Sports medicine

In reply: The "30/30" rule is a simple and easy-to-remember rule designed to reduce the probability of lightning strikes. Two important studies over recent years have led to its development. First, in 1993, Holle et al analysed the number of casualties relative to flash rates during thunderstorms and found that most casualties occur at the beginning and end of storms.1 They concluded that individuals typically wait too long to seek safe shelter and often resume too soon. Secondly, in 1999, Lopez and Holle examined the distribution of successive flashes for large numbers of different types of storms, and found that, although most were separated by less than 8 km, a significant number of successive flashes occurred up to 13 km apart.2 This was noted to be more likely with larger, more complex storms. Given that lightning can strike kilometres forwards or backwards from the storm front, being within 10 km of lightning activity (as estimated by a "flash-to-bang" count of 30 seconds) reflects a risk that the next flash might conceivably be at the observer's location, irrespective of whether there are blue skies overhead. This is why blue sky alone is not enough reason to break the 30/30 rule.

Michael Makdissi

To the Editor: I enjoyed reading Makdissi and Brukner's "Recommendations for lightning protection in sport",1 but I feel that in addressing an audience of renowned golf hacks the authors have made a glaring omission. It is well known in golfing circles that the first rule of lightning self-protection on the golf course is to always carry a 1-iron in the bag and in appropriate conditions to reach for it — because not even God can hit a 1-iron!

Michael Gullquist

Each year many people are killed or injured by lightning due to misinformation and inappropriate behaviour during thunderstorms.1 Analysis of the circumstances surrounding lightning strikes shows that, while there has been a large decrease in the number of lightning casualties in farming and outdoor work, there has been a smaller relative increase in sports-related casualties.2,3 Moreover, with large crowds gathering to participate in or watch an outdoor event, the potential exists for mass casualties to occur from a lightning strike at any one venue. Hence, there is a need to develop specific approaches for lightning safety at sports events. In Australia, fatality rates for lightning strikes have fallen from 0.21 per 100 000 population in 1910–19194 to about 0.01 per 100 000 population in the 1990s. From 1990 to 1999, 23 fatalities were directly attributable to lightning (Australian Bureau of Statistics, personal communication). Furthermore, from 1993 to 1998, lightning was responsible for 95 hospital admissions (Dr R Cripps, Research Centre for Injury Studies, Flinders University, 2001, personal communication). From these figures, we can estimate that the mortality rate from lightning strikes in Australia is currently about 10%. This is below the generally accepted mortality rate of 30%,5 although other authors have reported mortality rates as low as 5%.6 In 1998, the Lightning Safety Group, a group of lightning experts in the United States, developed guidelines for lightning safety,7 which have since been applied to a variety of sports and recreational pursuits.8-11 However, there have been no clear recommendations for lightning safety at events with large numbers of spectators. Our aim is to present specific, practical recommendations to reduce the risk of lightning casualties in outdoor sporting and recreational activities in Australia. General guidelinesThe general guidelines presented here are based on the recommendations made by the Lightning Safety Group and those adopted by the US National Athletic Trainers' Association (Box 1).6,7 Proactive planThe proactive plan should commence on the day before activity, where weather forecasts provide important warning of possible thunderstorm activity.8 Increased awareness of lightning risk should continue on the day of activity until play has finished and the crowd has dispersed. The most basic level of warning involves observation of the weather in the local area. The first flash of lightning or clap of thunder, no matter how far away, should heighten lightning-awareness. The level of risk depends to a large degree on one's location relative to the storm system, which can be determined by the "flash-to-bang" rule (see below). Further useful information can be obtained by liaison with the Bureau of Meteorology <http://www.bom.gov.au>. In recent years, major advances have been made in technology for identifying and locating lightning. In Australia, there is a network of sensors that enable cloud-to-ground flashes to be mapped to within a few hundred metres. Together with other details about local weather conditions, the Lightning Location System can provide real-time displays of lightning strikes and determine the speed and direction of movement of the thunderstorm. This information can be used to estimate the likely future path of the thunderstorms and their probable arrival times at various venues. Chain of commandDuring the formulation of specific lightning safety guidelines, a specific person should be given responsibility for monitoring the weather for signs of a developing thunderstorm. The nominated "weather watcher" should have the authority to postpone the event and have competitors, officials and spectators moved to safe areas. Appropriate people to nominate as weather watchers include the event supervisor, trainers or other medical personnel, or the ground manager. When lightning threatens, the weather watcher is responsible for recognising the danger and activating the lightning protection plan. This should include a signal to the referees and umpires, as well as a method of informing those at risk (ie, players, officials and spectators) of the action required. Safe structures and locationsNo place is absolutely safe from the lightning threat; however, some places are safer than others (Box 1).1,12 It is important to have already identified safe structures and the most appropriate way of moving people into these facilities. The best choice is a large, fully enclosed building. Criteria for suspension and resumption of activitiesThe "30/30" rule is recommended for lightning safety and serves as a guide for the suspension and subsequent resumption of activity.7,13 The first part of this rule (a flash-to-bang count of 30 s) is a guide to the suspension of activity. The flash-to-bang count is one of the most practical techniques for estimating the distance to lightning activity. It is based on the fact that light travels faster than sound. Given that sound travels at a speed of about one kilometre every three seconds, the time that elapses between the flash of lightning and clap of thunder can be divided by three to give a measure of how far away the storm is in kilometres.8,14 The overall message is to seek shelter when the lightning activity is too close, but how do we define what is meant by too close? Currently, most experts agree that the accepted "safe" distance is no less than 10 km.1,7-10,15 This means that as the flash-to-bang count approaches 30 seconds, all people at risk should be seeking or already inside safe shelters. The second part of the 30/30 rule provides the criteria for resumption of play. Here it is recommended that people wait 30 minutes after the last sight of lightning or sound of thunder. This figure is based on the observation that a typical storm moves at about 40 km/h. Thus, waiting 30 minutes allows the thunderstorm to be about 20 km away, minimising the probability of a nearby strike. It is important to emphasise that blue skies and lack of rainfall are not adequate reasons to breach the 30-minute return-to-play rule.1,7,9 Dissemination of InformationIt is important that all participants, officials and spectators are warned of the potential dangers of lightning and how to minimise their risk of lightning-related injury. Practical ways in which this can be achieved include: reading lightning safety messages over the public address systems; and placing notices and safety instructions in event programs and in high-traffic areas at each venue (eg, entrance, change rooms, clubhouse). The information should contain clear and specific instructions about: criteria for suspension and resumption of athletic and recreational activities; and locations of the safety shelters and the best way to access them, as well as suitable alternative shelters. It is important to have a back-up plan in the case of power or equipment failure. Crowd strategiesThe first critical issue in crowd safety is that of safe shelters for large numbers of people. Ideally, crowds should be evacuated to safe areas before the storm is within 10 km of the venue (30-second flash-to-bang count). Given the practical constraints of moving large crowds, it is imperative that a formal assessment is made of existing structures (eg, grandstands, lightning gantries), as simple, cost-effective modifications can dramatically improve the protection offered to the crowd by these structures. Guidelines are provided by the Australian Standard on Lightning Protection.16 Spectators present in structures that are certified as lightning-safe can be advised to remain seated at times of increased lightning risk. Conversely, spectators present in unsafe areas or in structures that have had no formal assessment must be evacuated to safe shelters (Box 1). The importance and size of the event are also critical in decisions regarding safety of spectators. When larger groups are involved, more time is required to properly secure the area. Thus, as time requirements change, the distance at which lightning is considered a threat must be increased. In their report to the Organising Committee for the Sydney Olympic Games, Andrews and Mackerras (personal communication) recommended three phases of lightning safety (Box 2). Their recommendations, which were based on use of the Bureau of Meterology's Lightning Location System, should be implemented for major events where large crowds are expected. ConclusionThe important components of any lightning safety policy include a proactive approach; vigilant monitoring of the local weather; a specific chain of command; a method of delivering the message to those at risk; definition of safe structures; and definition of the criteria for both suspension and resumption of activity. Large events require careful consideration of crowd numbers, length of time required to ensure protection for all present, and appropriate shelters. The more far-reaching the event and the more people involved, the more economical it may be to use formal lightning location systems in early-warning surveillance. 1: General lightning safety recommendations Develop a proactive approach that includes monitoring the local weather from the day before activity until play has finished and the crowd has dispersed. Establish a specific chain of command. This includes choosing a designated weather-watcher and specifying the method of warning the people at risk. Define and list safe structures and locations. Define the criteria for both suspension and resumption of activity. Safe structures Large/substantial building (with electric and telephone wiring and plumbing to provide a safe pathway for the current to the ground). Fully enclosed metal vehicle (acts as a Faraday cage and guides the lightning current around the passengers). Buses are an excellent shelter and can be strategically placed around a venue to protect larger groups of people. Unsafe locations and situations Open field. Close vicinity to the tallest structure in an area (eg, tree, communication tower, light pole). Small structures such as rain/picnic shelters, tents, interchange bench. Indoor and outdoor swimming pools. Use of indoor phones. Umbrellas, golf clubs, bats, or any other object that increases an individual's height. The "30/30" rule A flash-to-bang count of 30 seconds indicates that lightning is 10 km away. This is associated with significant risk that the next strike could be at the observer's location. Thus, activity should be suspended and people moved to designated safe shelters. Wait 30 minutes after the last lightning or thunder before recommencing play. 2: Three phases of lightning safety for the Sydney 2000 Olympic Games Yellow: State of increased lightning awareness Intended to give 60 minutes advanced warning of a storm front reaching 10 km from a venue. (The direction and speed of travel of the storm front are taken into consideration, so that the anticipated time taken for the storm to reach 10 km from the venue is 60 minutes.) Orange: Activation of the lightning protection plan Intended to give 30 minutes advanced warning of a storm front reaching 10 km from a venue. Depending on the venue's requirements, all competitors should be moved to protected areas. Patrons should be advised to remain in position if they are already in a safe area, or move to a protected area as shown on a map. Individuals in transit should be advised to complete their transit as soon as possible. People in cars and buses should be advised not to commence transit and to remain in their vehicles. Red: State of increased lightning risk Declared when lightning activity is within 10 km of a venue. By this stage, all movements and evacuations should be complete, with the venue now secure from lightning. (Adapted from Andrews and Mackerras, 2001, personal communication.)

Michael Makdissi MB BS, BSc(Hons) · Peter Brukner MB BS, FACSP

As lack of exercise is an established major risk factor for many chronic illnesses (particularly heart disease) and premature mortality, it is incumbent on government bodies to promote physical activity.1 However, one in five adult Australians is prevented from being more physically active by injury or disability.2 Thus, minimising injury associated with sports and physical exercise also needs to be a government priority. Sports injuries in Australia are treated by a combination of medical and paramedical services, occasionally in public or private hospitals, but mainly in an outpatient setting. Although the Australian healthcare system provides universal "safety net" coverage for sports injuries at a relatively affordable cost, it has no plan for prevention of sports injuries. Perhaps this is because the government departments concerned with sport and health consider there is insufficient evidence to show that the burden of sports injuries is substantial and that many of these injuries could be prevented. But government bodies would be unwise to ignore the recent trend in Australia towards the regular occurrence of serious sports injuries that are leading to an increase in liability claims. The flow-on increases in insurance premiums are placing many community sports events, active recreation facilities and voluntary service providers under great financial pressure. The burden of sports injuriesThe cost of sports injuries in Australia was an estimated $1 billion a year in 19903 (we are not aware of any more recent published figure). Extrapolating from cost estimates made in a 1998 Victorian study,4 we estimate that sports injuries now directly cost the Australian community at least $1.65 billion a year. Although this figure may be disputed, it is a circular argument to suggest that no resources should be devoted to accurately counting the costs of sports injuries in Australia because there is no hard proof that the costs are substantial. Both injury frequency and associated costs need to be counted to derive cost–benefit ratios for any countermeasures implemented.5,6 Moreover, injury surveillance is the first stage in any program of sports injury prevention.7 Various factors conspire to prevent the incidence and public health burden of sports injuries in Australia from being adequately monitored.6 The Burden of Illness and Injury estimates for Australia8 do not reflect the true burden of sports injuries because (a) such injuries are rarely fatal;9 (b) limitations of the International Classification of Diseases (ICD-9),10 upon which they are based, prevent adequate identification of sports injuries;11 and (c) most sports injuries are not treated in hospital settings, where patient data would be retained centrally.11 The Medicare system that operates outside hospitals does not collect information about diagnosis or associated factors for patient consultations. It also prevents any other body from providing rebates for outpatient doctor visits, so there is no other organisation that could easily collect information about the number and cost of sports injuries treated by doctors in private practice. Moves towards national injury surveillance and prevention in AustraliaThe Australian Sports Injury Data Working Party was established in 1997 to draw up guidelines for sports injury surveillance, but, despite the release of a working data dictionary,12 no national body has since been funded to implement an Australia-wide approach to sports injury surveillance. In 1997, a Federal Government partnership led to the development of a national sports safety framework.13 However, since the late 1990s, there has been a notable lack of national leadership to implement this framework. The Strategic Injury Prevention Partnership, a group set up in August 2000 that represents health departments in all jurisdictions, is responsible for implementing the National injury prevention plan: priorities for 2001–2003. However, the Plan does not list the prevention of sports injuries as a priority.14 One major reason for this is that considerably less is known about sports injuries and their risk factors than other injuries such as falls, drownings and road trauma.5,15 New Zealand's sports injury compensation schemeFor a model of sports injury surveillance, Australia could look to New Zealand, which already has in place the infrastructure to monitor sports injuries. New Zealand's Accident Compensation Corporation (ACC) monitors sport, traffic and work injuries as a distinct segment of the healthcare system. The ACC can accurately determine the cost of treating sports injuries in New Zealand (eg, the cost was NZ$100 million in 2000).16 Furthermore, ACC statistics have shown that the number of sports injuries in New Zealand has fallen over recent years.16 Perhaps this decline is partially due to the preventive efforts of the ACC. It is quite possible that, in relative terms, the cost of sports injuries in New Zealand is lower than the cost in Australia, as New Zealand's scheme focuses on preventing injuries.16 The New Zealand system also has the advantage of being a "no-fault" insurance scheme that prevents sporting participants taking common law action against either the doctors or administrators associated with sporting events. Similar restrictions to liability actions from sporting participants are needed in Australia to prevent the cost of running sports events from becoming prohibitive, and to remove the fear of lawsuits that is developing among volunteers (including doctors) who cover sporting events. Plaintiff advocate groups currently argue that common law actions should not be restricted because injured athletes in Australia have no form of redress other than through the courts. Australian initiativesAnterior cruciate ligament (ACL) injuries to the knee, which occur primarily during sporting activities, provide a concrete example of the way that preventive measures could result in huge cost savings to the community. The Australian Football League (AFL), which monitors the number and circumstances of ACL injuries, has estimated that these injuries cost the AFL well over $1 million a year.17 The AFL has found that ACL injuries are twice as likely to occur in the more northern States of Australia as in Victoria.17,18 Research into the reason for this difference is helping to develop ways to prevent these injuries among professional footballers.18 By the same token, any differential patterns of injury observed in the general population would become an important public health issue. However, because of the lack of national injury surveillance, it is not known whether there are significant regional or other differences in injury patterns at the community level. One Australian State government has established a body specifically for compensating serious sports injuries, the New South Wales Sporting Injuries Insurance Scheme. This is a successful, non-compulsory, non-profit government insurer for catastrophic sports injuries (ie, those involving more than 35% permanent loss of use of a body part). The Scheme is cost-neutral and provides an incentive to actively prevent injury through promotion of safe sport practice and funding of injury prevention research. It is possible that the existence of the Scheme has lowered the risk of catastrophic injury in New South Wales relative to other States, but, once again, comparisons are not possible with incomplete data — the NSW Scheme is not compulsory for all sports and no other State has good records of catastrophic sports injuries. The Federal Government body devoted to sport, the Australian Sports Commission (ASC), has been extremely successful in promoting and developing Australian sport at the elite level. However, it does not consider itself responsible, in any major way, for the promotion of safe sport at the community level, and devotes most of its resources to the areas for which it is accountable, such as Australia's performance in elite sporting events. The approach to road trauma in Australia is a good example of how the healthcare system could better manage sports injuries. Traffic accidents are managed entirely outside the Medicare system, through bodies such as the Transport Accident Commission in Victoria. These bodies provide an infrastructure to support and develop preventive measures and actively engage in data collection to monitor injury trends. That Australian roads are much safer today than they were 20–30 years ago is testament to the success and extent of this preventive approach. ConclusionThe New Zealand approach to managing the problem of sports injuries may not be perfect, but it is surely better than the Australian approach of having no overall plan. Australian government bodies concerned with health and sport need to establish a body with national responsibility for sports safety and injury surveillance, exploring options such as a New Zealand-style national sports injury insurance scheme. It is only with an established infrastructure for monitoring sports injuries that significant advances will be made towards preventing sports injuries and ensuring safe, lifelong participation in physical activity for all Australians.

