits of Chironex antivenom for severe envenomations by chirodropids worldwide need investigation. Chironex antivenom has been shown to be of little benefit in the "irukandji" syndrome (it neither relieves the pain of envenomation nor reduces any other systemic problem), 32 and is currently not recommended for envenomation from any other (non-chirodropid) jellyfish species. Conclusions Lethal, or potentially lethal, chirodropid jellyfish occur worldwide, around every major land mass in the tropical and some subtropical oceans, and deaths and serious morbidity are more common than previously believed. Physicians practising in these areas, or those advising people who travel to such areas, must be aware of the problem, and advise their patients on awareness, prevention and treatment (summarised in Box 3) of potentially lethal jellyfish envenomation. The toxicology of the venoms needs further study. Acknowledgments We would like to thank Associate Professor Nor Azila and Dr Iekhsan Othman (Malaysia), Loisette Marsh (Australia), Major (Dr) R Hooper (Sabah), Dr T K Chan, Bertha Cutress (Puerto Rico), Drs Y Tomihara, Y Araki and M Kohama (Japan) for assistance with compilation of data. The photograph at the beginning of this section was provided by Surf Life Saving Queensland Inc. References Burnett JW. International consortium of jellyfish stings [letter]. J Wilderness Med 1990: 1; 135-137. Fenner PJ, Williamson JA, Burnett J. Some Australian and international marine envenomation reports; progress summary to October 31 1993. Adelaide: International Consortium for Jellyfish Stings, Department of Hyperbaric Medicine, Royal Adelaide Hospital, 1994. Williamson JA, Fenner PJ, Burnett JW, Rifkin J, editors. Venomous and poisonous marine animals: a medical and biological handbook. Surf Life Saving Australia and University of New South Wales Press Ltd, Sydney, 1996. Currie B, Khanh DM, Alderslade P, et al. Jellyfish envenomation in the Northern Territory of Australia. Toxicon 1992: 30; 501. Fish CJ, Cobb MC. Noxious marine animals of the central and western Pacific Ocean. Res Rep US Fish Ser 1954; 36: 1-45. Bengston K, Nichols MM, Schnadig V, Ellis MS. Sudden death in a child following jellyfish envenomation by Chiropsalmus quadrumanus ; Case report and autopsy findings. JAMA 1991; 266; 10: 1404-1406. Fatal sting in Labuan. Malaysian Straits Times 1992 Jul 22: 1 (Cols 1-2). Cleland JB (Sir), Southcott RV. Injuries to man from marine invertebrates in the Australian region. Special report series no.12. Canberra: NHMRC, 1965. Haeckel E. System der Acraspeden: zweite halfle des System der Medusen . Jena: Gustav Fischer, 1880: 447. Barnes JH. Chironex fleckeri and Chiropsalmus quadrigatus : Morphological distinctions. North Queensland Naturalist 1965; 32: 13-22. Kramp PL. Synopsis of the medusae of the World. J Marine Biol Assoc UK 1961; 40: 304-310. Menon MGK. Scyphomedusae of Krusadai Island. Bull Madras Govt Museum, NS Nat Hist Sect 1936; 1(2): 1-9. Tan NH, Oo SL, Thambyrajah V, Azila N, editors. Advances in venom and toxin research. Proceedings of the Third Asia Pacific Congress on Animal, Plant and Microbial Toxins; 1993 27 Jun-1 Jul; Malaysia. Kuala Lumpur: Malaysian Society on Toxinology, 113-118. Guest WC. The occurrence of the jellyfish Chiro psalmus quadrumanus in Matagorda Bay, Texas. Bull Mar Sci Gulf Carib 1959: 9; 79-83. Burnett JW, Gable WD. A fatal jellyfish envenomation by the Portuguese man-o'-war. Toxicon 1989; 27: 823-824. Stein MR, Marraccini JV, Rothschild NE, Burnett JW. Fatal Portuguese man-o'war ( Physalia physalis ) envenomation. Ann Emerg Med 1989; 18: 312-315. Halstead BW. Poisonous and venomous marine animals of the world. Princeton, NJ; Darwin Press, 1978: 301. Gonzaga RAF. Mordeduras picadas pot animas da forna Portuguesa . Amber-Porto-Portugal. Premio Biol de Medicina Clinics 1984; 165-167. Burnett JW, Fenner PJ, Kokelj F, Williamson JA. Serious Physalia (Portuguese Man-o'-war) stings: implications for scuba divers. J Wilderness Med 1994: 5; 71-76. Mingliang Z. A study on nematocyst dermatitis caused by jellyfish Stomolophus numerai . Acta Acad Med Qingdao 1987; 4: 1. Mingliang Z. The marine stinger. Qingdao: Oceanology University Press, 1992: 51. Kramp PL. The Medusae of the tropical west coast of Africa. Atlantide [report 3]. Copenhagen: University of Copenhagen and British Museum (Natural History), 1955: 288-292. Pages F, Gili JM, Bouillon J. Planktonic cnidarians of the Benguela current. Scientia marina 1992; 56 (suppl): 1-444. Adiga KM. Brachial spasm as a result of a sting. Med J Aust 1984; 140: 180-181. Williamson JA, Burnett JW, Fenner PJ, et al. Acute regional vascular insufficiency after jellyfish envenomation. Med J Aust 1988; 149: 698-701. Hartwick RJ, Callanan V, Williamson JAH. Disarming the box jellyfish: nematocyst inhibition in Chironex fleckeri . Med J Aust 1980; 1: 15-20. Williamson JAH, Le Ray LE, Wolfhart M, Fenner PJ. Acute management of serious envenomation by box-jellyfish ( Chironex fleckeri ). Med J Aust 1984; 141: 851-853. Othman I, Burnett JW. Techniques applicable for the purifying of Chironex fleckeri (box-jellyfish) venom. Toxicon 1990; 28: 821-835. Freeman SE. Actions of Chironex fleckeri toxins on cardiac transmembrane potentials. Toxicon 1974; 12: 395-404. Baxter EH, Marr AGM. Sea wasp ( Chironex fleckeri ) antivenene: neutralising potency against the venom of three other jellyfish species. Toxicon 1974; 12: 223-229. Keen TEB. Comparison of tentacle extracts from Chiropsalmus quadrigatus and Chironex fleckeri. Toxicon 1971; 9: 249-254. Fenner P, Rodgers D, Williamson J. Box jellyfish antivenom and "Irukandji" stings. Med J Aust 1986; 144: 665-666. Authors' details Corner of Palmer and Grendon Streets, North Mackay, QLD. Peter J Fenner, FACTM, FRCGP, General Practitioner and Marine Stinger Officer, Surf Life Saving Queensland Inc. Hyperbaric Medicine Unit, Department of Anaesthesia and Intensive Care, Royal Adelaide Hospital, Adelaide, SA. John A Williamson, FANZCA, FACTM, Director and Associate Professor. No reprints will be available. Correspondence: Dr P J Fenner, PO Box3080, North Mackay, QLD 4740. To top of article - ©MJA 1996 <URL: http://www.mja.com.au/> © 1996 Medical Journal of Australia.

Peter J Fenner · John A Williamson

Silicone breast implants: implications for society and surgeons Stuart B Renwick Readers may print a single copy for personal use. No further reproduction or distribution of the articles in whole or in part should proceed without the permission of the publisher. For copyright permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au/>". Abstract - Introduction - Problems with silicone gel breast implants - Mechanical problems - Relationship to autoimmune diseases - Relationship to breast cancer - Summary - Medicolegal settlements in the United States - The future - References - Author's details - Register to be notified of new articles by email - - ©MJA1996 In the last two years, scientific studies have confirmed that there is no significant increase in risk of subsequent breast cancer, connective-tissue disease or symptoms in women with silicone gel-filled breast implants. Despite this evidence, a moratorium (in place since 1992) on the use of these prostheses in the United States has been maintained by the pressure of overwhelming litigation. At the same time, Australian authorities also announced a moratorium, restricting the availability of silicone breast implants. Huge damages awarded by United States courts forced Dow Corning, manufacturer of a large percentage of breast prostheses, to file for Chapter 11 bankruptcy in May 1995. This effectively terminated the major source of implantable silicone for medical use. The withdrawal of implantable silicone and other implantable prosthetic material will be a significant loss for surgeons and society. This paper will highlight the consequences if reasoned scientific data are not relied on by Australian courts to assess claims for damages relating to medical devices. (MJA 1996; 165: 338-341) Introduction In the late 1940s, a family of silicon-based polymers (plastics) was developed. These polymers had a molecular structure of silicon and oxygen atoms with various organic sidechains, which could be varied to make the silicones liquid or solid for use as lubricants, gels, flexible sheeting or solid blocks of low reactivity and great permanency. Silicones were rapidly taken up by surgeons as a compatible material for implanting into the human body. Breast augmentation was first performed by injecting paraffin wax into the breast and, in 1949, by the implantation of polyvinyl alcohol sponge. As these implants set like a rock after several years, injectable liquid silicone was tried in Asian countries (it was never legal in Australia). However, this produced granulomas with hard lumps and opacities which precluded mammographic detection of breast cancer. Silicone gel-filled prostheses were first used in 1964 and it has been estimated that about two million have been implanted over 30 years worldwide. The prostheses have been modified to include fixation patches, thinner outer envelopes of silicone, silicone cores with outer envelopes of saline, and textured outer envelopes. Regulations governing the use of breast implants in Australia are shown in Box 1. Silicones are currently used not only in gel-filled breast implants, but also in ventriculocaval shunts, artificial joints and tendon sheaths, intraocular lenses, cochlear implants, as well as implantable pumps, pacemakers and defibrillators. Problems with silicone gel breast implants Mechanical problems The fibrous tissue "capsule" that naturally forms around the implant can contract, increasing tension in the prosthesis and causing pain, hardening and changes in breast appearance. Sometimes "bleeding" of silicone gel into the space between the envelope and the capsule occurs with an apparently intact envelope. External trauma can rupture the implant, causing leakage of silicone gel into the capsule or migration of silicone to other body tissues. The prosthesis may cause local infection. A 1994 study reported that 10% of prostheses needed replacement and, of these, 85% were intact and 15% had bled or had ruptured (i.e., only 1.5% of all prostheses had bled or leaked and 98.5% were intact). 2 Relationship to autoimmune diseases During the 1980s, there were sporadic references in the literature to single cases or small series of cases where an association between silicone gel implants and autoimmune diseases was claimed. 3-6 The hypothesis that silicone induces connective-tissue diseases was generated from such descriptive uncontrolled studies. 7 Up to June 1993, about 300 patients have been reported worldwide with rheumatic symptoms after receiving gel-filled breast implants. 8 The most commonly reported connective-tissue disease was scleroderma, but several other connective-tissue disorders and vague musculoskeletal symptoms have also been described, particularly vague aches and pains (fibromyalgia), sleep disorders and fatigue -- symptoms which are extraordinarily common in the community. 9 It was not until 1994 that the first definitive studies to examine the relationship between silicone implants and autoimmune disease appeared. Englert et al. identified 556 cases of scleroderma in women who had resided in Sydney between 1974 and 1988, of whom 270 were living and 213 were deceased (73 were "living status unknown"). 10 They reported that the rates of augmentation mammoplasty were similar between the 251 women with scleroderma that they interviewed and 289 matched controls (the study carried a 90% chance of detecting a relative risk of 4.5). These results were validated in 1996 when the authors found no association between silicone breast implants and scleroderma (odds ratio [OR], 1.33; 95% confidence interval [CI], 0.26-6.71, and OR, 1.00; 95% CI, 0.16-6.16, after adjustment for confounders age, socioeconomic status and ethnicity). 7 Validation of augmentation mammoplasty status was possible in 532 of the original 556 cases of scleroderma. Larger epidemiological studies were conducted in the United States. In 1994, Gabriel et al., from the Mayo Clinic, performed a population-based case-control study of 749 women who had received a breast implant in Olmsted County, Minnesota, between 1964 and 1991. 11 Each subject was matched with two women of the same age who had not had a breast implant, but had had a medical evaluation within two years of the date of the subject's implant. The implant group were followed for a mean of 7.8 years and the control group for a mean of 8.3 years. The authors sought evidence from the medical records for a diagnosis of any connective-tissue diseases, autoimmune diseases or non-breast cancer, as well as for related symptoms. Only morning stiffness was significantly more common in the implant group. Five women with implants and 10 women without implants were diagnosed with one of the specified connective-tissue diseases. The authors found no statistically significant elevation in the relative risk of any of the specified connective-tissue diseases or other disorders in women with silicone breast implants. Box 2 shows the conclusion reached in 1994 by the Medical Devices Agency of the United Kingdom Department of Health, which reviewed all the evidence relating to silicone breast implants and connective-tissue disease. In 1995, Sanchez-Guerrero et al., from Harvard Medical School, reported on a cohort of over 120 000 registered nurses aged between 30 and 55 who had been followed up since 1976. 13 The mean follow-up period after surgery for the 1183 women with silicone breast implants was 9.9 years. The age-adjusted relative risk of definite connective-tissue disease in women with implants was 0.3 (95% CI, 0-1.9). The relative risk of self-reported signs or symptoms of connective-tissue disease for women with implants was 1.5 (95% CI, 0.9-2.4), and the risk of having any one of 41 signs, symptoms or laboratory features of connective-tissue disease was 0.7 (95% CI, 0.3-1.6). The authors concluded that there was no association between silicone breast implants and connective-tissue diseases, or signs or symptoms of these diseases. The American College of Rheumatology released a statement in October 1995 declaring that these studies provided compelling evidence that silicone implants expose patients to no demonstrable additional risk for connective-tissue or rheumatic disease. 14 The College affirmed that anecdotal evidence, while of importance in drawing attention to a potential problem, should no longer be used to support this relationship in the courts or by the Food and Drug Administration (FDA). They recognised that many women who have received silicone breast implants have musculoskeletal complaints that are also very common in the general population. They had stated in 1994 the importance and great need for scientific analysis of this question, and called upon the FDA and other regulatory agencies to allow professional societies to foster epidemiological studies. The only study suggesting a possible link was published in February 1996. 15 Hennekens et al. retrospectively reviewed a large cohort of 395 543 health professionals and found 10 830 women who reported breast implants and 11 805 who reported connective-tissue diseases between 1962 and 1991. The relative risk of any connective-tissue disease among those reporting implants was 1.24 (95% CI, 1.08-1.41; P = 0.0015). This indicated a small, but significant, increase in the risk of connective-tissue disease, but provided reassuring evidence against silicone implants being a large-scale hazard. The results fell within the 95% confidence limits of the other two major studies. The authors stress that biases from self-reporting of symptoms (questionnaires were sent to the women after the publicity surrounding the FDA ban) or a higher participation rate in women with such diseases must be considered as alternative explanations for their results. Relationship to breast cancer In a population-based non-concurrent cohort-linkage study of 11 676 women in Alberta, Canada, who underwent cosmetic breast augmentation from 1973 to 1986, Berkel et al. found that 41 women with implants had subsequently developed breast cancer. 16 By comparing these women to a cohort of women who had a first primary breast cancer diagnosed between 1973 and 1990, and by applying calendar-year-specific incidence rates of breast cancer, the expected number of breast cancer cases in the implant cohort was 86.2. The standardised incidence ratio was thus 47.6%, significantly lower than expected ( P < 0.01). They concluded that women with silicone breast implants have a lower risk of breast cancer than the general population. In a reanalysis of the data used by Berkel et al., Bryant and Brasher performed multiple estimates of the standardised incidence ratios on the basis of differing study-eligibility dates, indication periods and types of breast cancer (invasive or invasive plus in situ ). 17 They found substantial differences in the numbers of person-years at risk, resulting in higher standardised incidence ratios than in the original analysis, and concluded that the risk of women with silicone breast implants developing breast cancer was not higher or lower than in the general population. Summary Silicone breast implants have a low incidence of mechanical problems or leakage (about 1.5%). Silicone breast implants do not increase the risk of breast cancer. Three large and scientifically sound studies confirm that there is no strong link between silicone breast implants and connective-tissue diseases or symptoms. Medicolegal settlements in the United States In view of these findings, it must be asked how silicone breast implants were found wanting and how their main manufacturer was reduced to bankruptcy? The answer lies in the medicolegal settlements and judgments made against the company in the United States ( Box 3). The United States legal processes in the breast implant trials exemplified a growing divergence between science and the law, and the use and abuse of expert witnesses in an adversarial legal system. 20 In just four years, the litigation bar in the United States demolished the largest manufacturer of medical silicone products. The future So far, litigation has been aimed largely at the manufacturers of breast implants, but if they were unable to pay could individual surgeons who performed the implants be sued? What transpired in United States courtrooms and in the United States media, at least at the time of the FDA ban, were judgments allegedly based on anecdote and speculation. 16 Anecdote and fear prevailed over science and were successful. I only hope that Australian courts will admit reasoned scientific evidence and that settlements, if any, are commensurate with damages and not excessive. In Australia, we must maintain scientific objectivity, so that silicone continues to be available for implantation in its many forms. References Commonwealth Department of Human Services and Health. Breast implant information booklet. Canberra: AGPS, 1995. Duffy MJ, Woods JE. Health risks of failed silicone gel breast implants: a 30 year clinical experience. Plast Reconstr Surg 1994; 94: 295-299. Van Nunen SA, Gatenby PA, Basten A. Postmammoplasty connective tissue disease. Arthritis Rheum 1982; 25: 694-697. Kumagai Y, Shiokawa Y, Medsger TA, et al. Clinical spectrum of connective tissue disease after cosmetic surgery. Arthritis Rheum 1984; 27: 1-12. Spiera H. Scleroderma after silicone augmentation mammoplasty. JAMA 1988; 260: 236-238. Varga J, Schumacher R, Jimenez SA. Systemic sclerosis after augmentation mammoplasty with silicone implants. Ann Intern Med 1989; 111: 377-383. Englert H, Morris D, March L. Scleroderma and silicone gel breast prostheses -- the Sydney study revisited. Aust N Z J Med 1996; 26: 349-355. Brooks PM. Silicone breast implantation: doubts about the fears. Med J Aust 1995; 162: 432-434. Reilly PA. Fibromyalgia in the workplace -- a management problem. Ann Rheum Dis 1993; 52: 249-251. Englert HJ, Brooks P. Scleroderma and augmentation mammoplasty -- a causal relationship? Aust N Z J Med 1994; 24: 74-80. Gabriel SE. Risks of connective-tissue diseases and other disorders after breast implantation. N Engl J Med 1994; 330: 1697-1702. Medical Devices Agency. Silicone implants and connective tissue disease. London: Department of Health, 1995. Sanchez-Guerrero J, Colditz GA, Karlson EW, et al. Silicone breast implants and the risk of connective-tissue diseases and symptoms. N Engl J Med 1995; 332: 1666-1670. American College of Rheumatology. Issues Statement on Silicone Breast Implants, 24 October 1995 [press release]. Hennekens CH, Lee I-M, Cook NR, et al. Self-reported breast implants and connective-tissue diseases in female health professionals. A retrospective cohort study. JAMA 1996; 275: 616-621. Berkel H, Birdsell DC, Jenkins H. Breast augmentation: a risk factor for breast cancer? N Engl J Med 1992; 326: 1649-1653. Bryant H, Brasher P. Breast implants and breast cancer-- reanalysis of a linkage study. N Engl J Med 1995; 332: 1535-1539. Nocera J. Fatal litigation. Fortune 1995 Oct 16; No 20: 46-66. Nocera J. Fatal litigation. Fortune 1995 Oct 30; No 21: 137-158 Angell M. Evaluating the health risks of breast implants: the interplay of medical 1513-1518. Author's details Sydney Breast Cancer Institute, Royal Prince Alfred Hospital, Camperdown, NSW. Stuart B Renwick, FRACS, FRCS, Director. Reprints: Associate Professor S B Renwick, Sydney Breast Cancer Institute, Royal Prince Alfred Hospital, Missenden Road, Camperdown, NSW 2050. - Register to be notified of new articles by email - - To top of article - ©MJA1996 <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia. We appreciate your comments.