John W Orchard FACSP, PhD · Caroline F Finch PhD

Live stronger live longer: An exercise and lifestyle program for over 40s Mark Awerbuch. Sydney: McGraw-Hill, 2001 (xviii + 230 pp). ISBN 0 074 71087 7 This is a timely book on progressive strength training for older people which is made doubly useful because the program can be modified for people with arthritic conditions. The book is divided into two sections. The first provides a foundation for understanding changes to the body caused by ageing and arthritis. It discusses the impact of these changes on physical and psychological health, and presents the evidence supporting the benefits of strength and cardiovascular fitness training programs. Issues of nutrition and the importance of ensuring an appropriate diet are also discussed. Information is provided in an easy-to-read style, a user-friendly manner, and it is suitable for either health professionals or the interested layperson. A particularly useful chapter focuses on the barriers and motivators to starting and sustaining ongoing participation in exercise programs. The second section provides a step-by-step framework for conducting a strength and/or cardiovascular fitness training program — the book argues that these programs are complementary. Exercises are simply described, with many photographs. One criticism is that all of the photographs show only two participants, who appear quite fit. To older people, or people with mild to moderate arthritis, the photos may make them think the program is not suitable for them. (The book argues strongly that the program is appropriate for these groups as long as the framework is followed.) There is a very useful list of contact details on where to find further information (such as Fitness Australia-accredited gymnasiums), and a comprehensive bibliography of recent research in the area of exercise training for older people and people with arthritis. Overall, the book is a useful text for health practitioners, older people generally, and those with mild arthritic problems. People with more severe arthritis should discuss the issues with their medical practitioner, specialist or physiotherapist before beginning this type of program, as there is a need in this group to closely monitor initial response to exercise to avoid aggravation of joint pain.

Keith Hill

To the Editor: The conclusion of Holland et al that horse-related injuries in children account for a considerable number of deaths and injury is unarguable.1 In New Zealand, hospitalisation rates for falls from horses and rugby injuries are comparable.2 Despite these disconcerting facts, the data on horse-riding injuries need to be put in a balanced perspective. The frequency of injuries in adult equestrian activity, Pony Club riding, occupational riding (including professional jockeys) and riding for leisure are quite different. Collective raw data are misleading. The freak accident of actor Christopher Reeve in 1995, with the resulting much-publicised quadriplegia, brought public attention worldwide to the question of acute spinal cord injury (ASCI) in horse riding and led to widespread parental concern about "spine safety" in this sport. Spinecare Foundation was subsequently involved in a review of 32 patients with ASCIs from horse riding admitted to the spinal cord injury units at Royal North Shore and Prince Henry hospitals, Sydney, for the years 1976 to 1996.3 Occupational and leisure riding accounted for 88% of injuries. ASCIs occurred in only two riders under the aegis of the Equestrian Federation of Australia — one while competing and the other while training. There were no injuries in children younger than 14 years of age in any form of riding. Most importantly, in the study period, there had been no ASCIs in Pony Club riders, of which there were 22 000 in New South Wales in 1996. Neither had there been an ASCI in those who participated in Riding for the Disabled. In the context of these comments, it is relevant to briefly revisit the contentious topic of Down syndrome children taking part in Riding for the Disabled and in sport generally. Since 1970 (from when accurate records are available), no child with Down syndrome in NSW has had an ASCI in any sport, let alone in a well-defined non-sporting accident. There is simply no case for the radiological screening of the cervical spine for atlanto-axial instability in asymptomatic children with Down syndrome before they undertake Riding for the Disabled. The indications for this examination have been set down.4 We hold that the public and the medical profession can continue to be reassured by this information. Certainly, a child wearing a lap seat belt or other poorly fitting restraint in the rear passenger compartment of a car is at infinitely greater risk for spinal cord injury than when astride a horse at Pony Club. Further, as Holland et al have documented,1 if he or she is wearing a protective helmet the chances of head injury would be reduced significantly. Safety in all potentially dangerous sports should be foremost in the minds of those who administer, supervise and participate in such games. As yet there are no hard data to support the wearing of body protectors to reduce the risk of ASCI, or other vertebral injuries, in horse riding. In reply: One of the reasons for publishing our data was to raise the level of awareness of both the frequency and severity of horse-related trauma in Australian children.1 This trauma appeared to be associated with a low level of compliance with basic safety measures, in particular the use of a Standards-approved riding helmet.1,2 We stated clearly in our article that the risk of injury needed to be viewed in the context of the important social and health benefits of horse-riding as a sporting and leisure activity.1 Taylor and Roe have commented on the perceived benefits of Riding for the Disabled, especially in children with Down syndrome. Certainly, the available data suggest that in this strictly supervised scenario horse riding would appear to be very safe.3 However, the evidence for therapeutic benefit would appear to be relatively weak, and the risks of this form of equestrianism cannot be compared with the more common interaction that might occur between a normal child and horse.4 The incidence of spinal cord injury in children fortunately appears low, at less than 2% of children admitted with all forms of traumatic injury.5 In this context, the use of spinal cord injury as a measure of the safety of a sport for children is flawed. While children may be at greater risk of injury when inappropriately restrained in a motor-vehicle accident, this fact in itself does not make horse-riding, or indeed any other high-risk sporting activity, safe. The use of appropriate safety devices and responsible adult supervision does.

Thomas K F Taylor DPhil(Oxon), FRCS, FRACS · Justin P Roe MB BS, FRACS · Andrew J A Holland BSc, MB BS, FRACS, FRACS(Paed) · Gerard T Roy

Fitness and fads The epidemiology of dog walking: an unmet need for human and canine health Adrian E Bauman, Schroeder J Russell, Susan E Furber and Annette J Dobson MJA 2001; 175: 632-634 Abstract - Main findings - Further interpretation using DogEpi concepts - Authors' details - - More articles on Psychiatry Abstract Objective: To describe the prevalence of dog walking in New South Wales, and to identify potential health gains if more dogs were walked. Design: Cross-sectional analytical survey. Setting and participants: 894 adults in NSW in 1998 (among the owners of approximately two million domestic dogs in NSW who were potential participants in dog-walking behaviours). Interventions: None yet. Main outcome measures: Dog walking hours per week; other DogEpi concepts to illustrate the public health gains include the DAF (dog attributable fraction), and the BBR (benefits to bites ratio). Results: The response rate to the survey was 74%. 46% of households in NSW had a dog and, overall, dog owners walked 18 minutes per week more than non-dog owners. However, more than half of dog owners did not walk their dogs, and were less likely than non-owners to meet recommended levels of physical activity sufficient for health benefits. If all dog owners walked their dogs, substantial disease prevention and healthcare cost savings of $175 million per year might accrue. Conclusions: There are potential benefits of dog walking for human health; currently, among dog owners, much of this benefit remains to be realised. There are also likely benefits for canine health. Dog walking should be promoted through national strategies recommending "Walkies for all by the year 2010". About half of all homes in Australia have a pet, with dogs being the most prevalent, reported in about 40% of all households; these rates are similar to United States estimates for dog ownership.1,2 Although most dogs are loved and well cared for by their owners, a key question is whether dogs might improve human health. The notion that dogs might promote good health has been explored elsewhere, with studies of the psychological companionship and supportive role of dogs, and the use of "dogs as therapy" for older, institutionalised adults.3,4 Other, small-scale studies have associated dog ownership with lower blood pressure, or even reduced re-infarction rates, among people with coronary heart disease.5,6 One area which has been less studied is the concept of dog walking, which provides physical activity for both dogs and people. Some surveys have proposed that people who own dogs are more active than those who do not,5,7 although this is not always the case.2,8 Nonetheless, this area has received much less attention than other pet-related research. This article focuses on the epidemiology of dog walking, which generally has been ignawed by researchers, and eschewed by epidemiologists. Hence this report cuts to the bone and unleashes an incisive public health argument for increasing dog walking in Australia. The primary research question was whether dog owners were more active than non-dog owners. In addition, the potential benefits of increased dog walking were estimated, using innovative DogEpi concepts. Methods This study was based on two population-based physical activity surveys carried out in New South Wales in March and November 1998.9 Respondents were adults, randomly sampled from the Electronic White Pages. Questions were asked about dog ownership, and the amount of time the respondent had spent walking his or her dog in the previous week. Standard physical activity questions about walking and moderate and vigorous physical activity in the previous week were also asked.10 The study variables were total time engaged in dog walking, any walking and total physical activity. Respondents were considered to have achieved "recommended levels of physical activity" for health benefit (150 minutes of at least moderate activity a week), based on the US Surgeon General's report.11 Analyses were carried out with SPSS,12 and included bivariate comparisons of proportions and means, and adjusted odds ratios using forced-entry logistic regression models to adjust for possible confounders. Results Main findings Of the 1208 adults approached, 894 (74%) responded. They were aged 25-64 years, with a mean age of 44.4 years (95% CI, 43.9-44.9 years). Almost half (45.6%) were male, 75% were married or had a partner, and 28% reported some tertiary education. Overall, 47.1% achieved the US Surgeon General's recommended 150 minutes of total physical activity per week, and 27% achieved this only through walking. About 46% of the sample reported that they had a dog at home. Among dog owners, the mean reported time allocated specifically for dog walking each week was 0.95 hours (95% CI, 0.77-1.13 hours per week), which was less than half of the average of two hours in total from all types of walking reported by dog owners each week (see Box). Among dog owners, 59% reported no dog walking, 26% reported up to 2.5 hours per week, and 15% reported at least 2.5 hours per week. The Box shows the mean time spent in physical activity according to dog ownership status. Those who owned dogs walked only 0.3 hours (about 18 minutes) more per week than non dog-owners. However, those who owned dogs and walked them less than one hour per week walked less, in total, than non dog owners (P = 0.01). Only those who walked their dogs for more than an hour per week walked significantly more or were significantly more active in total than non dog-owners. Further, the median number of walking sessions per week was 3.0 for both dog owners and non-owners (P = 0.98). All dog-walker categories were slightly less likely to reach the 150 minute per week "health-enhancing" threshold, except for those who walked their dogs for 2.5 hours. For overall physical activity, similar proportions of owners and non-owners achieved 150 minutes of total activity per week (46.9% and 47.3%, respectively), and dog owners who did not walk their dogs were significantly less likely to meet the guidelines. Only those who walked their dogs for at least an hour a week were more likely (odds ratio, 1.89) than non-owners to achieve sufficient physical activity for health benefits (Box). Further interpretation using DogEpi concepts This section describes innovative interspecies epidemiological approaches to understanding the data. DogEpi concepts are not meant to hound researchers, nor meant to be a golden (standard) retriever of epidemiological wisdom, but they are descended from the litter of current epidemiological thought, some of which is scatological. Firstly, the notion of dog walking to total walking ratio (DWTWR) and dog walking to total physical activity ratio (DWTPAR). The DWTWR, which is the percentage of all walking that was dog walking, was 22.9%. For 12% of the population, dog walking was half of their total walking. As a percentage of all physical activity, the DWTPAR was 13%, with 9% of the population doing at least half their total activity as dog walking. More important is the DAF (dog attributable fraction), which is an epidemiological estimate of the proportion of disease which might be prevented if all of the dog owners walked their dogs for at least 150 minutes per week. If this occurred, the population prevalence of sufficient physical activity would increase from 47% to 71%. Such an increase in physical activity would be about 5-10 times as great as most population-level interventions designed to promote activity.9 From this level of change in dog walking, and assuming a population-attributable risk of 18% for physical inactivity and coronary heart disease (CHD),13 it can be estimated that the maximal DAFcardiovascular is about 9% of the total burden of CHD. Other estimates of the DAF for diabetes and colon cancer, along with other health benefits of being active, including reduced doctor visits and medication costs, could be estimated in addition to this cardiovascular DAF. Direct healthcare cost savings can be estimated for specific increases in physical activity levels.13 A conservative estimate suggested that A$36 million might be saved annually for coronary heart disease for every 5% increase in the prevalence of adults who are "sufficiently active".13 Thus, if all dog owners walked their dogs more, this would be a 24% increase, resulting in direct healthcare cost savings of around $175 million per year. These savings would accrue rapidly, as cardiovascular risk reduction occurs sooner following the initiation of physical activity than after smoking cessation or dietary change.14 Nonetheless, it is important to calculate the other benefits and also the potential adverse effects and costs of keeping dogs as pets in Australia. The benefits of mental health improvement and stress reduction may be considerable, but are not used here in order to provide a conservative estimate of overall dog benefit. The adverse effects include the risks of zoonoses, but these are low. One public health issue is dog bites, which are estimated to cost $1.5 million in Victoria in direct healthcare costs.15 This is clearly an overestimate for the risks of dog walking, as only a quarter of dog bites occur in open space, roads or paths.16 However, we can use this overestimate to calculate a preliminary population health benefits to bites ratio (BBR) for the increased risk of dog bites and the risk reduction for heart disease to estmate the potential benefits versus risks of dog walking. We find that, even if only half of dog owners increased their dog walking to 150 minutes per week, then the resulting national savings of $87.5 million, divided by national dog bite costs of around $7 million, would give a very favourable cost benefit to bites ratio. Discussion In general, dog owners are not more active than non-owners, unless they practise regular, sustained dog walking. This article identifies the human health benefits of dog walking, and points to the need to encourage those with dogs to walk them more. It is possible that adults in the household other than the survey respondent also contributed to the time dogs are walked, so, from the canine perspective, our data could be an underestimate. Nonetheless, it would be a useful health-promotion strategy for inactive non-dog owners to acquire a dog in order to initiate regular moderate walking. There are reciprocal benefits for canine health -- from the dog's perspective, the amount walked is generally "never enough". This may be one way in which dog and human health might be improved, providing a biologically plausible explanation for the xeno-transmission of mortality gradients shared between pets and their owners, and described recently in the British Medical Journal.17Dog walking is an important potential benefit of dog ownership. As about half of adult Australians are physically inactive, and the public health benefits of being active are comparable to those of smoking cessation,18 dog walking should become widely recommended by human and canine health advocates alike. We should paws then, put our best feet forward, and take "man's best friend" for a walk more often. We advocate a campaign to promote "Walkies for all by the year 2010". Acknowledgements We thank NSW Health for data collection. Competing interests None declared. References Beck AM, Meyers NM. Health enhancement and companion animal ownership. Ann Rev Public Health 1996; 17: 247-257. Headey B. Health benefits and health cost savings due to pets: preliminary estimates from an Australian national survey. Soc Indicat Res 1999; 47: 233-243. Robb S, Stegman CE. Companion animals and elderly people — a challenge for the evaluation of social support. Gerontologist 1983; 23: 277-282. Francis GM, Turner J, Johnson S. Domestic animal visitation as therapy with adult home residents. Int J Nurs Stud 1985; 22: 201-206. Anderson WP, Reid CM, Jennings GL. Pet ownership and risk factors for cardiovascular disease. Med J. Aust 1992; 157: 298-301. Friedmann E, Thomas SA. Pet ownership, social support and one year survival after acute myocardial infarction in the Cardiac Arrhythmia Suppression Trial (CAST). Am J Cardiol 1995; 76: 1213-1217. Serpell J. Beneficial effects of pet ownership on some aspects of human health and behaviour. J Roy Soc Med 1991; 84: 717-720. Simons LA, McCallum J, Simons J. Pet ownership and future health. Med J Aust 1997; 167: 231-232. Bauman AE, Bellew B, Owen N, Vita P. Impact of an Australian mass media campaign targeting physical activity in 1998. Am J Prevent Med 2001; 21: 41-47. Armstrong T, Bauman A, Davies J. Physical activity patterns of Australian adults (AIHW Catalogue No. CVD 10). Canberra: Australian Institute of Health and Welfare, 2000. US Department of Health and Human Services. Physical activity and health: a report of the Surgeon General. Washington DC: Department of Health and Human Services, Centers for Disease Control and Prevention, 1996. Statistical package for the social sciences [computer program]. Version 10. Chicago, Ill.: SPSS Inc, 2000. Stephenson J, Bauman A, Armstrong T, et al. The costs of illness attributable to physical inactivity. Canberra: Commonwealth Department of Health, 2000. Blair SN, Kohl HW III, Barlow CE, et al. Changes in physical fitness and all cause mortality: a prospective study of healthy and unhealthy men. JAMA 1995; 273: 1093-1098. Watson W, Ozanne-Smith J. The cost of injury to Victoria. Report No. 124. Melbourne: Monash University Accident Research Centre, 1997. Ashby K. Dog bites. Hazard no. 26. Victorian Injury Surveillance System. Melbourne: Monash University Accident Research Centre, 1996: 7-13. Moloo J, Waller JL, McKeown RE, et al. Xenotransmission of the socioeconomic gradient in health? A population based study. BMJ 1998; 317: 1686-1686. Mathers C, Vos T, Stevenson C. Burden of disease and injury in Australia. (AIHW Catalogue no. PHE 17). Canberra: Australian Institute of Health and Welfare, November 1999. (Received 15 Oct, accepted 2 Nov, 2001) Authors' details School of Public Health and Community Medicine, University of NSW, Sydney, NSW. Adrian E Bauman, PhD, FAFPHM, Professor of Public Health; Susan E Furber, PhD, Senior Lecturer. Strathfield, NSW. Schroeder J Russell, Canine Walking Advocate. School of Population Health, University of Queensland, Herston, QLD. Annette J Dobson, PhD, Professor of Biostatistics. Reprints: Professor A E Bauman, Epidemiology Unit, Hugh Jardine Building, Locked Mail Bag 7017, Liverpool BC 1871, NSW. Make a comment Walking and total physical activity time, and percentages meeting recommended physical activity levels, according to dog ownership and dog-walking status Total hours Achieved 150 minutes per week Category Number Walked per week (mean [95% CI]) Physical activity per week (mean [95% CI]) By walking only By total physical activity Adjusted odds ratio†(95% CI) Non-dog owner 484 1.7 (1.4-1.8) 3.3 (2.9-3.6) 121 (25.1%) 229 (47.3%) 1.0 (reference) Dog owner* 410 2.0 (1.8-2.2) 3.5 (3.1-3.8) 105 (29.7%) 191 (46.9%) 0.95 (0.72-1.23) Does not walk dog Walks dog up to 1 h/week Walks dog 1-2.5 h/week Walks dog > 2.5 h/week 240 33 73 61 1.3 (1.0-1.5) 1.3 (0.9-1.7) 2.2 (1.8-2.5) 5.0 (4.3-5.6) 2.5 (2.0-3.0) 1.9 (1.3-2.5) 4.1 (3.4- 4.8) 7.0 (6.0-8.1) 39 (16.3%) 5 (15.2%) 16 (21.9%) 45 (100%) 76 (31.7%) 9 (27.3%) 45 (61.6%) 61 (100%) 0.55 (0.39-0.77) 0.45 (0.2-1.01) 1.89 (1.1-3.1) n/a * Data on dog-walking time were missing for three dog owners. † Odds ratios for meeting the recommended physical activity guidelines, adjusted for age, sex, education, marital status. n/a = not available. 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Adrian E Bauman · Schroeder J Russell · Susan E Furber · Annette J Dobson

Fitness and fads Estimating historical changes in physical activity levels Garry J Egger, Neeltje Vogels and Klaas R Westerterp MJA 2001; 175: 635-636 Abstract - Methods - Results - Discussion - References - Authors' details - - More articles on Psychiatry Abstract Objective: To compare activity levels between a simulated "historical" lifestyle and a "modern" lifestyle to try to validate earlier estimates of secular changes in activity. Design: Triaxial accelerometers (TRACMORs) were used to measure activity levels in a "historical" group of seven male actors who were paid to live like early Australian settlers at a theme park north of Sydney (eg, minimising the use of modern technology) for a week. Results were compared with those from a group of seven "modern" sedentary office workers. Results: Activity levels were up to 2.3 times greater in the historical group than the modern group. Calculations based on body weight and energy expenditure suggest the difference is the equivalent of walking up to 16 km per day more in the past than today. Conclusions: These findings accord with two previous estimates of changes in daily activity levels over time and suggest that recent public health guidelines for increasing physical activity may be inadequate. An inactive lifestyle has been linked to a range of diseases, many of which are mediated through obesity.1 Intuitively, it seems apparent that average activity levels have decreased with modern industrial development and have mirrored the worldwide rise in obesity. Proxy measures of inactivity, such as the sale of motor vehicles and television viewing time, show a clear relationship to the development of obesity in the presence of a declining food intake. For this reason, some obesity experts suggest that the modern phase of the obesity epidemic (from 1980 onwards) is probably mediated more by inactivity ("sloth") than overconsumption ("gluttony"). However, the quantitative dimensions of a change in physical activity are difficult to estimate.2 If they could be (even roughly) determined, they might provide valuable information against which to assess modern physical activity guidelines for weight loss and maintenance. A "back of an envelope" calculation suggested an average decline in energy expenditure in the United Kingdom from the years after World War II to 1995 of around 800 kcal/d.3 At an energy cost of around 50 kcal/km for a 70 kg man,4 this suggests a decline in activity levels equivalent to walking about 16 km less per day. More recently, a comparison of activity levels of hunter-gatherer populations with those of individuals in modern Western societies suggested that the average daily difference may be equivalent to walking about 19 km.5 In an attempt to validate these estimates, we recently mocked up a small experiment for a lifestyle television production (Burke's Backyard). Our experiment was designed to compare activity patterns in Australian settlers of 150 years ago with modern-day sedentary office workers. We then attempted to calculate differences in terms of distance walked daily to compare with the previous estimates. Methods Movement levels were monitored in two groups of men by use of a triaxial accelerometer (TRACMOR, Maastricht University, Maastricht, the Netherlands) worn around the waist during waking hours. This has recently been validated against doubly-labelled water,6 and is regarded as one of the most sophisticated modern ambulatory measurement monitors. The device measures movement in activity units on three axes (forwards, sidewards and upwards), and includes even relatively minor movements such as fidgeting and upper-body actions. Seven male actors aged 30-60 years who work at "Old Sydney Town", a historic theme park north of Sydney set around the early 19th century, were selected to represent a historically active group. The men are paid to play the role of early Australian soldiers, convicts and settlers for about eight hours every day. They agreed to wear a TRACMOR during waking hours for one week, and were asked to avoid the use of modern technology as much as possible when they were not working at the park during the week. In an attempt to further authenticate this process, five of the men lived on the premises in convict huts for up to four days and nights. A second group of seven male modern sedentary workers, aged 30-60 years, including accountants, information technology personnel, doctors, a taxi driver and an entertainer, were also given TRACMORs to wear during waking hours, and were asked to continue their normal lifestyle over the course of a week. All records were downloaded into a computer program developed by the developers of the TRACMOR at Maastricht University in the Netherlands for analysis of results. Results The mean activity level (arbitrary units) for the historical group was 88 533 (95% CI, 33 697-143 369; range, 62 204-129 924), compared with 54 920 (95% CI, 32 019-77 821; range, 38 322-70 399). Thus, the historical group were on average 1.6 times more active than the modern group. However, the task was taken more seriously by some in the historical group than others (eg, some still used cars and televisions to some extent during the week). Hence, the two main outliers in the group, who kept rigidly to the experimental requirements, may provide a better reference point for calculations. These two individuals (with activity levels of 129 924 and 125 800 units) were 2.3 times more active than the modern group. Using estimates derived from energy expenditure tables (see Box), it was calculated that the difference in activity levels between the means of the two groups was equivalent to walking about 8 km per day. However, when the two outliers in the historical group were compared with the mean of the modern group, the difference was equivalent to walking about 16 km per day. Discussion A difference in daily activity levels equivalent to walking 8-16 km per day between previous and modern times represents a huge secular change in daily energy expenditure. At the upper level, this coincides roughly with previous estimates.3,5 It probably also accords with the levels of movement required for foraging for survival throughout most of human evolution. Anthropological evidence suggests that early humans, like modern hunter-gathers, may have transported tools, weapons and game over a daily range of about 15 km.8 Given their other daily tasks, this would have added up to a substantial daily energy use which was rarely, if ever, likely to be exceeded by food intake over an extended period, thus reducing the chances of energy imbalance. As a result, human populations, up until the past 2-3 decades, have not been significantly overweight. The growth of time-saving and time-using technologies,9 however, means that these activity levels are unlikely ever to be reached without conscious effort. In the presence of an abundant (and energy-dense) food supply, obesity, at least at the population level, is almost an inevitable consequence of modernisation. More telling are the implications this has for physical activity recommendations for optimal health and weight management. Recent government recommendations suggest an added daily energy requirement of 30 minutes of accumulated mild- to moderate-intensity activity.10,11 However, for a 96 kg sedentary office worker, such as in this study, this would account for perhaps an extra 200 kcal/d, which is 300-800 kcal (the equivalent of walking 5-13 km) short of the 500-1000 kcal difference estimated here. These findings support the suggestion that, if the evolutionary perspective (which has dominated almost all of human existence) is indicative of requirements for optimal health, an increase in activity levels up to three times those recommended in modern guidelines may be necessary.5 Supporting this, data from the United States Weight Control Registry, a database of people who have lost more than 14 kg and maintained this for at least five years, have shown that people who achieve the greatest benefits are consciously active for up to 80 minutes a day.12 This is about three times greater than current recommendations.10,11 These figures are based on people who have been previously obese, and maintenance of weight loss may be more difficult than prevention of weight gain. Nevertheless, it is an awesome task, in the absence of a major environmental change, to expect these activity levels to be met in our society. The figures presented in this study should be interpreted with caution. Although we used a validated modern movement-sensing device,13 the results involve only small numbers under artificial conditions. In their present form, they merely add support to other attempts to calculate human activity levels over time and provide an indication of the activity requirements needed to correct these secular changes. References Powell KE, Blair SN. The public health burdens of sedentary living habits: theoretical but realistic estimates. Med Sci Sports Exerc 1994; 26: 851-856. Prentice A, Jebb S. Obesity in Britain: Gluttony or sloth? BMJ 1995; 311: 437-439. James WPT. A public health approach to the problem of obesity. Int J Obes Relat Metab Disord 1995; 19: S37-S45. Ainsworth BE, Haskell WL, Whitt MC, et al. Compendium of physical activities: an update of activity codes and MET intensities. Med Sci Sports Exerc 2000; 32 (9 Suppl): S498-504. Cordain L, Gotshall RW, Eaton SB. Physical activity, energy expenditure and fitness: an evolutionary perspective. Int J Sports Med 1998; 9: 328-335. Bouton C, Verboeket-van de Venne WP, Westerterp KR. Physical activity assessment: comparison between movement registration and doubly labelled water. J Appl Physiol 1996; 81: 1019-1026. Movahedi A. Simple formula for calculating basal energy expenditure. Nutr Res 1999; 19: 989-995. Gowlett J. Mental abilities of early man: a look at some hard evidence. In Foley R, editor. Hominoid Evolution and Community Ecology. New York: Academic Press, 1984; 167-192. Bowden S, Offer A. Household appliances and the use of time: the United States and Britain since the 1920s. Econ Hist Rev 1994; XLVII: 725-748. United States Surgeon General. Physical activity and health: a report of the Surgeon General. US Department of Health and Human Services. Atlanta: Centers for Disease Control, 1996. Egger G. National physical activity guidelines for Australians: scientific background report. Canberra: Commonwealth Department of Health and Aged Care, 1999. Klem ML, Wing RR, McGuire MT, et al. A descriptive study of individuals successful at long-term maintenance of substantial weight loss. Am J Clin Nutr 1997; 66: 239-246. Westerterp K. Pattern and intensity of physical activity. Nature 2001; 410: 539. (Received 25 Sep, accepted 22 Oct, 2001) Authors' details Deakin University, Melbourne, VIC, and GutBusters Pty Ltd, Sydney, NSW. Garry J Egger, MPH, PhD Adjunct Professor of Health Sciences. Masstricht University, The Netherlands. Neeltje Vogels, BBiolSc Student; Klaas R Westerterp, PhD, Professor of Human Energetics, Department of Biological Sciences. Reprints will not be available from the authors. Correspondence: Professor G J Egger, PO Box 313, Balgowlah, NSW 2094. eggergjATozemail.com.au Make a comment Calculation of distance equivalents Activity units measured by the TRACMOR are not readily convertible to energy units (kilocalories). However, an estimate of relative differences in activity levels can be made by assuming a total daily energy expenditure 1.4 times that of resting metabolic rate for the men in our modern group.5 With an average weight of 96 kg and age of 44 years, a mean resting metabolic rate of about 2000 kcal/d can be estimated.7 Therefore, total energy expenditure would be 1.4 x 2000 = 2800 kcal/d, of which 800 kcal represents daily physical activity. As activity counts in our historical group ranged from 1.6 times those of the modern group on average to 2.3 at the extremes, this implies a total daily physical activity level in this group of 1280-1840 kcal/d, or a net difference of about 500-1000 kcal/d between the groups. Using energy values for walking of 0.716 kcal/kg per kilometre (or about 61 kcal/km for a 90 kg man),4 this implies a net difference between the groups equivalent to walking about 8-16 km per day. Back to text