Stuart B Renwick

Position Statement Paediatric advanced life support The Australian Resuscitation Council Guidelines The Advanced Life Support Committee of the Australian Resuscitation Council MJA 1996; 165: 199-206 Basic cardiorespiratory resuscitation - Advanced life support - Techniques in paediatric advanced life support - Medications and fluids used in paediatric advanced life support - Management after resuscitation - Cessation of cardiopulmonary resuscitation - Contributors - References - Register to be notified of new articles by email - These guidelines by the Australian Resuscitation Council (ARC) provide brief step-by-step outlines of the management of common life-threatening emergencies in infants and children. The guidelines are similar, but not identical, to guidelines published by the American Heart Association 1 and the European Resuscitation Council. 2 An international liaison committee (including representation from the ARC) is attempting to resolve differences and will in due course publish common advisory statements. The current guidelines are specifically for advanced life support, but some essential techniques of basic life support are presented. Further details of basic life support for infants and children 3 and specific guidelines for resuscitation of asphyxiated newborn infants have been published. 4,5 Basic cardiorespiratory resuscitation Cardiorespiratory arrest should be suspected when the infant or child loses consciousness, appears pale or cyanosed, or is apnoeic or pulseless (see definitions in Box 1). Assess airway and breathing by observing movement of the chest and feeling for expired breath. Position the head and neck to maintain an open airway. Movement of the chest without expiration implies an obstructed airway. If the obstruction is not relieved by backward head tilt and chin lift or by forward jaw thrust, the pharynx should be inspected with a laryngoscope and cleared of any secretions, vomitus or blood with a sucker (Yankauer). Forceps (Magill) may be needed to extract a foreign body. If spontaneous ventilation is not immediately resumed, artificial ventilation is commenced with mouth-to-mask expired air, a self-inflating resuscitation bag or an oxygen-inflated bag and mask circuit. Supplemental 100% oxygen should be added. Insertion of an oropharyngeal airway (Guedel) may facilitate ventilation. Assess the circulation by palpating the carotid, brachial or femoral pulse. Commence external cardiac compression (ECC) if a pulse is not palpable or it is: < 80 beats per minute (bpm) in a newborn or infant; < 60 bpm in a small child; < 40 bpm in a large child. Precede ECC with 2-5 slow breaths to reinflate the lungs. The patient should be placed on a firm surface, and compression directed to the lower sternum to a depth approximating a third of the anteroposterior diameter of the chest, or at a depth of 2-3 cm and rate of 100/min for a newborn or infant; depth of 3-4 cm and rate of 100/min for a small child; depth of 4-5 cm and rate of 80-100/min for a large child. ECC for a newborn or infant can be performed with two fingers, although a better technique is to encircle the chest with both hands, compressing the sternum anteriorly with the thumbs while stabilising the vertebral column posteriorly with the fingers. The rescuer's hands must encircle the chest freely and not restrict chest expansion. ECC for a small child can be performed with the heel of one hand and, for a large child or teenager, with two hands. A cycle should be 50% chest compression and 50% relaxation. Combine ECC and assisted ventilation in an infant or small child in a ratio of 5 : 1. For a large child or teenager in whom a two-handed technique of ECC is required, a single rescuer may achieve better circulation and ventilation with a ratio of compression to ventilation of 15 : 2. If a mask is used, breaths should be delivered between successive compressions to allow adequate expansion of the lungs, but if an endotracheal tube is used coordination is less crucial as effective ventilation can be given against the resistance imposed by ECC. For the asphyxiated newborn, ECC should be at a rate of 120/minute and ventilation at 40-60/min (i.e., in a ratio of 3 : 1). 5,6 Advanced life support Advanced life support implies a patent airway by endotracheal intubation, mechanical ventilation with oxygen, the treatment of cardiac arrhythmias, the treatment of the cause of cardiorespiratory arrest and of complications arising from its management. When several rescuers are in attendance, tracheal intubation and ventilation, display of the electrocardiograph (ECG) and access to the circulation should be attempted simultaneously. Thereafter treatment should be guided by the cardiac rhythm (see Flowchart in Box 2). Tracheal intubation is the first priority. This establishes and maintains a patent airway, facilitates mechanical ventilation with 100% oxygen, minimises pulmonary aspiration, enables suctioning of the trachea and provides a route for the administration of selected drugs. If intubation cannot be accomplished easily, ventilate and oxygenate the patient using a mask before reattempting intubation. Assess the cardiac rhythm by displaying the ECG via chest leads or the defibrillator paddles. Proceed with drug therapy or immediate direct current (DC) shock (Box 2), while maintaining ECC and mechanical ventilation with supplemental 100% oxygen. Secure access to the circulation with a peripheral intravenous (IV) cannula. If cannulation is difficult, do not waste time (more than 90 seconds) with repeated unsuccessful attempts -- instead use the intraosseous (IO) route or the (less effective) respiratory tract via the endotracheal tube (ETT). 7 All drugs and resuscitative fluids may be given via the IO route but only adrenaline, atropine and lignocaine may be given via the ETT. Central venous cannulation of the subclavian or internal jugular veins should not be attempted initially as it wastes time and is potentially hazardous. However, cannulation of an external jugular or femoral vein may be easily accomplished. Surgical cutdown onto a vein may be required. Intracardiac injection should not be attempted unless all alternative methods of access to the circulation are impossible. The doses of drugs, DC shock and fluid therapy are based on body weight, which may be estimated according to age if the weight is unknown: Newborn: 3.5 kg 1 year: 10 kg 1-9 years: (age in years x 2) + 8 kg 10 years and over: age in years x 3.3 kg. Doses may also be prescribed on the basis of height. 8,9 Drug doses according to the 50th percentiles of weight and height for age are given in Box 3. Asystole or severe bradycardia If the cardiac rate is unresponsive to ventilation with 100% oxygen, asystole or pulseless severe bradycardia ( < 80 bpm in an infant, < 60 bpm in a small child, < 40 bpm in a large child or teenager) should be treated with adrenaline (10 µg/kg IV or IO, or 100 µg/kg via the ETT). The subsequent dose of adrenaline by any route is up to 100 µg/kg. If sinus rhythm cannot be restored, sodium bicarbonate (1 mmol/kg IV or IO) and/or atropine (20 µg/kg IV, IO or ETT), with additional doses of adrenaline, may be successful. If facilities are available, cardiac pacing (via the oesophageal, transcutaneous, transvenous or epicardial routes) may be effective. Ventricular fibrillation and pulseless ventricular tachycardia The only effective treatment of ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT) is DC shock. If the onset of VF is recent or is observed, a precordial thump may be given (although its efficacy has not been proven) and defibrillation should be attempted before any other treatment. The initial DC shock treatment of VF or pulseless VT is 2 J/kg, increasing to a maximum of 4 J/kg 10,11 in a series of three shocks. If sinus rhythm does not occur, give adrenaline (10 µg/kg IV or IO, or 100 µg/kg ETT) and a further three shocks of 4 J/kg. Persistent or refractory VF or VT may be treated with lignocaine (1 mg/kg IV, IO or ETT) followed by another series of up to three shocks of 4 J/kg. If the VF or VT remains refractory, alternative agents (bretylium tosylate 5 mg/kg, sodium bicarbonate 1 mmol/kg, magnesium sulfate 0.05-0.1 mmol/kg) may be tried, in combination with adrenaline (100 µg/kg IV, IO or ETT) and a series of three shocks of 4 J/kg. However, no drug has been conclusively proven to improve the efficacy of DC shock. Electromechanical dissociation (pulseless electrical activity) Electromechanical dissociation exists if pulses are absent despite relatively normal coordinated electrical activity on the ECG. It may be due to poor intrinsic myocardial contractility or secondary to a number of remediable causes, including hypoxaemia, hypovolaemia, severe acidosis, tension pneumothorax, pericardial tamponade, hyperkalaemia, hypocalcaemia, poisoning with a calcium channel blocker or hypothermia. It may also be due to massive pulmonary embolism. Treatment is with adrenaline, 10 µg/kg IV or IO or 100 µg/kg ETT initially, with subsequent doses up to 100 µg/kg by any route. If the electromechanical dissociation is persistent, consider hypovolaemia or severe acidosis and give a bolus of crystalloid or colloid fluid (20 mL/kg IV or IO) and/or sodium bicarbonate (1 mmol/kg). An underlying cause should be sought by clinical examination and investigations, including a chest x-ray, 12-lead ECG and echocardiograph if possible. Supraventricular tachycardia Supraventricular tachycardia (SVT) may cause severe hypotension or pulselessness. Synchronised DC shock (0.5-1 J/kg) should be given immediately to a pulseless patient. If blood pressure is adequate, vagal stimulation or drug therapy may be used. Adenosine is the drug of first choice. Alternatives are