Garry J Egger · Neeltje Vogels · Klaas R Westerterp

Olympic Games Drug testing at the Sydney Olympics With pre-Olympic and out-of-competition testing, as well as a new, validated test for erythropoietin, athletes will be exposed to more comprehensive drug testing at the Sydney Olympics Brian Corrigan and Ray Kazlauskas MJA 2000; 173: 312-313 See also, Kennedy Drug screening - Sample collection - Analysis - Conclusion - References - Authors' Details - - More articles on Sports medicine Testing for drugs used to enhance performance has been carried out at the Olympic Games since they were held in Mexico in 1968, when Australia's Ron Clarke became the first athlete to be tested. Doping at the Olympic Games is banned for two very good reasons: the use of drugs is cheating, and drugs have adverse effects on the health of athletes.1 The International Olympic Committee (IOC) has maintained a list of proscribed substances and methods for their detection since 1967, and this list is updated each year to form the basis for determining banned substances in all sport.2In much the same way as random breath testing is used to deter drink driving, drug testing is intended as a deterrent rather than a method of catching all offenders. Thus, in Olympic final events, the competitors who gain the first four places, plus one other usually chosen at random, are subjected to a drug test. During Olympic heats, any athlete may be selected at random for testing. In past Olympic Games, athletes were not tested for drugs until after they had competed in their events. At the Sydney Olympics, for the first time, many athletes will be subject to pre-Olympic, out-of-competition testing, as it is during this period that some drugs, such as anabolic steroids, may be best detected. This represents a huge change in the IOC position and has occurred after much lobbying by, among others, the Drug Committee of the Sydney Organising Committee for the Olympic Games (SOCOG). Drug screening Although blood testing has been performed in a limited fashion at Winter Olympics since 1994, screening for drugs at the Summer Games has, until these Sydney Games, been restricted to urine testing. Urine samples are generally preferable to blood samples for testing for most substances banned by the IOC, as it is easier to collect adequate volumes of urine, and collection of urine is not so invasive. Also, drug and metabolite levels are much higher in urine than in blood, so their detection has greater retrospectivity.3 However, there is a subset of drugs -- the peptide hormones such as erythropoietin (EPO) and human growth hormone (hGH) -- for which establishing a reliable urine test has proved a major obstacle. However, a validated test for EPO has just been accepted by the IOC and will be available for use at the Sydney Games. It involves both a blood test perfected by Australian scientists, and a urine test perfected by the French. Sample collection The procedures of urine collection for doping control are rigorously controlled.1 First, a chaperon meets the chosen athlete at the conclusion of the event, provides documentation of his or her selection, and obtains the athlete's signature for verification. The chaperoned athlete attends the doping control station, where forms are filled in to document all prescribed, complementary and other medicines he or she may be taking. The athlete selects his or her own container and provides a urine sample under the observation of the chaperon, and possibly a team representative. Athletes are required to provide a specimen of approximately 75 mL. This can take some time if the athlete is dehydrated, and athletes are permitted to attend press conferences or receive medals in the interim, provided they are always accompanied by their chaperons. Fluids (not containing caffeine) are provided in the waiting room. The urine sample is checked for volume, pH, and specific gravity (SG). A low SG (< 1.010) could indicate an attempt to dilute the urine by taking a diuretic or drinking litres of water. Athletes may have taken sodium bicarbonate to prevent the build-up of lactic acid and so delay the onset of fatigue. While it is difficult to detect sodium bicarbonate, its use markedly elevates the pH (normally about p H 5-6 post-exercise).4 Also, at high pH, basic drugs such as the amphetamines are very poorly excreted,5 so, if a urine sample is dilute or has a high pH, the athlete will be asked to remain in the collection area and to produce further samples. Athletes divide their own 75 mL urine specimens into two aliquots in bottles labelled A and B, which have the same unique identifying number. These are secured for shipment to the laboratory. There are at least three copies of the associated paperwork -- one for the athlete, one for the testing authority (the IOC) and a third, abbreviated version (that does not identify the athlete) for the laboratory. The athlete verifies that the process was satisfactory. The information recorded at the doping control station initiates a chain of custody, which identifies the custodian of the sample at every stage. This extends from urine collection through storage, transport, delivery to the drug-testing laboratory, testing and then the final report sent to the appropriate authority. Correct storage of the urine sample is important and refrigeration is essential to inhibit bacterial growth and endogenous steroids, which can be modified under some conditions to produce, or, more usually, break down, testosterone.6 Analysis State-of-the-art technology and quality control are integral to the whole analytical procedure. The 27 laboratories around the world currently accredited by the IOC are subjected to rigorous reaccreditation testing each year.7 The IOC-accredited laboratory in Sydney has been accredited since 1990 and performs about 4000 tests within Olympic sports each year as part of the Australian program to eliminate doping in sport (Australian Sports Drug Agency, annual report, 1998). Medical practitioners cannot request testing for competing athletes outside this system unless the athletes have bona fide medical conditions and proper documentation is supplied. During the two weeks of the Sydney Olympic Games, up to 2000 samples will be analysed (some 10 000 individual drug tests). Samples are screened for banned substances by means of sophisticated instruments such as gas chromatography mass spectrometers. Such instruments can provide unambiguous identification of drugs or metabolites to confirm a positive result. To obtain higher sensitivity for anabolic steroids, and hence longer detection periods of banned substances that may have been used during training but not at event time, the IOC has introduced the use of high-resolution mass spectrometry. This technique can detect smaller quantities and was made compulsory by the IOC for the Atlanta Olympics. The techniques have been refined and extended and will play an integral part of the testing protocol at the Sydney Olympics. The most common method of detecting exogenous testosterone, rather than natural testosterone, is the testosterone/epitestosterone (T/E) ratio.8 Epitestosterone is normally secreted as an epimer of testosterone, and testosterone is not converted to epitestosterone, so the population mean for the T/E ratio is approximately one.9 An elevated T/E ratio remains an excellent indicator of exogenous testosterone abuse,10 and the IOC has determined that values above six indicate doping. However, a very small group of individuals have a naturally elevated T/E ratio. An endocrinological investigation must be performed to detect individuals with an elevated T/E ratio due to either a medical condition or low normal epitestosterone production.9 More recently carbon isotope ratio mass spectrometry has been used11 and this technique may also assist in deciding these cases. All testing is carried out on one of the duplicate samples from each athlete (the A sample). The presence of a banned substance or its metabolites is sufficient to constitute a positive test -- it is not the responsibility of the testing authorities to determine how that substance got into the body. However, positive results are further investigated by the IOC Medical Commission. This may require analysis of the second (B) sample, during which the athlete or his or her representative may be present.1 If this analysis supports the initial result, a hearing is held to determine if a doping offence has occurred. The IOC Code clearly specifies the penalties that apply for doping offences. Conclusion Use of performance-enhancing drugs demeans both sport and the athletes who use them. Now that sport is a multi-billion dollar business, antidoping programs must be correctly undertaken so as not to allow evasion by the use of legal arguments and loopholes. This requires constant research into doping practices and programs. It goes without saying that the whole drug-testing process has to be, like Caesar's wife, beyond suspicion. References Olympic Movement Anti-Doping Code. Lausanne, Switzerland: International Olympic Committee, 1999. Kicman AT, Cowan DA. Peptide hormones and sport: misuse and detection. Br Med Bull 1992; 48: 496-517. Donike M, Geyer H, Gotzmann A, et al. Blood analysis in doping control. Advantages and disadvantages. In: Hemmersbach P, Birkeland K, editors. Proceedings of the Second International Symposium on Drugs in Sports. Towards the use of blood samples in doping control? Lillehammer, Norway, 1993. Oslo, Norway: On Demand Publishing, 1994: 75-92. Tiryaki GR, Atterbom HA. The effects of sodium bicarbonate and sodium citrate on 600m running time of trained females. J Sports Med Physical Fitness 1995; 35: 194-198. Mottram DR. Drugs in sport. 2nd ed. London: Spon, 1996: 8-9. Ayotte C. Evaluation of elevated testosterone epitestosterone values in athlete's urine samples. IAAF Quarterly 1997; 2: 87-94. Doping. An IOC white paper. Lausanne, Switzerland: International Olympic Committee, 1999. Anguilera R, Becchi M, Casabianca H, et al. Improved method of detection of testosterone abuse by gas chromatography combustion isotope ratio mass spectrometry analysis of urinary steroids. J Mass Spectrom 1996; 31: 169-176. Dehennin L, Matsumoto AM. Long-term administration of testosterone enanthate to normal men: alteration of the urinary profile of androgen metabolites potentially useful for detection of testosterone misuse in sport. J Steroid Biochem Biol 1993; 44: 179-189. Catlin DH, Hatton CK, Starcevic SH. Issues in detecting abuse of xenobiotic anabolic steroids and testosterone by analysis of athletes' urine. Clin Chem 1997; 43: 1280-1288. Becchi M, Anguilera R, Farizon Y, et al. Gas chromatography/combustion/isotope-ratio mass spectrometry analysis of urinary steroids to detect misuse of testosterone in sport. Rapid Commun Mass Spectrom 1994; 8: 304-308. Authors' Details Institute of sport, Concord Hospital, Sydney, NSW. Brian Corrigan, AM, FRACP, FRCP, Director. Australian Sports Drug Testing Laboratory, Pymble, NSW. Ray Kazlauskas, PhD, Director. Reprints will not be available from the authors. Correspondence: Dr B Corrigan, 1 Lookout Avenue, Dee Why, NSW 2009. abcATsouthernx.com.au Make a comment

Brian Corrigan · Ray Kazlauskas

Olympic Games Newer drugs used to enhance sporting performance Michael C Kennedy MJA 2000; 173: 314-317 Controversy surrounding drug use in sport makes this a difficult area for rigorous research. However, it is striking that what data there are on drugs currently used for performance enhancement rarely indicate any clear benefit. Testosterone precursors - 5 Alpha-dihydrotestosterone - Clenbuterol - Erythropoietin - Insulin - Growth hormone - Insulin-like growth factors - β-Hydroxy-β-methylbutyrate - Conclusions - Disclaimer - Acknowledgements - References - Authors' details - - More articles on Sports medicine Historically, many different drugs have been used in attempts to enhance sporting performance. Strychnine, cocaine, heroin and ethyl alcohol were in common use at the turn of the century, but they were later supplanted by amphetamines, pseudoephedrines and anabolic steroids. Caffeine has remained popular for over a hundred years and anabolic steroids have been in steady use since the early 1960s.1Nevertheless, the magic elixir of sporting performance remains elusive. The search continues in the face of unsatisfactory results, adverse reactions and drug control efforts within sport and through legislation. With advances in drug development there is also the further hope that new drugs will be difficult for laboratories to detect. My aim in this article is to provide a brief review of some of the newer drugs that have become popular over about the past 10 years, providing, where possible, doses used, their International Olympic Committee (IOC) status, their adverse reaction profiles, and methods used to detect them. The best known of these newer drugs are the testosterone precursors, dihydrotestosterone, clenbuterol, growth hormone, insulin-like growth factor, insulin, erythropoietin and β-hydroxy-β-methylbutyrate. Unfortunately, there are few published data quantifying the present use of these drugs in Australia. The doses of drug taken are difficult to ascertain -- those in this article have been obtained largely from Internet searches. There are many difficulties in deciding whether a drug actually enhances sporting performance. While a laboratory study may find a small change in strength or some other physiological parameter such as maximal oxygen uptake, this may not translate to increased performance in actual competition. When considering adverse reaction profiles it must be remembered that most of the drugs mentioned here are not subjected to the postmarketing surveillance procedures used for newly released therapeutic drugs. It is necessary to rely almost entirely on reports by interested professionals or projections made from the known pharmacological properties of the drug. There are no data on the effects of these agents on developing fetuses, children or adolescents. Testosterone precursors The pathway of testosterone synthesis is shown in the Box. Testosterone precursors are taken with the aim of increasing testosterone levels without the need for testosterone injections, and also in the hope of foiling current drug detection methods. The most popular agents in this group of drugs are dehydroepiandrosterone and androstenedione. Dehydroepiandrosterone (DHEA) has been the subject of a recent comprehensive review in the Journal.2 This drug is a weak androgen that circulates in two interconvertible forms -- unconjugated DHEA and DHEA sulfate, the latter in higher concentration. The physiological role of DHEA remains unclear. Concentrations fall with age and it has been trialled as therapy in a wide variety of conditions with little evidence of a positive effect, apart from increasing well-being and sexuality (term derived from a psychometric questionnaire) in women with adrenal insufficiency.3 While one study showed an increase in lean body mass, this was not confirmed in another. There is one study of the effects of DHEA on strength and aerobic performance; a comparison of DHEA, androstenedione and placebo in 40 healthy middle-aged men did not show any advantage of the steroid precursors over placebo.4 The effects of long-term, high-dose administration are unknown.2 In Australia, there has been one high-profile case involving a footballer receiving DHEA for chronic fatigue syndrome. After legal argument, the player was allowed to continue playing if he ceased taking the drug.2 Androstenedione and related compounds, such as 5-androstenedione, 4-androstenediol, 5-androstenediol, 19-norandrost-4-enedione, 19-norandrost-5-enediol and 19-norandrost-4-enediol, have become extremely popular in the United States since baseball home run record holder Mark McGwire admitted using androstenedione.5 As with DHEA, androstenedione is used in an attempt to increase testosterone concentrations. There is a well-conducted, double-blind controlled trial evaluating the effects of androstenediones on endocrine function, body composition and strength. In the first part of this study, 10 people received 100 mg of androstenedione orally for two days, and then received the same regimen of placebo one week later; the effects on serum testosterone, luteinising hormone (LH) and follicle-stimulating hormone (FSH) were measured. In the second part of the study, 300 mg of androstenedione or placebo was given in a cyclical dosing regimen over eight weeks to 20 men, only one of whom had any previous experience in resistance training. Strength was assessed by a number of resistance exercises and training was standardised over eight weeks. Compared with placebo, androstenedione did not increase concentrations of free or total testosterone and did not increase strength or alter lean body mass, but it did increase serum concentrations of oestradiol. Levels of high-density lipoprotein (HDL) became depressed in the treatment group compared with pretreatment levels. While this study used lower doses than are often used by athletes, these results suggest it is unlikely that androstenedione increases sporting performance.6 While it did not evaluate sporting performance, one study found that 300 mg of oral androstenedione given to 14 volunteers caused a significant rise in testosterone levels.7 There was also considerable individual variation in the levels, which suggests variations in metabolism of the drug. Dose: Up to 1100 mg/day of DHEA; athletes take doses of androstenedione which exceed the dose used in these studies. IOC status: Banned (but androstenedione is not banned in major league American baseball). Adverse reactions: There do not appear to be any immediate clinically detectable adverse effects. Long term administration of testosterone precursors will reduce HDL, and so predispose some athletes to coronary disease. Elevated levels of oestrone and oestradiol could have effects on malignant processes and also cause gynaecomastia. Detection: The testosterone/epitestosterone (T/E) ratio in urine is used to detect exogenous testosterone. A ratio greater than 6:1 is usually taken as an indication of misuse. DHEA has been reported to increase the T/E ratio in some, but not all, studies. Doses as low as 50 mg for three days can alter the ratio to more than 6:1 in some, but not all, individuals, suggesting there may be individual differences in the metabolism of this drug.8 In addition to the T/E ratio there has been considerable progress in detecting exogenous testosterone by measuring the ratio of the carbon isotopes 12C and 13C. This method may become one of the major means of detecting steroid misuse in the near future. 5 Alpha-dihydrotestosterone 5 Alpha-dihydrotestosterone (DHT) is the principal active metabolite of testosterone and has a greater binding affinity to the androgen receptor than testosterone. It transforms more readily to the steroid receptor complex and dissociates from this complex more slowly than does testosterone. It is used to enhance performance in a variety of sports. DHT has been a licensed pharmaceutical in some countries and gained considerable prominence when 11 Chinese swimmers were found to have taken the drug in the 1994 Asian Games in Tokyo. There are no published data showing there is any effect on sporting performance. Dose: Probably greater than 25 mg twice daily, percutaneously. IOC status: Banned. Adverse reactions: While there are few data, it is reasonable to expect that typical androgenic adverse effects such as baldness in males, hirsutism in females and acne will occur. Detection: DHT does not alter the T/E ratio, but it can be detected by determining the ratios of other steroids to epitestosterone and LH.9 Clenbuterol Clenbuterol is a β2-agonist with a half-life of 35 hours which came to prominence during the Barcelona Olympics.10,11 It is marketed in some countries as a bronchodilator and is not approved for human use in Australia. There are excellent data showing that other β2-agonists allow asthmatic athletes to compete at international level, but few showing that these drugs improve strength or aerobic performance in people who do not have asthma. In animals large doses of clenbuterol have been shown to increase lean body mass.12 Athletes usually take clenbuterol to increase muscle mass, and it is taken orally in conjunction with anabolic steroids. There are no data showing clenbuterol alters athletic performance or strength in healthy people. Dose: Up to 60-120 mg/day may be taken in cycles of 6-12 weeks' duration. IOC status: Banned. Adverse reactions: Clenbuterol will produce a predictable tremor and tachycardia. There are anecdotal reports of sudden death in two bodybuilders.13 Detection: Clenbuterol can be easily detected in urine by mass spectroscopy. Erythropoietin Autologous and homologous transfusions, commonly known as blood doping, have been used to enhance performance since the 1970s. This practice received considerable prominence when some members of the 1984 United States Olympic cycling team confessed to receiving transfusions. Endurance athletes experience very complex physiological adaptations such as an increase in red cell mass and a decrease in haemoglobin concentration resulting from a considerable increase in plasma volume. It appears that aerobic performance is improved by blood transfusion in some circumstances.14The ready availability of synthetic erythropoietin (r-HuEPO) scandalised the 1998 Tour de France.15 This substance has been commercially available since that time and has essentially replaced transfusion as a means of blood doping. There is no doubt that rHuEPO can enhance physical performance in patients with anaemia secondary to renal failure. Both haemoglobin levels and physical performance were shown to have increased in 24 young healthy males who received r-HuEPO for seven weeks.16 As it seems to be widely accepted that r-HuEPO will increase aerobic performance, it is not surprising that it is widely misused in endurance sport. As the haematocrit may be measured to detect misuse, plasma expanders are sometimes used to avoid detection. Dose: Often three injections per week for six weeks. Vials contain varying concentrations, so doses are likely to vary considerably. IOC status: Blood transfusions and r-HuEPO are both banned. Adverse reactions: As dehydration will increase blood viscosity during any endurance event, the most serious adverse reactions to r-HuEPO seem likely to result from vascular events caused by thromboses when blood viscosity is markedly increased. However, there are no reported cases of this in the refereed literature. Sporting magazines and the lay press have reported deaths allegedly caused by r-HuEPO. These deaths have not occurred during exercise, but during periods of physical inactivity or sleep.17 Detection: Difficult because of its short half-life of 5-6 hours and the long duration of action on erythropoiesis. r-HuEPO differs from the endogenous hormone in its carbohydrate moiety, and this confers different physicochemical properties, thus allowing the potential for it to be detected in both blood and urine.18 Alternative methods of detection rely on measurement of various haematological and ferruginous parameters in capillary samples of blood.19,20 At present there are a number of studies under way to ascertain which of these methods would be fair to athletes and also stand up to the rigours of legal argument in the setting of a tribunal. On 1 August 2000, the Scientific Committee of the IOC approved a test based on urine and blood analysis (N Vance, Programme Manager, Doping Control, Sydney 2000 Olympics, personal communication). Insulin Insulin is an anabolic hormone, so it is not surprising that it has become popular in power sports. There are no studies showing an enhancement of sporting performance and, not surprisingly, there are reports of hypoglycaemia in users.21Insulin is often used in association with anabolic steroids. Clearly, medical practitioners need to be mindful of this area of misuse should unknown patients request renewal of a prescription for insulin. Insulin is also available in Australia without a prescription if the patient is prepared to pay the over-the-counter price, so this caution also applies to dispensing pharmacists. Dose: 2-15 U 20-40 minutes after exercise with a carbohydrate load, or as 10 U twice daily.22 IOC status: Allowed for athletes with insulin-dependent diabetes. Adverse reactions: Hypoglycaemia. Detection: There are numerous analytical methods of detecting insulin. No criteria have been set for insulin misuse in sport. Growth hormone Growth hormone (GH) has become popular since the advent of DNA-derived production removed concerns about human pituitary sources and Creutzfeldt-Jakob disease. Athletes usually take it in association with anabolic steroids. There is no doubt about the anabolic effects of the hormone -- the increase in muscle strength in hypopituitary patients receiving treatment and observations that the hormone is released in response to exercise. There is also no doubt that legitimate sources are being diverted into the sporting area.23 In spite of its widespread use there are no data showing an enhancement of sporting performance. One well conducted investigation in experienced training weightlifters showed that 14 days of growth hormone use did not alter protein synthesis or breakdown.24 Another study of exercising elderly men did not show any increase in strength.25 While muscle protein is probably not altered, a placebo-controlled trial showed that lean body weight increased as a result of decreasing body fat. In that study supraphysiological doses of GH were given thrice weekly for six weeks to eight progressive-resistance weight-trained athletes.26Dose: 2.1 U 2-4 times per week. Cycle length varies depending on availability, but is usually about six weeks. IOC status: Banned. Adverse reactions: Clinical acromegaly would be expected, yet a case has yet to be reported in the refereed literature. Detection: Difficult to detect in urine. The synthetic form can be detected by measurement of isoform ratios in serum,27 as recombinant GH manufacture produces only one isoform, while the pituitary releases principally the single 191 amino acid polypeptide chain with a molecular mass of 22 kDa, a smaller 20 kDa form and some smaller and larger forms. Insulin-like growth factors Insulin-like growth factor (IGF) production is principally regulated by GH. IGF is an important factor for some of the actions of GH, such as its anabolic and growth-promoting effects, but not its effects on carbohydrate and lipid levels, which are a direct action of GH on a GH receptor.28,29 At present there are few established clinical applications for IGF and, in sport, it is probably used less than growth hormone. There are no studies of IGF in sporting performance. Dose: Unknown. IOC status: Banned. Adverse reactions: No data from athletes. High-dose intravenous use causes hypoglycaemia; hypophosphataemia causing hypotension and asystole has been reported. Longer-term effects are parotidomegaly, facial pain, hand oedema, sinus tachycardia, gynaecomastia, Bell's palsy and avascular necrosis of the femoral head.28 Detection: Detecting IGF in urine is difficult and, as for GH, determining compound ratios in serum may be a means of detecting misuse. β-Hydroxy-β-methylbutyrate Infusions of some branched-chain amino acids will decrease protein breakdown in postoperative patients. This is probably the result of an inhibitory action on protein metabolism by metabolites of leucine such as a-ketoisocaproate.30 More recently, its further metabolite, β-hydroxy-β-methylbutyrate (HMB), has been considered to be more active in inhibiting protein breakdown. HMB is available as a food supplement in the US, which means that it avoids many of the regulatory hurdles that are required of a drug. A state of clinical deficiency of HMB is yet to be described. This substance has no approved use in Australia. It is currently widely used by athletes in a variety of sports and has no clinical applications in medicine at present. A randomised trial of doses of 0 g, 1.5 g and 3 g per day and three levels of protein supplementation in 41 subjects showed increases in strength during resistance training.31 A further study in eight cyclists has shown a small increase in maximal oxygen consumption.32 At present there are too few data to ascertain whether the compound has a positive effect on sporting performance and whether high doses have significant toxicity. Dose: Up to 15 grams/day are sometimes consumed. IOC status: Not banned. Adverse reactions: None have been described to date. Detection: Can be quantified in urine. Conclusions Despite the paucity of data showing that any of these drugs, except probably erythropoietin, have positive effects on sporting performance, they are used increasingly for performance enhancement. As toxicity and adverse reactions do not seem to deter such use, detection and its consequences appear to be the main deterrent in top-level sport. Detection methods therefore need to be constantly updated and enhanced, and possibilities in this area include the introduction of blood sampling, the use of carbon isotope ratios to detect anabolic steroid misuse, and widening the scope of out-of-competition testing. Doctors need to bear in mind that drug misuse is not restricted to elite athletes -- indeed, most drug use in sport occurs at a non-elite level. The possibility that a patient has used unusual drugs to enhance performance, and that this may be either causing or confounding the clinical state, should always be considered in athletes presenting with an unusual illness. Disclaimer While all efforts have been made to ensure the correct information about the IOC status of the drugs mentioned, this may vary between sports. The IOC status of any drug is subject to frequent revision. Athletes and coaches should check the latest status of any drug mentioned in this article with the relevant sporting body or with the Australian Sports Drug Agency. Acknowledgements I thank Ms Dianne James, Librarian, Manly Hospital. References Laura R, White S, editors. Drug controversy in sport. Sydney: Allen and Unwin, 1991: 1-4. Corrigan AB. Dehydroepiandrosterone and sport. Med J Aust 1999; 171: 206-208. Arlt W, Callies F, van Vlijmen JC, et al. Dehydroepiandrosterone replacement in women with adrenal insufficiency. N Engl J Med 1999; 341: 1013-1020. Wallace MB, Lim LA, Cutler A, Bucci L. Effects of dehydroepiandrosterone vs androstenedione supplementation in men. Med Sci Exercise Sports 1999; 31: 1788-1792. Yesalis CE. Medical, legal, and social implications of androstenedione use. JAMA 1999; 281: 2043-2044. King DS, Sharp RL, Vukovich MD, et al. Effect of oral androstenedione on serum testosterone and adaptations to resistance training in young men. JAMA 1999; 281: 2020-2028. Leder BZ, Longcope C, Catlin DH, et al. Oral androstenedione administration and serum testosterone concentrations in young men. JAMA 2000; 283: 779-782. Bowers LD. Oral dehydroepiandrosterone supplementation can increase the testosterone/epitestosterone ratio. Clin Chem 1999; 45: 295-297. Kicman AT, Coutts SB, Walker CJ, Cowan DA. Proposed confirmatory procedure for detecting 5 alpha-dihydrotestosterone doping in male athletes. Clin Chem 1995; 41: 1617-1627. Muscling in on clenbuterol [editorial]. Lancet 1992; 340: 403. Kamburoff PL, Prime FJ, Schmidt OP. The bronchodilator effects of NAB 365. Br J Clin Pharm 1977; 4: 67-71. Harahan JP, editor. Beta-agonists and their effects on animal growth and carcass quality. London: Elsevier Applied Science, 1987. Prather ID, Brown DE, North P, Wilson JR. Clenbuterol: a substitute for anabolic steroids? Med Sci Sports Exercise 1995; 27: 1118-1121. American College of Sports Medicine. The use of blood doping as an ergogenic aid. Med Sci Sports Exercise 1996; 28: 1-8. Peddling drugs to the pedal pushers [editorial]. Lancet 1998; 352: 415. Ekblom B. Blood doping and erythropoietin, the effects of variation in haemoglobin concentration and other related factors on physical performance. Am J Sports Med 1996; 24 (6 Suppl): S40-42. Leith W. EPO and cycling. Athletics Magazine (Willowdale, Ontario, Canada) June 1992: 24-26. Choi D, Kim M, Park J. Erythropoietin: physico- and biochemical analysis. J Chromatog 1996; 687: 189-199. Saris WHM, Sneden JMG, Brouns F. What is a normal red-blood cell mass for professional cyclists? [letter]. Lancet 1998; 352: 1758. Gareau R, Audran M, Baynes RD, et al. Erythropoietin abuse in athletes. Nature 1996; 380: 113. Willey WJ. Insulin as an anabolic aid? A danger for strength athletes. Physician Sports Med 1997; 25: 103-104. Dawson RT, Harrison MW. Use of insulin as an anabolic agent. Br J Sports Med 1997; 31: 259. Council on Scientific Affairs. Drug abuse in athletes. Anabolic steroids and human growth hormone. JAMA 1988; 259: 1703-1705. Yarasheski KE, Zachwieja JJ, Angleopoulos TJ, Bier DM. Short-term growth hormone does not increase muscle protein synthesis in experienced weight lifters. J Appl Physiol 1993; 74: 3073- 3076. Taaffe DR, Pruitt L, Reim J, et al. Effect of recombinant human growth hormone on the muscle strength response to resistance exercise in elderly men. J Clin Endocrinol Metab 1994; 79: 1361-1366. Crist DM, Peake GT, Egan PA, Waters DA. Body composition response to exogenous GH during training in highly conditioned adults. J Appl Physiol 1988; 65: 579-584. Wu Z, Bidlingmaier M, Dall R, Strasburger CJ. Detection of doping with growth hormone. Lancet 1999; 353: 895. Bach LA. The insulin-like growth factor system: Basic and clinical aspects. Aust N Z J Med 1999; 29: 355-361. Ascoli M, Segaloff DL. Adenohypophyseal hormones and their hypothalamic releasing factors. In: Goodman & Gilman's the pharmacological basis of therapeutics. 9th ed. New York: McGraw-Hill, 1996: 1363-1382. Sapir DG, Mackenzie W, Moyer ED, et al. Effects of alpha-ketoisocaproate and of leucine on nitrogen metabolism in postoperative patients. Lancet 1983; 1: 1010-1014. Nissen S, Sharp R, Ray JA, et al. Effect of leucine metabolite β-hydroxy-β-methylbutyrate on muscle metabolism during resistance-exercise training. J Appl Physiol 1996; 81: 2095-2104. Vukovich MD, Adams GD. HMB may improve Vo2peak [abstract]. Med Sci Sports Exerc 1997; 29: S252. Authors' details Department of Clinical Pharmacology and Toxicology, St Vincent's Hospital, Sydney, NSW. Michael C Kennedy, MD, FRACP, Physician. Reprints will not be available from the author. Correspondence: Dr M C Kennedy, Manly Non Invasive Cardiac Laboratory, 22 Darley Road, Manly, NSW 2095. drmkennATozemail.com.au Make a comment Back to text