digoxin, a beta-blocker or a calcium channel blocker. Calcium channel blockers should not be used to treat SVT in infants because their negative inotropic effect may be fatal. Techniques in Paediatric advanced life support are given in Box 4. Medications and fluids used in paediatric advanced life support are summarised in Box 5. Management after resuscitation The cause of cardiorespiratory arrest should be sought and specifically treated. Complications of the resuscitation procedure should also be sought, especially if secondary deterioration occurs. This includes a chest x-ray to check the position of the endotracheal tube, to exclude pneumothorax, lung collapse or aspiration and to check the cardiac silhouette, and a blood sample for estimation of the haemoglobin level, pH, gas tensions and electrolyte and glucose concentrations. Supportive therapy should be provided until there is recovery of function of vital organs. This may include oxygen therapy, mechanical ventilation, inotropic infusion and renal support for several days or longer. Recovery in infants and children is usually slow because cardiorespiratory arrest is often secondary to prolonged global hypoxaemia and ischaemia with prior damage of other organs. Particular care should be taken to ensure adequate cerebral perfusion with well oxygenated blood and adequate blood pressure. Cessation of cardiopulmonary resuscitation The decision to cease cardiopulmonary resuscitation should be based on a number of factors, including the patient's pre-arrest condition, response to resuscitation, remediable factors, likely outcome and the opinions of experienced medical personnel. References Emergency Cardiac Care Committee and Subcommittees of the American Heart Association. Guidelines for cardiopulmonary resuscitation and emergency cardiac care. JAMA 1992; 268: 2171-2302. Paediatric Life Support Working Party of the European Resuscitation Council. Guidelines for paediatric life support. BMJ 1994; 308: 1349-1355. Manual Australian Resuscitation Council. Policy Statements. Policies 12.1-12.9, November 1995. (Located at the Royal Australasian College of Surgeons, Spring Street, Melbourne.) Emergency Cardiac Care Committee and Subcommittee of the American Heart Association. Guidelines for cardio resuscitation and emergency cardiac care. JAMA 1992; 268: 2276-2281. Roy RN, Betheras FR. The Melbourne chart -- a logical guide to neonatal resuscitation. Anaesth Intens Care 1990; 18: 348-357. The Advanced Life Support Committee of the Australian Resuscitation Council. Adult advanced life support. The Australian Resuscitation Council Guidelines. Med J Aust 1993; 159: 616-621. Tibballs J. Endotracheal and intraosseous drug administration for paediatric CPR. Aust Fam Physician 1992; 21: 1477-1480. Lubitz SL, Seidel JS, Chameides L, et al. A rapid method for estimating weight and resuscitation drug dosages from length in the pediatric age group. Ann Emerg Med 1988; 17: 576-581. Oakley P, Phillips B, Molyneux E, Mackway-Jones K. Updated standard reference chart. BMJ 1993; 306: 1613. Chameides L, Brown GE, Raye JR, et al. Guidelines for defibrillation in infants and children. Report of the American Heart Association Target Activity Group: cardiopulmonary resuscitation in the young. Circulation 1977; 56 (suppl): 502A-503A. Gutgesell HP, Tacker HA, Geddes LA, et al. Energy dose for ventricular defibrillation of children. Pediatrics 1976; 58: 898-901. Rogers FB. Technical note: a quick and simple method of obtaining venous access in traumatic exsanguination. J Trauma 1993; 34: 142-143. Hornchen U, Schuttler J, Stoeckel H, et al. Endobronchial instillation of epinephrine during cardiopulmonary resuscitation. Crit Care Med 1987; 15: 1037-1039. Jasani MS, Nadkarni VM, Finkelstein MS, et al. Effects of different techniques of endotracheal epinephrine administration in pediatric porcine hypoxic-hypercarbic cardiopulmonary arrest. Crit Care Med 1994; 22: 1174-1180. Patterson M, Boenning D, Klein B. High dose epinephrine in pediatric cardiopulmonary arrest (CPA). Pediatric Emerg Care 1994; 10: 310. Goetting MG, Paradis NA. High-dose epinephrine improves outcome from pediatric cardiac arrest. Ann Emerg Med 1991; 20: 22-26. Contributors This document was drafted and revised by Dr James Tibballs at the request of the Australian Resuscitation Council. Submissions were received from members of the Advanced Life Support Committee of the ARC and from Dr R Henning, Dr F Shann, Ms S Kinney (Melbourne); Dr A Duncan (Perth); Dr J McEniery, Dr G Delbridge, Dr B Lister (Brisbane); Dr B Wilkins, Dr R Choong, Dr B Duffy, Dr T Gratten-Smith, Dr I Alexander, Dr M Schindler, Dr J Gillis, Dr A O'Connell, Dr D Schell, Dr O Miller (Sydney); Dr S R Keeley, Dr A J Slater, Dr G M Shaw, Dr J Raftos (Adelaide); Dr E R Segedin (Auckland); Dr L Quan (Seattle); and Dr D Zideman (London). Members of the Advanced Life Support Committee: Dr M Allen (ARC South Australian Branch). Dr R A Capps (Australian Defence Force). A/Prof V Callanan (ARC Chairman; and Australian and New Zealand College of Anaesthetists). Ms J Dennett (Confederation of Australian Critical Care Nurses). Mr M Draheim (ARC Tasmanian Branch). Ms J Finn (Royal College of Nursing, Australia). Dr L Grigg (Cardiac Society of Australia and New Zealand; and National Heart Foundation). Mr A Hadj (Royal Australasian College of Surgeons). Mr J Hall (Institute of Ambulance Officers, Australia). Mr K Hambrecht (Co-opted member). Prof G A Harrison (Chairman, ARC Advanced life Support Committee; and Australian and New Zealand College of Anaesthetists). Dr I Jacobs (ARC Western Australian Branch). Mr O Juul (ARC New South Wales Branch). Mr S Leahy (Surf Lifesaving Association of Australia). Ms J Maclean (Royal Lifesaving Society, Australia). Dr P Morley (ARC Victorian Branch). Dr J O'Callaghan (Co-opted member). Dr A Phillips (Royal Australian College of General Practitioners). Mr C Smith (ARC Queensland Branch). Dr J Taylor (Co-opted member). Dr J Tibballs (Australian and New Zealand Intensive Care Society). Mrs E P Tyler (Australian Red Cross Society). Dr J Wassertheil (Australasian College for Emergency Medicine). Dr J Williamson (St John Ambulance Australia). No reprints will be available. Correspondence: Dr J Tibballs, Intensive Care Unit, Royal Children's Hospital, Flemington Road, Parkville, Melbourne, VIC 3052. ©MJA 1996 Home |

Suspected snakebite in children: a study of 156 patients over 10 years Helen J Mead and George A Jelinek Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au/>". Abstract - Introduction - Methods - Results - Discusssion - References - Authors' details - - ©MJA1997 Abstract Objective: To describe the epidemiology and clinical features of children presenting to an emergency department with suspected snakebite. Design: A retrospective study of patient records. Setting: An emergency department of a children's teaching hospital (Princess Margaret Hospital) in Perth, Western Australia. Participants: All children attending the emergency department from 1984 to 1993 with suspected snakebite. Main outcome measure: Clinical and laboratory evidence of envenomation. Results: Over the decade studied, 156 children (mean age, six years and eight months) presented with suspected snakebite; over two-thirds (68%) were boys. In at least 31% of cases, no appropriate first aid had been applied. Only 14 children were envenomed according to clinical and laboratory criteria: 10 of these had coagulopathy; one of the 10 also had rhabdomyolysis. A Venom Detection Kit was used in 117 children. The test gave a positive result in 21 children (13%). Antivenom was given to 18 children, 14 of whom were definitely envenomed. Four of the envenomed children returned a negative result of Venom Detection Kit testing at all sites tested, and in five patients not clinically envenomed the urine specimen tested positive with the Venom Detection Kit (presumably a false positive result or subclinical envenomation). Of the 156 children, 130 were admitted to hospital, and 26 were discharged directly from the emergency department. All children recovered completely. Conclusions: (i) Many children did not receive appropriate first aid for snakebite; (ii) Most children with suspected snakebite presenting to the emergency department were not envenomed; (iii) Envenomation was best diagnosed by clinical features and laboratory investigations, with the Venom Detection Kit being used to determine the appropriate antivenom; (iv) Discharging children directly from the emergency department is not recommended. MJA 1996; 164: 467 Introduction Three major Australian studies of snakebite in children have been published.1-3 Two were from south-east Queensland1,2 and the third from Victoria.3 No similar studies have been reported from Western Australia, but one has been published on patterns of envenomation in 193 adults admitted to Perth teaching hospitals.4 There are also no published data on children presenting to Australian emergency departments with snakebite. Our aim was to describe the presenting features, treatment and outcome in children with suspected snakebite attending an emergency department. We also examined aspects of the use of the Venom Detection Kit, which was widely used as an adjunct in the diagnosis and management of these children. Methods We studied the records of all children presenting to Perth's Princess Margaret Hospital for Children with suspected or definite snakebite between 1 January 1984 and 31 December 1993. If parents or other carers had a reasonable suspicion that a child may have been bitten by a snake, this was classified as "suspected snakebite", and in "definite snakebite" a reliable history was available of a snake striking the child (whether or not envenomation occurred), or there was