Michael C Kennedy

Sports Medicine Deaths due to brain injury among footballers in Victoria, 1968-1999 Paul R McCrory, Samuel F Berkovic and Stephen M Cordner MJA 2000; 172: 217-219 Abstract - Introduction - Methods - Results - Discussion - References - Authors' details - - More articles on Sports medicine Abstract Objectives: To determine the frequency and nature of fatal brain injuries occurring in Australian football. Setting: State of Victoria, January to July 1999. Design: Retrospective case series of football-related deaths identified from the coronial autopsy records of the Victorian Institute of Forensic Medicine (1990-1999) and newspaper reports (1968-1989). Main outcome measures: Coronial autopsy findings and circumstances of injury. Results: 25 deaths associated with Australian football were identified, nine due to brain injury. Coronial findings in the brain-injury deaths were intracranial haemorrhage in eight patients and infarct in the territory of the middle cerebral artery in one. In three of four cases of subarachnoid haemorrhage, vertebral artery trauma was noted. In all but one case, injury occurred as an accidental part of play. Conclusions: The most common findings in deaths due to brain injury in Australian football were intracranial haemorrhage, including subarachnoid haemorrhage from vertebral artery injury. Introduction Traumatic brain injury is common in contact and collision sports. In Australian (rules) football the epidemiology of mild head injury has been well studied. Based on prospective studies, the incidence of concussion in professional play is about 4 per 1000 player hours or 1 per 125 player games.1,2 However, a concern for team physicians is the very rare possibility of severe brain injuries, including intracranial haematomas, sometimes complicated by diffuse cerebral oedema, leading to permanent neurological impairment or death.3-7 To our knowledge there is no systematic, published information on severe and fatal brain injury in any code of football in Australia. Our study aimed to determine the frequency and nature of fatal brain injuries that occurred in football played in the State of Victoria, comprising Australian football and rugby union, in the 32 years to 1999. Methods In Victoria, the Coroners Act 1985 (Vic.) requires all unexplained deaths or deaths due to accident or injury to be reported to the Coroner. In such cases, an autopsy is usually performed and the circumstances surrounding the death are investigated by the Coroner before a formal finding is made.8 The Victorian Institute of Forensic Medicine (VIFM) is responsible for providing pathology services and medical expertise to the Coroner. VIFM records from 1990 onwards are available on a computerised database, while earlier records are filed chronologically according to date of death and archived off-site. We performed a computerised search of the VIFM database for the period January 1990 to July 1999. A keyword search for the term "football" was used, noting where this word occurred in the coronial findings or the forms detailing the circumstances of the injury. Deaths of officials and spectators at football matches were excluded from the study. As pre-1990 VIFM records are not on a computerised database, we could not search by text word. Further, as they comprise more than 50 000 case records stored with limited accessibility, a manual search was considered logistically unfeasible. Instead, we searched the clipping libraries of the major daily Victorian newspapers (The Age, the Herald-Sun) for the period January 1968 to December 1996 for cases of football-related fatalities. Reported details of names, injuries and dates of events were compared against coronial case records. The original records of identified cases were extracted for analysis of the circumstances surrounding the injury and the neuropathological findings. The coronial autopsy always involved gross examination of the brain, but histological and detailed neuropathological examination was not always performed. When necessary, original hospital records were obtained for further details of injuries and neurosurgical findings. This study was approved by the VIFM Ethics Committee and by the Ethics Committee of the Austin & Repatriation Medical Centre, Melbourne, Vic. Results We identified 25 football-related deaths in the period 1968-1999. Fourteen of these occurred in the 10 years 1990-1999 and were found by computerised search of the VIFM database, while 11 occurred in the 22 years 1968-1989 and were found by newspaper searches. Both search strategies were used for the period 1990-1996, and each identified the same nine cases. Details of the 25 deaths are shown in the Box. All but three were in Australian rules players, with the remainder in rugby union players (Patients 9, 21 and 22). Nine deaths were due to brain injury, all but one in Australian rules players. The remaining 16 were due to other causes, predominantly unrecognised ischaemic or congenital heart disease. For the brain-injury deaths, coronial findings were intracranial haemorrhage (in eight patients) and infarct in the territory of the middle cerebral artery (in one). In three of four cases of subarachnoid haemorrhage, vertebral artery trauma was noted. Diffuse cerebral oedema was noted in five patients -- in conjunction with surgically treated subdural haematomas (Patients 2, 6 and 8), a large subdural haematoma that was not surgically treated (Patient 9), and infarct in the territory of the middle cerebral artery (Patient 7). Analysis of the circumstances of the fatal injury from coronial depositions, police records and newspaper reports suggested that all but one of the nine brain-injury deaths occurred largely because of accidental injury during normal play. In Patient 9, no injury was noted. Discussion This study adds to knowledge of the severe end of the brain-injury spectrum in Australian football. We identified nine deaths due to brain injury associated with Australian football in Victoria in the 32 years to 1999. The most common coronial finding was intracranial haemorrhage, including three cases of traumatic subarachnoid haemorrhage from vertebral artery injury. Determination of football-related deaths is limited in part by the difficulties of case ascertainment. Computerisation of Victorian coronial records began in 1990, and text-word searches are limited to this period. Mortality data based on death certification through the Australian Bureau of Statistics do not adequately identify injury risk factors such as sport participation. We used a novel case-ascertainment method -- searching newspaper records -- on the assumption that deaths from football are likely to be "newsworthy" and that the reports are likely to contain narrative details of the incident. Indeed, we found that when the searches overlapped (1990-1996), the two methods had identical case ascertainment (nine cases). The presence of diffuse cerebral oedema was noted in five cases, all of which were associated with a major intracranial lesion. The mechanism of the middle cerebral artery territory stroke was not established at autopsy. However, given that hemiplegia was evident within minutes of the injury, it was more likely to have been caused by a traumatic middle cerebral artery occlusion than by raised intracranial pressure. An area of concern shown in epidemiological studies of football injury is the higher concussion rates that occur in elite junior competitive football (age under 18 years) compared with senior levels of competition.9-11 It has been postulated that junior players may not have fully developed the necessary evasive strategies to avoid the elements of the game that put them at risk of brain injury. In our study, three of the nine fatal brain injuries were in teenagers and were associated with vertebral artery injury. Traumatic vertebral artery dissection is the most common reported mechanism of stroke in sport.12 The combination of unilateral neck pain or headache after head or neck trauma should prompt suspicion of vertebral artery dissection, even in the face of seemingly trivial trauma.12 Focal neurological signs, such as vertigo, diplopia, ataxia, dysarthria, cranial nerve palsies or altered mental function, should be an absolute indication for urgent neurological consultation and hospital admission.13 Our results show that, although Australian football has one of the highest participation rates of sports in Victoria, the potential for fatal brain injury is extremely low. We did not identify any risk factors that could be modified to prevent brain injury. All team physicians, regardless of the level of participation, need to be conversant with the appropriate clinical pathways for the safe and efficient triage of neurologically injured athletes.14 Many deaths were due to cardiac causes, such as congenital cardiac disease, unrecognised ischaemic cardiac disease and commotio cordis (sudden death due to low-energy trauma to the chest wall, mechanism unknown, but presumed to be arrhythmia). The first two occurred mostly in teenagers, whereas the last occurred exclusively in players aged between 35 and 44 years. A high frequency of ischaemic cardiac death in football has also been observed in Aboriginal players in the Northern Territory.15 Pre-participation medical screening should be considered by football administrators throughout the country for high-risk groups. The role of a body to monitor injury over a range of sports in this country should also be considered. Although sport-related deaths are few, detecting injury patterns and identifying injury risk factors are important to ensure safe participation in sport. This task will be easier once the National Coroners' Information System, administered by the Monash University National Centre for Coronial Information, becomes fully functional in six to 12 months' time. References Seward H, Orchard J, Hazard H, Collinson D. Football injuries in Australia at the elite level. Med J Aust 1993; 159: 298-301. McCrory P. Neurological injuries in rugby and Australian rules football. In: Jordan B, Tsaris P, Warren R, editors. Sports Neurology. 2nd ed. Philadelphia: Lippincott-Raven Publishers; 1998: 441-449. Jennett B. Epidemiology of head injury. J Neurol Neurosurg Psych 1996; 60: 362-369. Jordan B, Tsaris P, Warren R, editors. Sports neurology. 2nd ed. Philadelphia: Lippincott-Raven Publishers, 1998: 45-71. Adams J. Head injury. In: Adams JH, Duchen LW, editors. Greenfield's neuropathology. 5th ed. London: Oxford University Press, 1992: 106-152. Cantu RC, Voy R. Second impact syndrome: a risk in any contact sport. Phys Sportsmed 1995; 23: 27-34. McCrory PR, Berkovic SF. Second impact syndrome. Neurology 1998; 50: 677-683. Breen K, Plueckahn V, Cordner S. Ethics, law and medical practice. Sydney: Allen and Unwin, 1997. Orchard J, Wood T, Seward H, Broad A. Comparison of injuries in elite senior and junior Australian football. J Sci Med Sport 1998; 1: 83-88. McMahon KA, Nolan T, Bennett CM, Carlin JB. Australian Rules football injuries in children and adolescents. Med J Aust 1993; 159: 301-306. National Health and Medical Research Council. Football injuries of the head and neck. Canberra: NHMRC, 1995. McCrory P. Stroke in athletes. In: Cantu R, editor. Neurologic athletic head and spine injuries. Philadelphia: WB Saunders and Co, 2000. In press. Showalter W, Esekogwu V, Newton K, Henderson S. Vertebral artery dissection. Acad Emerg Med 1997; 4: 991-995. McCrory PR. Were you knocked out? A team physician's approach to initial concussion management. Med Sci Sports Exerc 1997; 29 (7 Suppl): S207-S212. Young M, Fricker P, Thomson N, Lee K. Sudden death due to ischaemic heart disease in young Aboriginal sportsmen in the Northern Territory, 1982-1996. Med J Aust 1999; 170: 425-428. (Received 12 Jul 1999, accepted 21 Jan 2000) Authors' details Department of Medicine (Neurology), University of Melbourne, Austin and Repatriation Medical Centre, Melbourne, VIC. Paul R McCrory, FRACP, FACSP, Neurology Research Fellow; Samuel F Berkovic, MD, FRACP, Professor. Department of Forensic Medicine, Monash University, and Victorian Institute of Forensic Medicine, Melbourne, VIC. Stephen M Cordner, FRCPA, FRCPath(UK), Professor and Director. Reprints will not be available from the authors. Correspondence: Dr P R McCrory, 31 Grosvenor Parade, Balwyn, VIC 3103. pmccroryATcompuserve.com Make a comment Football-related deaths* in Victoria, 1968-1999 Patient Age (years) Details of injury Time to death Coronial findings Brain Injury 1 15 Accidental blow to neck when shepherded during play, fell to ground unconscious and died in hospital 6 hours Traumatic subarachnoid haemorrhage from vertebral artery injury, subdural haematoma 2 17 Accidental knock to the head during game, complained of tinnitus and headache, found unconscious next morning; craniotomy performed because of computed tomography evidence of extradural haematoma 16 hours Extradural and subdural haematomas cerebral contusion, cerebral oedema noted postoperatively 3† 19 Collision during normal play, no head contact reported, collapsed several minutes later and died in hospital 1 day Traumatic subarachnoid haemorrhage from vertebral artery injury 4 20 Accidental blow to occipital region during match, immediate collapse and declared brain dead at hospital 1 day Traumatic subarachnoid haemorrhage from vertebral artery injury 5 21 Forearm to face in tackle during match, may have subsequently hit head on ground, immediately confused and then suffered generalised seizure 2 days Subarachnoid haemorrhage (no comment on vertebral artery findings), cerebral contusion 6† 24 Accidental clash of heads during match and died in hospital after craniotomy 3 days Extradural haematoma, cerebral oedema noted postoperatively 7 26 Accidental knock to the back of the head while marking ball, noted to be "dazed" by team mates and collapsed about 10 minutes later; described as hemiplegic at that time 3 days Cerebral oedema, middle cerebral artery territory infarction 8† 36 Collision during play, fell backward hitting head on ground, immediately unconscious followed by respiratory arrest; craniotomy performed in hospital 6 hours Large subdural haematoma, cerebral noted oedema postoperatively 9† 41 Rugby union player, collapsed during match; no obvious trauma 4 hours Large subdural haematoma, cerebral oedema Other causes 10† 16 Collapsed after a football game, past history of heart problems DOA Hypertrophic obstructive cardiomyopathy with acute cardiac failure 11 19 Collapsed at football during game DOA Hypertrophic obstructive cardiomyopathy with acute cardiac failure 12 16 Collapsed and died during game DOA Myocardial ischaemia and arrhythmia associated with congenital aortic valve stenosis 13 19 Collapsed and died at football during match DOA Anomalous origin of left coronary artery 14† 20 Collapsed on field, no obvious trauma DOA Anomalous origin of left coronary artery 15 19 Bumped on chest during play, took kick and then collapsed, unable to be revived DOA Commotio cordis‡ 16† 19 Hit on chest in collision, took free kick then collapsed DOA Commotio cordis 17 24 Hit in the chest and collapsed DOA Commotio cordis 18 35 Collapsed and died during game DOA Coronary artery occlusion 19 37 Collapsed and died during game DOA Coronary artery occlusion 20† 37 Collapsed and died during game DOA Coronary artery occlusion 21† 43 Rugby union player, collapsed and died during game DOA Coronary artery occlusion 22† 44 Rugby union player, collapsed and died during game DOA Coronary artery occlusion 23† 24 Collision followed by respiratory distress DOA Acute asthma complicated by tension pneumothorax 24 22 Collision during match DOA Liver rupture and haemorrhage 25 18 Collapse during football match; no obvious trauma DOA No obvious abnormalities, neuropathological findings DOA=dead on arrival at hospital. *All deaths were associated with Australian rules football unless otherwise stated. †Deaths in the period 1990-1999, found by computerised database search. ‡ Sudden death after low-energy trauma to the chest wall, characteristically with no structural damage to the chest wall, thoracic cavity or heart -- mechanism unknown, presumed arrhythmia. 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Paul R McCrory · Samuel F Berkovic · Stephen M Cordner