clinical and/or laboratory evidence of envenomation in circumstances consistent with snakebite. To ensure all records were found, multiple data sources were accessed, including hospital morbidity coding for inpatient admissions; intensive care unit records; and emergency department records. Data extracted from the records were entered onto a Microsoft Access 2.0 database to assist with analysis.5 To facilitate a comparison with the study in adults from Perth hospitals,4 data on patients' snakebite history and envenomation status were extracted and patients were grouped in the categories listed in the Perth study4 and shown in Box 1. Systemic envenomation was deemed present if there was clinical (vomiting, abdominal pain, or neurotoxic effects -- ptosis, convulsions, or difficulty with breathing or swallowing) or laboratory evidence (coagulopathy, haemolysis, rhabdomyolysis or renal failure). Results Over the 10 years, 160 children presented to the Emergency Department at Princess Margaret Hospital with suspected snakebite. Patient records were available for 156 children. The snake was brought in with the patient for identification on 16 occasions (on one occasion the snake was still alive!). Thirty-one children were admitted to the Intensive Care Unit, 87 to a general ward, 12 to the Emergency Department observation ward and 26 were discharged directly from the Emergency Department. Age and sex distribution The mean age of the children was six years and eight months (range, 15 months to 14 years 4 months), and over two-thirds (68%) were boys. Athough there was an even age distribution among children who were envenomed, there were 46 (29%) toddlers (less than three years) among the children presenting. Location Most snakebites occurred in the victims' garden (59 cases; 38%) or surrounding suburban bushland (51 cases; 33%). Eight (5%) occurred in a house or outbuilding and 26 (17%) children were bitten in open country. The location of the remaining 12 (7%) was not specified. Seasonal distribution Most children presented in the summer months, with very few presentations during winter; only three of the 14 children who were envenomed were bitten outside the months of October to April. Bite site Most children were bitten on a limb (lower limb: 103 cases, 66%; upper limb: 43 cases, 28%). There was one bite to the torso and one to the head, with the site not recorded in eight cases. Puncture marks were noted in 81 cases (52%). First aid It was often difficult to determine from the patient records whether first aid had been applied. However, in 39 cases it was clearly documented that no first aid was used, and inappropriate first aid (such as washing the site or use of an arterial tourniquet) was recorded in 10 cases (i.e., at least 49 children [31%] did not have effective first aid). The pressure- immobilisation first aid technique was used in 75 children (48%), although in some it was noted that the bandage had been applied only loosely or the limb was not fully immobilised. There was no record of whether first aid was applied in 32 children (21%). In some cases first aid measures were inappropriately left in place for a prolonged period after reaching hospital. Envenomation Fourteen children had systemic envenomation and 17 possible systemic envenomation according to the criteria used in this study (Box 1). The details of the clinical features, management and outcome of the 14 envenomed children are summarised in Box 2. In two children with possible envenomation, laboratory coagulation tests gave values just outside the normal range; both had an uneventful course and were not given antivenom. Four other child ren classified with possible envenomation received antivenom early for non-specific symptoms, without confirmatory laboratory evidence of envenomation. Venom detection Of the 117 cases in which the Venom Detection Kit was used, a positive result was obtained in 21 children (12 from wound swabs, 10 from urine, and four from blood). In nine of these child ren with no evidence of systemic envenomation, venom was detected in urine in five, and in skin swabs in the other four. In a child with borderline coagulopathy, the Venom Detection Kit gave a positive result in blood, but a negative one in urine. Another child treated for possible envenomation tested positive for venom at the "bite site", but tests of urine and blood gave a negative result with the Venom Detection Kit (Case D under "Use of antivenom"). The venom type detected by the Venom Detection Kit in envenomed patients is shown in Box 2. Use of antivenom Antivenom was given to 18 children (polyvalent in eight cases, brown snake in seven and tiger snake in five; two patients received more than one type of antivenom). Four children who were given antivenom may not have been envenomed. Case A: An eight-year-old boy with a witnessed bite received antivenom for regional lymphaden o pathy and headache. No venom was detected at the bite site, nor in blood or urine. Case B: A 10-year-old girl (no snake was seen) had a negative result of a Venom Detection Kit test of a bite site, and urine and coagulation studies showed no abnormality, but she was given antivenom because of symptoms of tiredness and non-specific weakness. Case C: A nine-month-old girl who was crying and vomiting and noted to have a mark on her arm was given polyvalent antivenom before transfer to Princess Margaret Hospital. No venom detection tests were undertaken. Her symptoms of fever and intermittent vomiting were subsequently thought to be due to a viral illness. Case D: A six-year-old girl had tiger snake venom detected at a possible bite site (but no venom detected in blood or urine). She was given tiger snake antivenom for symptoms of headache, fever, abdominal pain and nausea. A groin abscess was noted the next day, which may possibly have been the cause of her illness. Other supportive treatment Three children were administered fresh frozen plasma. No child required artificial ventilation. Outcome All children were discharged well from hospital; no permanent morbidity was recorded. Discusssion As in the previous epidemiological studies of snakebite in children in Australia,1-3 most of the children who presented to hospital with suspected snakebite were not envenomed (Box 3). In our study the over-representation of toddlers in the children presenting, despite an even age distribution of children with envenomation, probably reflected heightened parental concern and the difficulty obtaining a history from this age group. Patterns of envenomation and treatment for snakebite in Perth children were similar to those reported previously in adults.4 The sex distribution of victims, the seasonal pattern of envenomation and the site of bites were also similar. The venoms of the two snake genera responsible for most bites in Perth, Pseudonaja (brown snake) and Notechis (tiger snake), have powerful procoagulants, and coagulopathy was present in most (71%) of the envenomed patients. Among Perth snakes, only the tiger snake produces myolysis, and only one patient in this series had rhabdomyo lysis. Despite local differences in fauna, these findings are very similar to those in children with snakebite in Victoria.3 Despite continuing confirmation of the great efficacy of the pressure-immobilisation first aid technique in delaying venom spread,6,7 it is disturbing that this method is still not being used widely. In many cases it is also being applied incorrectly. More public education on first aid in snakebite is needed. The role of the Venom Detection Kit in patients with suspected snakebite attending emergency departments is discussed in Box 4. Although it appeared that no child came to harm after discharge from the Emergency Department, this practice is fraught with danger, as a case from 1973 illustrates. A two-year-old girl with restlessness and dry retching presented to hospital with an unclear history; the possibility of snakebite was raised by the parents. The examining medical officer concluded that she had been bitten by an insect, no investigations were ordered and she was discharged. The next morning she was found dead in bed, and it was later confirmed that tiger snake envenomation had been the cause of death. The Coroner found that there had been a lack of care on the part of the hospital, contributing to her death.10 In most children presenting to an emergency department there is no way of determining absolutely whether a venomous snakebite has occurred. There are special difficulties in obtaining a reliable history from young children and it may be tempting to use a negative result of a Venom Detection Kit to facilitate early discharge. Indeed, a number of children in this study were discharged from the Emergency Department without laboratory investigations, apart from use of the Venom Detection Kit. However, all children in whom snakebite is suspected, whether a snake was seen or not, should be admitted to hospital for observation and investigation (including coagulation profiles). In a number of cases of envenomation in our series, no snake bite was observed, and in two cases no snake was seen. Discharging children with suspected snakebite directly from emergency departments without a period of observation is not recommended. References Munro JGC, Pearn JH. Snake bite in children. A five year population study from South-East Queensland. Aust Paediatr J 1978; 14: 248-253. Jamieson R, Pearn J. An epidemiological and clinical study of snake-bites in childhood. Med J Aust 1989; 150: 698-702. Tibballs J. Diagnosis and treatment of confirmed and suspected snake bite. Implications from an analysis of 46 paediatric cases. Med J Aust 1992; 156: 270-274. Jelinek GA, Hamilton T, Hirsch RL. Admissions for suspected snake bite to the Perth adult teaching hospitals, 1979 to 1988. Med J Aust 1991; 155: 761-764. Microsoft Access [database]. Version 2.0. Redmond, WA: Microsoft Corporation, 1989-1994. Howarth DM, Southee AE, Whyte IM. Lymphatic flow rates and first-aid in simulated peripheral snake or spider envenomation. Med J Aust 1994; 161: 695-700. Sutherland SK. The pressure immobilisation technique. Med J Aust 1994; 161: 700-701. CSL Diagnostics. Snake venom detection kit. Product information leaflet. Melbourne: CSL Diagnostics, 1992. Wentworth B, Moisidis A, Jones S. Performance of the new snake venom detection kit at high and low concentrations [abstract]. Proceedings of the 22nd Annual Scientific Meeting of the Australasian Society of Immunology; 1992 Dec 2-4; Auckland. Parkville: Australasian Society of Immunology, 1992. Snake and lack of care killed girl. The West Australian 1973 19 Jun: 3 (col. 3, 4 and 5). (Received 6 Jul, accepted 20 Dec 1995) Authors' details Department of Emergency Medicine, Fremantle Hospital, Fremantle, WA. Helen J Mead, FRACP, FACEM, Staff Specialist; formerly, Senior Registrar, Intensive Care Unit, Princess Margaret Hospital for Children, Perth, WA; George A Jelinek, MD, FACEM, Assistant Director and Staff Specialist. No reprints will be available. Correspondence: Dr George A Jelinek, Department of Emergency Medicine, Fremantle Hospital, PO Box 480, Fremantle, WA 6160. ©MJA 1997 <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

Helen J Mead · George A Jelinek

For Debate Trauma in pregnancy and cerebral palsy: is there a link? The link between maternal trauma during pregnancy and cerebral palsy remains to be proven Marisa T Gilles, Eve Blair, Linda Watson, Nadia Badawi, Louisa Alessandri, Vivienne Dawes, Aileen J Plant and Fiona J Stanley MJA 1996; 164: 500-501 Introduction - Acknowledgements - References - Authors' details - - Articles on similar material Introduction Maternal trauma during pregnancy has been implicated in the aetiology of cerebral palsy in the surviving offspring.1,2 In 1991, a child with cerebral palsy received a settlement of three million dollars after it was alleged that the mother's negligent driving of a motor vehicle resulted in an accident which caused cerebral palsy in the child.1 The case rested on the testimony of an expert witness whose argument was based on a case series of six children with cerebral palsy born to mothers who had been involved in motor vehicle accidents. (Bergin AM, Stack JP, Stephenson JBP, King M. Cerebral palsy after motor accidents in pregnancy. Proceedings of the British Paediatric Neurology Association, Dublin, 1990 [unpublished data].) Possible mechanisms for the association between pregnancy trauma and cerebral palsy include reduced placental bloodflow, placental embolisation and placental abruption. To address the issue of trauma in pregnancy and subsequent cerebral palsy, we examined the Western Australian Cerebral Palsy Register3 (a subset of the Maternal and Child Health Research Database)4 which collects information on all children in the State who develop cerebral palsy (updated to the age of five years). We also examined the Hospital Morbidity Data System, which collects information on all acute hospital admissions. These two databases were selected in order to compare the rates of cerebral palsy in the offspring of women who, during their pregnancy, had trauma that required hospitalisation with the rates of cerebral palsy in the children of women who did not experience trauma. The Box outlines the methods and results of our study. Despite the fact that this was a population-based study over 11 years (1982-1992), the unadjusted relative risk of having a child with cerebral palsy after exposure to trauma was 1.4 (95% confidence interval, 0.34-5.77), which was not statistically significant. It was inappropriate to adjust for gestational age or low birth weight as they may have been factors in the aetiological pathway (e.g., trauma may induce a premature birth). Trauma occurs more commonly during the third trimester of pregnancy than at any other time in a woman's life.5 The incidence of trauma during pregnancy is reported to be about seven to eight per cent, but hospitalisation for trauma in pregnancy is rare. In the years of our study, only 0.3% of pregnant women were hospitalised. However, the severity of maternal trauma does not correlate well with the degree of fetal damage. Even minor trauma can cause fetal death and preterm labour,6-8 but few studies have considered the effect on long-term fetal outcome.2 Women who are not hospitalised (because of apparently minor trauma) may still have fetal compromise. In addition, women experiencing domestic violence may avoid medical attention, and hence such women may be under-represented in our study. Domestic violence during pregnancy, reported at rates between 8% and 17%, has been linked to fetal death, fetal distress and intrauterine growth retardation.9-11 The existence of one woman who was admitted to hospital for trauma at 28 weeks' gestation but had not been recorded as pregnant in the Hospital Morbidity Data System calls into question the validity of this data system in recording certain admission and discharge details relevant to our study. For example, in the presence of major trauma a pregnancy may be overlooked or not recorded, especially if the woman is in early pregnancy. This would lead to an underestimation of the number of women experiencing trauma during pregnancy who did not have a child with cerebral palsy, as only those women who were coded as being pregnant in the Hospital Morbidity Data System were included in the sample population. Our study has not resolved whether major trauma during pregnancy is associated with long term neurological problems in the child. In view of increasing litigation in this area, larger analytical studies into the outcomes following physical trauma during pregnancy are needed. This will best be achieved when better mechanisms for recording details of trauma during pregnancy, including domestic violence, are developed. Acknowledgements This study would not have been possible without the financial support of Healthway and PHRDC, who fund the Cerebral Palsy Register; data provided by the Health Department of WA; the expertise of Dr Richard Hockey, who carried out the linkage; and the editorial support generously supplied by Dr Ian Rouse and Dr Jennifer Kurinczuk. References Lynch v Lynch & Anor. Supreme Court of New South Wales (1991). Australian Tort Reports 81-117. Anquist KW, Parnes S, Cargill Y, Tawagi G. An unexpected fetal outcome following a severe maternal motor vehicle accident. Obstet Gynecol 1994; 84: 656-658. Stanley FJ, Watson L. Methodology of a cerebral palsy register. The Western Australian experience. Neuroepidemiology 1985; 4: 146-160. Stanley FJ, Croft ML, Gibbins J, Read AW. A population database for maternal and child health research in Western Australia using record linkage. Paediatr Perinat Epidemiol 1994; 8: 433-447. Patterson RM. Trauma in pregnancy. Clin Obstet Gynecol 1984; 27: 32-38. Williams JK, McClain L, Rosemurgy AS, Colorado NM. Evaluation of blunt abdominal trauma in the third trimester of pregnancy: Maternal and fetal considerations. Obstet Gynecol 1990; 75: 33-37. Farmer DL, Adzick S, Crombleholme WR, et al. Fetal trauma: relation to maternal injury. J Pediatr Surg 1990; 25: 711-714. Murdoch Eaton DG, Ahmed Y, Dubowitz LMS. Maternal trauma and cerebral lesions in preterm infants. Case reports. Br J Obstet Gynaecol 1991; 98: 1292-1294. Macfarlane J, Parker B, Soeken K, Bullock L. Assessing for abuse during pregnancy. Severity and frequency of injuries and associated entry into prenatal care. JAMA 1992; 267: 3176-3178. Dye TD, Tolliver NJ, Lee RV, Kenney CJ. Violence, pregnancy and birth outcome in Appalachia. Paediatr Perinat Epidemiol 1995; 9: 35-47. Webster J, Sweett S, Stolz TA. Domestic violence in pregnancy. A prevalence study. Med J Aust 1994; 161: 466-470. Stanley FJ, Watson L. Trends in perinatal mortality and cerebral palsy in Western Australia, 1967 to 1985. BMJ 1992; 304: 1658-1663. World Health Organization. International Classification of Diseases. 1975 revision, Vol 1. Geneva: Presses Centrales, 1977. Gee V. The 1991 Western Australian Birth Cohort. Statistical Series 34. Perth: Health Department of Western Australia, 1994: 5. Authors' details Health Statistics Branch, Health Department of Western Australia, Perth, WA. Marisa T Gilles, FAFPHM, Research Registrar; and Research Registrar, National Centre for Epidemiology and Population Health, Canberra. TVW Telethon Institute for Child Health Research, Perth, WA. Eve Blair, PhD, Senior Research Officer; Linda Watson, Research Assistant; Nadia Badawi, MSc, MRCPI, Paediatric Research Fellow; Louisa Alessandri, BSc(Hons), PhD, Research Officer; Fiona J Stanley, MD, FAFPHM, Professor of Paediatrics. Department of Public Health, The University of Western Australia, Perth, WA. Aileen J Plant, PhD, FAFPHM, Senior Lecturer. Women's Cancer Screening Service, Health Department of Western Australia, Perth, WA. Vivienne Dawes, FAFPHM, Medical Officer. No reprints will be available. Correspondence: Linda Watson, TVW Telethon Institute for Child Health Research, PO Box 855, West Perth, WA 6872. E-mail: Linda@ichr.uwa.edu.au Material trauma and cerebral palsy: a Western Australian population-based study, 1982-1992 Cerebral Palsy Register The study population was extracted from the Cerebral Palsy Register, a data subset of the Maternal and Child Health Research Database, and consisted of mothers of all children with cerebral palsy born between 1982 and 1992 inclusive, excluding those children who had a documented postnatal cause of cerebral palsy. A year-of-birth cohort of the Cerebral Palsy Register