Water Hazards Dead in the water: how safe are our water sports? We now have the Australian Water Safety Council and its National Water Safety Plan: the impact of these initiatives remains to be seen MJA 1999; 171: 584-586

Robyn M Walker

Water Hazards Patterns of drowning in Australia, 1992-1997 Ian J Mackie MJA 1999; 171: 587-590 For editorial comment, see Walker Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on Public and environmental health Abstract Objective: To determine patterns of victims, circumstances and locations of drownings in Australia in 1992-1997, inclusive. Methods: Population figures and available details of all drownings were obtained from the Australian Bureau of Statistics. Accidental non-boating drownings (ICD E910), boating incidents (E830-832), homicide (E964), suicide (E954), and other deaths without a drowning E code but "flagged" because drowning was involved (although not the primary cause of death) were included. Results: The overall accidental non-boating drowning rate was 1.44/100 000 population/year. The commonest sites for non-boating drowning were ocean or estuary (22%), private swimming pools (17%), non-tidal lakes and lagoons (17%), surfing beach (10%) and bathtub (7%). 22% of victims were aged under 5 years; this group had a drowning rate of 4.6/100 000 population/year. Very few young children drowned in the ocean or in boating incidents. The rate of boating drownings was 0.29/100 000 population/year. Overseas tourists comprised 4.7% of all non-boating drownings, 18% of surf and ocean drownings, and 25% of all scuba drownings. Indigenous people had a much higher drowning rate than the general population. Conclusions: Drownings in children aged less than 5 years continue to be the greatest challenge for water safety organisations and legislators. Drownings in the Indigenous community and among tourists requires more detailed study and action. To assist in developing preventive strategies, the National Water Safety Council will need to clarify the categories described as "ocean/estuary" and " lake, lagoon, dam and waterhole". Introduction Accidental drowning is a largely preventable cause of death. Water safety organisations, the general public and legislators need adequate information about the circumstances of drowning to target preventive action effectively. While the 1993 National Drowning Study concluded that the risk of accidental drowning in Australia and other countries has steadily decreased since 1920,1 that study and a later report2 did not provide detailed national information on where drownings occurred. Although the Australian Bureau of Statistics (ABS) has provided figures on accidental drownings in Australia dating from 1920, it has only reported the locations of accidental drownings since 1992. Currently, drowning is classified under the International Classification of Diseases (ICD) Supplementary classification of external causes of injury and poisoning codes.3 The relevant "E" codes and brief descriptions are shown in Box 1. In addition to the E codes, in 1992 the ABS introduced a nationally consistent system of "flags" for all drownings and other conditions where drowning is cited as one of two or more causes of death, but not the primary cause. These flags form the basis of specialised drowning tables in which flags 1-36 are for non-boating drownings and flags 37-53 are for various boating deaths. In this study, I examined both the international E codes and the ABS flag system4 to present new data which may help target those most at risk in the different locations where drownings occur. Methods Figures on accidental drownings in Australia from 1992-1997, inclusive, were obtained from the ABS. Accidental non-boating drownings (ICD E910: "Accidental drowning and submersion") were divided into locations and activities, which were then examined separately for age and sex distribution. Boating incidents (E830-832), homicide (E964), suicide (E954), and other deaths without a drowning E code but with the drowning flag applied were also studied. Implementation issues in 1992 and 1993 resulted in very slight discrepancies in drowning figures between the "E" code and "flag" systems. Five groups were subjected to detailed analysis. These were children aged under five years, people aged over 65 years, Indigenous people, overseas tourists, and those who drowned in the bathtub. Results Overall, 2673 people drowned in Australia in 1992-1997. These included 1551 non-boating drownings (E910; see Box 2), 292 drownings in boating incidents (E830-832; see Box 3), 390 suicides in the water (E954), and 28 homicides (E964), as well as several accidental drownings that appeared under a "drowning flag" rather than an E code (46 people with epilepsy who drowned, 13 who drowned because they had a heart attack or stroke while in the water, and 86 who drowned in motor vehicles accidents in the water). The remaining 267 deaths were "incidental" drownings -- generally those for which the coroner could not decide on a classification. The distributions of locations of all Australian accidental non-boating drownings and for selected groups are shown in Box 4, as is a summary of features of drowning deaths for children aged under five years, people aged 65 or more years, Indigenous people and overseas tourists. The age and sex distribution and detailed findings for bathtub drownings are shown in Box 5. Discussion Overall, this study shows that children aged under five years are most vulnerable to drowning in Australia. It also shows, with data not previously presented, that a considerable number of overseas tourists drown in our waters, and that the frequency of drownings of Indigenous people is disproportionately high, with an unusual number of drownings in young men. Twenty-two per cent of all drowning victims are in the 0-4-years age group, although this group comprises only 7% of the population. The rate of drownings in this age group (4.6 per 100 000 population per year) for 1992-1997 has changed little from that for 1986-1990 (4.7 per 100 000 population per year).1 It is thus clear that the high frequency of drowning in very young children is not improving. The figures provide strong backing for the recommendations of Nixon and colleagues,2 which were compilation of better coronial information, better police investigation of toddler drownings to include information on fencing and other vital details, detailed study of adolescent drownings, investigation of surveillance methods, support for advocacy of fencing of swimming pools, community education on the dangers of mixing alcohol with aquatic activities, and making first aid training mandatory for all pool owners. In particular, legislation on fencing for private pools is inadequate -- it varies from State to State, and local government areas have their own rules which are not always enforced. There is a real need for uniform national legislation for pool fencing that complies with the recommendations of the Australian Standards Association to help arrest this high rate of drowning in very young children. Details of drownings involving overseas tourists have not previously been published, and this is clearly an area in which government must work through the Water Safety Council to reduce the risk. Tourists and new migrants must be provided with suitable information and perhaps increased supervision when near the ocean. The ocean and recreational snorkelling or scuba diving present the greatest risks for tourists. Drowning in Aboriginal and Torres Strait Islander people also requires urgent government action through the appropriate established organisations. Differences in drowning incidence in different racial groups have been previously documented.6-8 The pattern of drownings in the Australian Indigenous population (Box 4) is quite different from that of the population as a whole, with a very high incidence in children under five years and in the 25 to 34 years age group. Further, ABS advice indicates that "death data for indigenous persons is undernumerated. While indigenous status is now a question on all State and Territory death forms, the ABS only regards data for South Australia, Western Australia and Northern Territory as having sufficient coverage to be of publishable standard" (ABS, personal communication). Bathtub drownings are disturbingly common on a national basis and preventive approaches need to vary for different age groups. The frequency of infant and toddler bathtub deaths has been documented in State reports for two decades,1 but this is the first national survey. The bathtub is the only site where female deaths predominate. This has been reported in previous studies,1 but the reasons for this phenomenon are not apparent. Most bathtub deaths require much more careful forensic scrutiny than they have received to date in most countries. Carbon monoxide, epilepsy, drugs and alcohol, cardiac arrest, suicide, homicide and child abuse have all been implicated, and there is little doubt that death in the bathtub at any age should be investigated carefully to determine whether the cause was natural or deliberate. Confirmation of true accidental drowning in bathtubs may be less common with such an approach. The quality of the information available needs to be improved to help target preventive action. For example, as pointed out previously,4 reliance solely on E codes would result in many drownings remaining unidentified. There were 80 drownings in motor vehicle accidents and a large number of suicides (390, making suicide more common than drowning in boating accidents [292]), and others, such as deaths from myocardial infarction, stroke and spinal injuries, where the involvement of drowning was only obvious from the ABS flag system. Further, there is a lack of detailed information on drownings listed within the E codes. "Lake, lagoon, dam and waterhole" and ocean/estuary drownings cover many different locations requiring different preventive measures -- this needs further investigation by the recently formed National Water Safety Council in conjunction with coroners, police and the National Injury Surveillance Unit. The most comprehensive review of measures to prevent drowning in Australia was published in 1995 by the Commonwealth Department of Human Services and Health, and contains most of the references of importance up to that time.2 The data for 1992-1997 in this study will provide the new National Water Safety Council with added information to assist more informed targeting of individual risk groups in specific areas. Acknowledgements I received great assistance from the officers of the Australian Bureau of Statistics, the executive officers of the Royal Life Saving Society Australia and Dr George Stathers. Purchase of the statistical computer disk with relevant data was funded by the Royal Life Saving Society Australia. References Mackie I, Tebb N, Eady T. National drowning study, Parts 1 to 4. Sydney: Royal Lifesaving Society Australia, 1993. Nixon J, Pearn J, Oldenburg B, Pitt W. Review of countermeasures to reduce drowning, near drowning and spinal injuries fron diving into shallow water. Canberra: Commonwealth Department of Human Services and Health, 1995. Department of Health and Human Services. The international classification of diseases, 9th revision, clinical modification (ICD-9-CM). 5th ed. Vol. 1: Diseases tabular list, October 1994. Bethesda, Md: United States DHHS (Publication No. PHS 94-1260). Smith G, Langley J. Drowning surveillance: how well do E codes identify submersion fatalities. Injury Prevention 1998; 4: 135-139. Australian Bureau of Statistics. Population by age and sex. Canberra: ABS, 1997. (Catalogue no. 3201.0.) Dietz P, Baker S. Drowning: epidemiology and prevention. Am J Public Health 1974; 64: 303-312. Branche C. Who drowns in the United States? Proceedings of International Medical-Rescue Conference. San Diego: International Lifesaving Federation, 1997. Mael F. Staying afloat: within-group swimming proficiency for whites and blacks. J Appl Psychol 1995; 80: 479-490. (Received 5 May, accepted 28 Oct, 1999) Authors' details Royal Life Saving Society Australia, Sydney, NSW. Ian J Mackie, AM, FRACP, National Medical Adviser. Reprints: Dr I J Mackie, PO Box 280, Cronulla, NSW 2230. ianmackieATmsn.com.au 1: International Classification of Diseases (ICD) Supplementary classification of external causes of injury and poisoning codes relating to drowning*E830Accident to watercraft causing submersionE832Other accidental submersion or drowning in water transport accidentE910Accidental drowning and submersionE954Suicide and self-inflicted injury by submersion (drowning)E964Assault by submersion (drowning)E984Submersion (drowning) undetermined whether accidentally or purposefully inflicted.*Drowning is defined by the Medical Commission of the International Lifesaving Federation as death resulting from suffocation within 24 hours of submersion in a liquid medium. Back to text2: Accidental non-boating drownings in Australia in 1992-1997 (E910) Overall There were 1551 drownings, a national rate of 1.44 per 100000 population per year (based on 1996 population data5) 77% of victims were male. Of 1096 victims aged over 14 years, the presence of drugs including alcohol was recorded in 148 (14%); 117 of these were male. The highest prevalence was in the 0-4 years age group Males made up 64% of the 0-4 years age group and 62% of people aged over 64 years who drowned. Locations of drownings Most non-boating drownings (22%) occurred in ocean/estuary (tidal) sites. - 90% of the victims were male and very few were aged under 15 years. 17% of drownings occurred in private swimming pools. - 64% involved children aged under four years, two-thirds of whom were male. - Of all those aged over 34 years who drowned in private pools, 63% were female. - Only 3% of accidental drownings occurred in public and "other" pools (28 drownings in public pools [20 males] and 18 in "other" pools [11 males]). 17% of drownings occurred in non-tidal lagoons and lakes. - 82% of victims were male, and there was a high frequency of drownings in 0-4-year-olds. 10% of drownings (162) occurred at surfing beaches. - 144 victims (89%) were male. - No one aged less than 5 years and few aged 5-14 years drowned at a surfing beach. 5.8% of drownings occurred while victims were fishing. - They comprised 54 victims (one female), all aged over 15 years, who were washed from rocks, and another 36 people (35 male) who drowned in tidal water. - The only female was 10 years of age, one male was four years old; there were no drownings in males aged 5-14 years, then deaths were relatively evenly distributed for age, with the greatest number, eight, in the over 65 years age group. 3.6% of the 1551 people drowned while using scuba equipment. - 44 (79%) were male, 15 (27%) were overseas tourists. - 36% of scuba deaths occurred in Queensland, 21% in Western Australia and 18% in New South Wales. 15 people drowned while snorkelling (11 males, 3 overseas tourists). 36 people (34 males) drowned while attempting rescues; 12 in surf, one in a public pool and 23 at other sites. Back to text 3: Drowning in boating incidents in Australia in 1992-1997 (E830, E832) There were 292 boating drownings, an average of 52 per year and a rate of 0.29 per 100000 population per year 94% of victims were male. The presence of a drug was reported in 7% of victims, all aged between 35 and 54 years (alcohol in 19, and a different drug in two others). Back to text 4: Drownings in selected groups Children aged <5 years There were 353 drownings in this group (64% boys), a rate of 4.6 per 100000 population/year. - In addition to the locations shown, 6% of toddlers drowned in an object such as a bucket and 2% drowned in an irrigation canal. - 37 infants (22 boys) drowned in their first year of life, 26 in the bathtub, 4 in a private pool, 3 in an object such as a bucket, 2 in a lake, 1 in the ocean and 1 in an irrigation canal. People aged 65+ years 12% of all accidental drowning victims were in this group (38% were women), a rate of 1.5 per 100000 population/year. - More women than men drowned in pools (22 v.11) and bathtubs (18 v. 4). Indigenous people The 63 non-boating drownings of Aboriginals and Torres Strait Islanders represent 4.2% of the national total, while they constitute only 1.8% of the population. - 30% of all Indigenous drownings were in the 25-34 years age group (95% of these male). - Only 7 Indigenous people drowned in boating incidents. All victims except one were in motorised craft; all were male. Overseas tourists 88 tourists from 12 countries drowned in Australia during 1992-1997 (age range, 3-78 years; 16 female) - 73 drowned in non-boating incidents, 5 in boating incidents and 10 in unspecified circumstances. - 38 tourists came from Europe (15 from the United Kingdom, 10 from Germany), 35 from Asia (17 from Japan), 7 from the United States and 8 from other countries. - 89% of tourists drowned in the ocean and 11% drowned in fresh water. 61% drowned at surfing beaches or elsewhere in the "ocean" and a further 24% drowned while scuba diving or snorkelling. Tourist drownings comprised 4.7% of non-boating drownings, 18% of surf and ocean drownings, 25% of scuba and snorkelling drownings and 1.6% of boating drownings. Back to text 5: Bathtub drownings in Australia, 1992-1997 There were 112 bathtub drownings (64 female [57%]). Bathtub drownings comprise 7% of all drownings. 47% of victims were aged <5 years. 20% of victims were aged over 64 years. Alcohol was present in 14% of victims aged over 15 years. Of these, all except one were aged over 60 years. An unspecified drug (but no alcohol) was detected in three younger people who drowned in the bathtub. Back to text