is only considered complete at the age of five years. Thus, by including the years 1990 to 1992 it is possible that as yet unregistered cases of cerebral palsy may have been misclassified as not having cerebral palsy. However, because cerebral palsy is rare (approximately 2 per 1000 live births),12 the effect of this error is very small. Hospital Morbidity Data System The sample population comprised all women between the ages of 14 to 50 with an ICD-9 external cause of injury (excluding poisons, drugs and medical misadventure)13 and the additional code for pregnancy in the Hospital Morbidity Data System. To validate the Hospital Morbidity Data System, a second method of identifying cases was used. The period of pregnancy was defined as the time between the second postmenstrual week and delivery, and the dates defining this period were identified for each pregnancy that resulted in a child with cerebral palsy. Database linkage Data from the Cerebral Palsy Register were linked with the births file, another subset of the Maternal and Child Health Research Database, to obtain identifying data for each mother in the study group, such as surname, maiden name, date of birth and address at the time of delivery. Using these identifying data, mothers were linked to the Hospital Morbidity Data System to determine exposure to trauma requiring hospitalisation during pregnancy. Statistical analysis Data were analysed using two-by-two contingency tables, and the relative risk was calculated with 95% confidence intervals. Results 529 children were born with cerebral palsy between 1982 and 1992, inclusive (extracted from the Cerebral Palsy Register). (See Box.) 770 pregnant women were hospitalised for trauma between 1982 and 1992 (extracted from the Hospital Morbidity Data System). The details of two of the mothers hospitalised for trauma during their pregnancy matched the details of two mothers of children with cerebral palsy. The incidence of cerebral palsy in children of women hospitalised for trauma during pregnancy was 2.6 per 1000 pregnant women. The incidence of cerebral palsy in children of women who did not experience trauma requiring hospitalisation during their pregnancy was 1.8 per 1000 pregnant women. A woman exposed to trauma requiring hospitalisation during pregnancy had 1.4 times the risk of having a child with cerebral palsy compared with a woman who had not had this experience (unadjusted relative risk, 1.4; 95% confidence interval, 0.34-5.77). The number of cases was small and this result was not statistically significant (Box). One mother who had a child with cerebral palsy and had been hospitalised for trauma during pregnancy was not recorded as being pregnant on the Hospital Morbidity Data System. Inclusion of this case in the two-by-two analysis increased the relative risk to 2.2 (95% confidence interval, 0.66-6.69), but only those women coded as being pregnant in the Hospital Morbidity Data System were included in the sample population (see text). Back to text

Marisa T Gilles · Eve Blair · Linda Watson · Nadia Badawi · Louisa Alessandri · Vivienne Dawes · Aileen J Plant · Fiona J Stanley

AbstractObjective: To assess the effectiveness of the flashlamp-pumped pulsed dye laser in the treatment of port-wine stains. Design: A retrospective review of medical records and patients. Setting: Royal Perth Hospital (a tertiary referral hospital), August 1989 to December 1992. Subjects: 186 consecutive patients with port-wine stains treated with a flashlamp-pumped pulsed dye laser. Outcome measures: Degree of lesion fading; adverse reactions. Results: Of 131 patients who completed treatment, 78% had better than 50% fading of the lesion and only 9% had less than 25% fading. An average 3.4 treatments were needed to achieve more than 50% fading. The response was better in children than in adults, although the difference was not significant. Anaesthesia was needed for 44% of patients. Pigmentary change (usually transient) occurred in 6.1% of patients and permanent and significant adverse effects in only 4.6%. Conclusion: This study confirms the efficacy of the flashlamp-pumped pulsed dye laser in the treatment of port-wine stains in children and adults. Early treatment of port-wine stains should be encouraged to reduce the physical and psychological morbidity of disfiguring lesions. IntroductionPort-wine stains (now termed capillary malformations) are congenital vascular malformations characterised by ectatic vessels within the cutaneous superficial vascular plexus.1 They affect 0.3% of children at birth, with an equal sex distribution.2 Most port-wine stains are found on the head and neck, with 85% occurring in a unilateral, dermatomal distribution.3 Their natural history is to progress from a pink, macular lesion at birth to a dark red (or even purple), nodular, proportionately larger lesion in adulthood.1,4 Cosmetic disfigurement can cause considerable psychological morbidity, and be socially disadvantageous.5,6 Hypertrophic, nodular lesions may bleed, either spontaneously or after trauma, encroach on essential facial structures or even develop into pyogenic granulomas.7 All port-wine stains should be treated, preferably early in life, to prevent or reduce the potential physical and psychological complications. Before the development of laser technology, treatment for port-wine stains was often unsatisfactory.8 Earlier lasers, including ruby, carbon dioxide and argon lasers, improved the lesions in most patients, but, as they were non-selective in their effects on tissue, the frequency of side effects, such as scarring and pigmentary changes, was unacceptably high.9 The flashlamp-pumped pulsed dye laser (PDL) was the first laser to be based on selective photothermolysis;10 it produces vascular- specific damage without affecting surrounding dermal structures or the epidermis.11-13 Studies have confirmed its effectiveness in the treatment of port-wine stains in adults, children and infants, with an extraordinarily low incidence of side effects.14-19 The PDL is now regarded as the first-line treatment for port-wine stains whenever possible.8,9,20-22 In Australia, the PDL has been in use since the late 1980s for the treatment of cutaneous vascular lesions, especially port-wine stains. However, no Australian study of its effects has been published. Therefore, we undertook a retrospective clinical review of all patients with port-wine stains treated with PDL at Royal Perth Hospital between August 1989 and December 1992. MethodsThe study was a retrospective review of patient medical records. If response to treatment was not recorded, attempts were made to review the patient between January and December 1993. PatientsAll patients (adult and paediatric) with a port-wine stain treated with PDL at Royal Perth Hospital between August 1989 and December 1992 were eligible. Patients attended outpatient clinics, where the site and size of the port-wine stain and demographic data were recorded and the treatment procedure and its risks and benefits were explained. Patients were photographed before treatment by a professional photographer in a studio dedicated to medical photography, with efforts to use the same magnification, lighting and exposure. Laser and techniqueA flashlamp-pumped pulsed dye laser (Candela SPTL-1, Candela Corp, Wayland, Mass, United States) was used. It emitted yellow light at a wavelength of 585 nm, with a pulse duration of 450 µs and a 3 s pause between pulses. The laser beam was transmitted down a 1 mm fibre by a planoconvex lens and focused as a 5 mm spot beam. Energy densities were measured by an energy meter (Ophir, Jerusalem, Israel), calibrated to 10% accuracy. Both the physicians and the patients eyes were protected from laser light during treatment. Some patients had a small initial test patch treated, depending on patient anxiety and time of presentation (before 1991, most had a patch test). Otherwise, the entire lesion was treated at once, unless it involved a large surface area (> 100 cm2). Treatments were repeated at intervals of 23 months. The energy density used varied with the age of the patient and colour, nodularity and location of the lesion and was adjusted according to the degree of purpura produced and the patients response to the previous treatment. Pulses were overlapped by a maximum of 10% across the affected area. The anaesthetic varied according to the site and area to be treated and the level of patient cooperation. EMLA cream (eutectic mixture of 2.5% lignocaine and 2.5% prilocaine cream, Astra Pharmaceuticals, North Ryde, NSW) was used for topical anaesthesia, applied under occlusion for 60120 minutes before treatment. Local anaesthesia involved an injection of 1% lignocaine, either locally or as a regional nerve block. General anaesthesia was given to children who had extensive lesions or were uncooperative with topical or local anaesthesia. The treated area developed purpura within a few minutes, usually persisting for 710 days. No immediate postoperative care was necessary, except for an occasional ice pack to reduce oedema in those with large treatment areas. Postoperative instructions were to protect the area from trauma, avoid excessive exposure to sunlight and use a topical antiseptic cream for any scaling or crusting. Treatment evaluationEach port-wine stain was evaluated, either before the next treatment or 34 months after the final treatment. Lesional lightening was assessed as the percentage reduction in colour compared with the pretreatment photo (fading < 25%, poor; 25% to 50%, fair; > 50% to 75%, good; and > 75%, excellent) (Figures 1-4). Adverse effects, such as scarring and textural or pigmentary changes, were also noted. All patients were individually assessed by one or both investigators. The endpoint of treatment was assessed clinically. Data analysisData were analysed with the Statistical Analysis Systems software package.23 The chi-squared statistic was used to assess the difference in response between age groups. ResultsThere were 186 patients treated by PDL: 131 completed treatment (55 either did not complete treatment or were having ongoing treatment). Patients were either Caucasian or Asian and aged 8 months to 66 years (mean, 25.6 years). There were 59 males (32%) and 127 females (68%). Most of the treated lesions were present from birth (97%). Acquired lesions appeared most commonly between the ages of six and 12. Most lesions were on the face and neck (87%), with the rest distributed unilaterally on the arms (4%), legs (5%), back (2%) and chest (2%). The size of treated lesions ranged from 1 cm2 to 280 cm2 (mean, 42 cm2). All responded to energy fluences between 5 and 10 joules/cm2(mean, 6.7 joules/cm2). Sixty-two per cent of the patients had a patch test before treatment. Anaesthesia was used for 44% of patients (general anaesthesia by 20%, topical by 19% and local or regional block by 5%). Responses of patients who completed treatment are shown in the Box. A good-to-excellent response was achieved in 78% and a poor response in only 9%. An average 3.4 treatments per lesion were required to achieve a good-to-excellent response. Adverse side effects occurred in 11% of patients who completed treatment; all had some fading of the lesion. The most common adverse effect was pigmentary change (6.1%), which was usually transient and resolved in 23 months. Only 4.6% had significant permanent adverse effects; two had scarring (in both the port-wine stain was on the face and neck region). More children than adults had a good or excellent response, but the difference was not significant when compared with a 2 x 2 contingency table and chi-squared test (r = 0.60). Similarly, fewer children than adults had a poor response. DiscussionOur results compare favourably with those of other studies. A good-to-excellent response (more than 50% fading) was obtained in 78% of our patients (including both adults and children, with lesions on sites including the trunk and lower limbs), with an average 3.4 treatments required. Others have found more than 50% fading in 73%-95% of patients after 2.4-2.8 treatments.14-17,24,25 Response to treatment varies between sites: the periorbital area, temple, lateral aspect of the cheek, neck and chin have been observed to be more responsive18,25 and the centrofacial area and lower leg to be less responsive.18,19 We found that a poor response was more common in adults than in children (although the difference was not significant), possibly because port-wine stains become progressively hypertrophied and nodular in adults. We found a higher rate of adverse effects (11%) than in other studies. The most common (usually transient) adverse effect was pigmentary change (increase or decrease), possibly because of excessive sunlight exposure after treatment. This transient change may not have been recorded in other studies; when it was excluded from our figures, the rate of adverse reactions was reduced to less than 5%, which is comparable with that found in other studies. Scarring was seen in two of our patients, with lesions on the face and neck, where damage to dermal structures with fibrosis occurs when excessive energy fluence is used. A low energy fluence should be used initially when treating port-wine stains on the neck and anterior chest. The PDL is the first laser specifically designed for cutaneous vascular malformations. It is based on the theory of selective photothermolysis, which predicts selective destruction of blood vessels without damage to the surrounding tissues.10 Laser light emitted by the PDL is absorbed by oxyhaemoglobin in the dilated vessels of the lesion, producing agglutination of erythrocytes, thrombus formation and eventual destruction of the vessels.11 They are replaced by non-dilated superficial dermal blood vessels with a normal appearance.12 A recent comparison of PDL and the copper vapour laser showed that PDL produced significantly better fading of port-wine stains.22 The characteristics and degree of pain associated with PDL treatment have been well described.26 Initially, there is a sharp stinging pain, very similar to the snap of a rubber band against the skin. Accompanying this is a second distinct heat sensation that can be at least as unpleasant as the initial sting. Pain rapidly subsides but seems to build up if successive pulses are used for a moderately sized lesion. Our current practice is to give general anaesthesia to all children from four weeks of age, until they are able to co-operate with topical or local anaesthesia, usually at eight to 10 years. Young children undergoing multiple painful treatments with inadequate anaesthesia under restraint may develop phobic responses. Furthermore, a struggling child may compromise the clinicians ability to perform the procedure optimally. In conclusion, this study supports the contention that all port-wine stains should be treated with PDL, as it has a high therapeutic index with a low incidence of adverse effects. Patients should preferably be treated in infancy or childhood, under general anaesthesia, to minimise the potential psychological morbidity of disfiguring lesions. In addition, the response to treatment seems better in children than in adults, although the difference was not significant, possibly because of the relatively small sample size. Laser treatment of port-wine stains should no longer be considered just cosmetic, but a medical necessity for a problem that can cause psychological and physical morbidity. References Mulliken JB. Capillary (port-wine) and other telangiectatic stains. In: Mulliken JB, Young AE, editors. Vascular birthmarks -- haemangiomas and malformations. Philadelphia: W B Saunders, 1988: 179-195. Jacobs AH, Walton RG. The incidence of birthmarks in the neonate. Pediatrics 1976; 58: 218-222. Tallman B, Tan OT, Morelli JG, et al. Location of port-wine stains and the likelihood of ophthalmic and/or central nervous system complications. Pediatrics 1991; 87: 323-327. Barsky SH, Rosen S, Geer DE, Noe JM. The nature and evolution of port-wine stains: a computer-assisted study. J Invest Dermatol 1980; 74: 154-157. Lanigan SW, Cotterill JA. Psychological disabilities amongst patients with port wine stains. Br J Dermatol 1989; 121: 209-215. Pickering JW, Butler PH, Ring BJ, Walker EP. Copper vapour laser treatment of port wine stains: a patient questionnaire. Lasers Med Sci 1990; 5: 43-49. Geronemus RG, Ashinoff R. The medical necessity of evaluation and treatment of port-wine stains. J Dermatol Surg Oncol 1991; 17: 76-79. Wheeland RG. Treatment of port-wine stains for the 1990s. J Dermatol Surg Oncol 1993; 19: 348-356. Van Gemert MJ, Carruth JA, Shakespeare PG. Laser treatment of the port-wine stains. BMJ 1993; 306: 4-5. Anderson RR, Parrish JA. Selective photothermolysis: precise microsurgery by selective absorption of pulsed radiation. Science 1983; 220: 524-527. Nakagawa H, Tan OT, Parrish JA. Ultrastructural changes in human skin after exposure to a pulsed laser. J Invest Dermatol 1985; 84: 396-400. Morelli JG, Tan OT, Garden J, et al. Tunable dye laser (577 nm) treatment of port wine stains. Lasers Surg Med 1986; 6: 94-96. Tan OT, Morrison P, Kurban AK. 585 nm for the treatment of port-wine stains. Plast Reconstr Surg 1990; 86: 1112-1117. Garden JM, Polla LL, Tan OT. The treatment of port-wine stains by the pulsed dye laser: analysis of pulse duration and long-term therapy. Arch Dermatol 1988; 124: 889-896. Tan OT, Sherwood K, Gilchrest BA. Treatment of children with port-wine stains using the flashlamp-pulsed tunable dye laser. N Engl J Med 1989; 320: 416-421. Reyes BA, Geronemus RG. Treatment of port-wine stains during childhood with the flashlamp-pumped pulsed dye laser. J Am Acad Dermatol 1990; 23: 1142-1148. Ashinoff R, Geronemus RG. Flashlamp-pumped pulsed dye laser for port-wine stains in infancy: earlier versus later treatment. J Am Acad Dermatol 1991; 24: 467-472. Renfro L, Geronemus RG. Anatomical differences of port-wine stains in response to treatment with the pulsed dye laser. Arch Dermatol 1993; 129: 182-188. Garden JM, Bakus AD. Clinical efficacy of pulsed dye laser in the treatment of vascular lesions. J Dermatol Surg Oncol 1993; 19: 321-326. Geronemus RG. Pulsed dye laser treatment of vascular lesions for children. J Dermatol Surg Oncol 1993; 19: 303-310. Hruza GJ, Geronemus RG, Dover JS, Arndt KA. Lasers in dermatology Ñ 1993. Arch Dermatol 1993; 129: 1026-1035. Sheehan-Dare RA, Cotterill JA. Copper vapour laser (578 nm) and flashlamp-pumped pulsed tunable dye laser (585 nm) treatment of port-wine stains: results of a comparative study using test sites. Br J Dermatol 1994; 130: 478-482. Statistical Analysis Systems [computer program], version 6.08. Cary (NC): SAS Institute Inc, 1994. Goldman MP, Fitzpatrick RE, Ruiz-Esparza J. Treatment of port-wine stains (capillary malformation) with the flashlamp-pumped pulsed dye laser. J Pediatr 1993; 122: 71-77. Holy A, Geronemus RG. Treatment of periorbital port-wine stains with the flashlamp-pumped pulsed dye laser. Arch Ophthalmol 1992; 110: 793-797. Rabinowitz LG, Esterly NB, Frieden IJ, et al. Anesthesia and/or sedation for pulsed dye laser therapy. Pediatr Dermatol 1992; 9: 132-153. Authors detailsDepartment of Dermatology, Royal Perth Hospital, Perth, WA. Ernest Tan, MB BS, Dermatology Registrar; Carl Vinciullo, FACD, Visiting Dermatologist. No reprints will be available. Correspondence: Dr C Vinciullo, Department of Dermatology, Royal Perth Hospital, Wellington Street, WA 6000. E-mail: carlATdermlaser.com.au

Ernest Tan · Carl Vinciullo