Ian J Mackie

Water Hazards Snorkelling deaths in Australia, 1987-1996 Carl W Edmonds and Douglas G Walker MJA 1999; 171: 591-594 For editorial comment, see Walker Abstract - Introduction - Methods - Results - Discussion - Acknowledgments - References - Authors' details - - More articles on Travel, aviation and underwater medicine

Carl W Edmonds · Douglas G Walker

Water Hazards Scuba diving medical examinations in practice: a postal survey Graham Simpson and David Roomes MJA 1999; 171: 595-598 For editorial comment, see Walker Abstract - Introduction - Methods - Results - Discussion - References - Authors' details - - More articles on Travel, aviation and underwater medicine

Graham Simpson · David Roomes

To the Editor: My first reaction to reading "On dry land" (in In this Issue, in the 5 April issue of the Journal1) was to ask myself, "hang on, isn't the Australian Medical Association (AMA) based in Canberra now, and surely Canberra wouldn't be crowing about the superiority of its winters over Melbourne's?". Then, of course, a quick look at the first page of that issue revealed that the Journal is published in . . . surprise, surprise ... Sydney! It seems that The Medical Journal of Australia is as Sydneycentric as the ABC: "Most of us [my italics] have long suspected that Aussie Rules football should not be played outside of Melbourne". Most Sydneysiders, perhaps (although you may want to look at the number of people attending matches played by the Swans compared with those at rugby league games before you get too confident), but, in any case, Australian Rules has completely dominated football south and west of the Murray River. This is an area which contains nearly half of Australia's population, and, more importantly, nearly half of the members of the AMA. You then proffer the gratuitous insult that knee injuries could be reduced if "grounds were prepared with constant watering and little exposure to the sun -- simulating the conditions of a typical Melbourne winter!". I wonder if the same terms would have been used if the In this Issue item had been written more recently, in light of Sydney's weather in the last few months compared with Melbourne's glorious autumn and mild early winter. A David Grounds Physician Richmond, VIC 1. On dry land [In this Issue]. Med J Aust 1999; 170: 191. In reply: We stand castigated for our Sydneycentricity. Grounds' observations about the weather in the two cities during the 1999 football season aroused some curiosity in our editorial office, so we obtained the recent weather statistics (derived from Bureau of Meteorology data) from a very helpful Western Australian website.1 As the Figure shows, Sydney, although slightly warmer, had a much wetter six months in 1999. Further, the statistics for average rainfall between 1840 and 1989 show that Sydney's football season is always wetter than Melbourne's. So, it seems the answer to where we would rather spend winter, and which football code we would rather support, lies not in the weather... Whether the weather be fine, Or whether the weather be not, Whether the weather be cold, Or whether the weather be hot, We'll weather the weather, Whatever the weather, Whether we like it or not! Anon Comparison of (a) average temperatures (minimum/maximum) and (b) total monthly rainfall for Melbourne and Sydney in the 1999 football season. Ruth M Armstrong Assistant Editor The Medical Journal of Australia 1. Australian Weather Statistics. <http://cygnus.uwa.edu.au/~cloader/weather//>

Sports Medicine Ethics of prescribing drugs to enhance sporting performance Crossing the line between good medicine and cooperating with unhealthy or illegal behaviour Michael C Kennedy and Judith R Kennedy MJA 1999; 171: 204-205 See also Corrigan Introduction - What should be done for athletes - Patient autonomy - Harm minimisation - Acknowledgements - References - Authors' details - - More articles on Sports medicine Introduction There are two groups of people who undertake sporting activity while taking drugs. The first are those who require medication for chronic conditions such as hypertension and hyperlipidaemia, in specific circumstances such as paraplegia or organ transplant, or for acute intermittent conditions such as inflamed joints, infections and injuries. The second group comprises healthy people who take drugs to enhance sporting performance. We include bodybuilders in this category. Doctors are always the prescribers for the first group and are often the prescribers for the second.1 In this article, we provide an overview of ethical practice when consulted by individuals in this second category. The use of drugs for enhancing sporting performance is widespread and has been documented in Europe, North America and Australia.2-5 Some drugs seem to have enduring appeal, while others come and go in fashion. Anabolic/androgenic steroids (AAS) have been popular for over four decades; in 1990, an estimated one million people in the United States were either current or former users of AAS.6 Over the past 15 years there has also been a steady increase in the use of growth hormone,7 erythropoietin8 and insulin.9 The use of stimulants is still common, although the popularity of amphetamines has decreased since the 1960s. The media's focus on high-profile athletes who test positive for a banned substance overshadows the pattern of use: most non-therapeutic drug use is at the non-competitive, non-elite level of sport where there is no drug testing.6 Particularly troubling is the use of AAS on and by adolescents2,3 and the known connection between some of the drugs and myocardial infarction, stroke and psychiatric episodes in apparently healthy athletes.10,11 It is therefore important that doctors carefully consider their actions before prescribing drugs to those who wish to enhance their sporting performance. The doctor's purpose should be no more than assessment of the clinical state and the management of this as best suits the patient within prevailing social and ethical constraints. There is no authority for either the patient or the doctor to widen the purview to include the creation of social rights, coaching in how to cheat, or violating regulations.12 What should be done for athletes It is important to incorporate questions about sporting activities into clinical history-taking. Before prescribing to athletes, the following points should be routinely addressed: Banned drugs: If the athlete is competing at competition level it is essential that care be taken to avoid a drug on the banned list. Mistakes can be easily avoided by checking the drug details in publications such as MIMS or the Drugs in sport handbook2 (published by the Australian Sports Drug Agency [ASDA], or by contacting the ASDA hotline on 1800 020 506). Exposure conditions: Doctors should be aware that athletes will often expose themselves to extremes of endurance, so care is needed when using agents such as non-steroidal anti-inflammatory drugs, prochlorperazine and pseudoephedrine, which can affect heat regulation or cardiac rhythm. Patients should also be informed of the effects a drug may have on their sporting performance per se. For example, if β-blockers are medically indicated, the trade-off will be a decrease in aerobic performance. Professional competence: It is the responsibility of each prescriber to know the pharmacological facts about a drug and the medical facts about the patient. For example, AAS are not only widely abused, but also are a drug group about which there is much published information. A healthy athlete has no medical condition that will require prescribing of AAS, which will worsen, not improve, tendon and muscle injuries.13 There are no studies showing that AAS enhance skilled performance. There are data showing AAS increase muscle size and strength,14 although these data need to be interpreted conservatively.15 There are also a number of predictable adverse reactions that occur with their use, such as acne and gynaecomastia.10In the absence of a clinical reason for prescribing drugs, and in the presence of good clinical reason for not doing so, any case for prescribing a drug must then rely on over-riding, non-medical considerations. The patient-autonomy and harm-minimisation arguments are the most ethically powerful of these. Patient autonomy Patient autonomy is the right to self-determination. Starting with this notion, it is argued that non-medical use of drugs is simply a matter of personal liberty and individual experimentation: if athletes are aware of possible adverse reactions and are willing to accept the risks in the hope of other rewards, there should be no prohibition on doctors' prescribing. It follows that the doctor's task is merely to ensure informed consent. Clearly, society does not agree with this argument. Prescribing is restricted to those with both clinical and pharmacological knowledge for good reason -- the expectation is that there will be a causal link between specific drug use and clinical benefit. Predictable negative effects -- and, for athletes, this may be exclusion from competition -- are traded off against the required medical outcome. There is no suggestion that medical practitioners should do whatever the patient asks. We are not obliged to prescribe a drug simply because it has been asked of us. Another important issue needs to be considered in relation to autonomy: athletes are in an environment where competition is fierce and selection is never assured. Therefore, they may be in no position to object to proposed medical interventions and sports-health supervision by doctors who are not their usual practitioner. An extreme example of the type of abuse possible under these circumstances occurred in the former German Democratic Republic.16 One lesson from this is that it may be difficult for an athlete to refuse even seemingly innocuous procedures such as vitamin injections or the taking of supplements to "boost the immune system" when suggested by those in official positions. Respect for the athlete's autonomy requires that administration of substances occurs only when the athlete is fully informed and truly free to refuse. Harm minimisation The harm-minimisation argument is that some athletes will take drugs irrespective of whether supervised or not, and that giving drugs under medical supervision potentially results in less harm as there is control over the quality of the drugs supplied and early detection and treatment of adverse reactions. The controlled use of heroin in registered addicts is one example of the application of the harm-minimisation argument in medicine.17 However, this model is not applicable to drugs in sport. Both types of drug-taking may involve unfortunate victims and major criminal and financial enterprises,18 but there the similarity ends. In contrast to heroin, little is known of the pharmacokinetics and pharmacodynamics of high doses of AAS taken as single agents. There is even less knowledge of their pharmacokinetics and pharmacodynamics when taken in various multiple doses ("stacking") or in increasing doses ("pyramiding"). In addition, experience has shown that when a doctor prescribes low doses of AAS, this may lead to the prescriber's being used as one of a number of sources of supply.19 Under these circumstances, the doctor faces a new dilemma when an adverse reaction follows: to cease prescribing the offending agent or to prescribe yet another drug (for example, tamoxifen when oestrogenic side effects occur). The absurdity of this argument becomes evident when extended to justify prescribing insulin, erythropoietin or amphetamines. Respect for the general principle of autonomy and individual freedom means an acceptance that individuals -- both doctors and patients -- "own" their actions and are responsible for what they do. Athletes can request what they like, but doctors need not comply. Non-maleficence means that medical actions must cause as little harm as possible, not that medical skills should be used to fine-tune enterprises of harm. If approached about prescribing drugs to enhance sporting performance, the proper medical response is to provide accurate information and advice in a non-judgemental manner. If the patient has been or is exposed to a known health risk it is reasonable to diagnose and treat any ill-effects. This applies to drug use as much as it does to smoking, and does not require crossing the line between good medicine and cooperating with behaviour that is unhealthy, illegal or just plain wrong. If requested to prescribe drugs to enhance sporting performance the proper response is to refuse. Saying "no" to unreasonable requests is not always easy, but to do otherwise is to miss the point of what practising medicine is all about. Acknowledgements Ms Dianne James, Librarian, Manly Hospital, Manly, NSW. References Copeland J, Peters R, Dillon P. A study of 100 anabolic-androgenic steroid users [letter]. Med J Aust 1998; 168: 311-312. Nilsson S. Androgenic anabolic steroid use among male adolescents in Falkenberg. Eur J Clin Pharmacol 1995; 48: 9-11. Korkia P, Stimson GV. Indications of prevalence, practice and effects of anabolic steroid use in Great Britain. Int J Sports Med 1997; 18: 557-562. Yesalis CE, Barsukiewicz CK, Kopstein AN, Bahrke MS. Trends in anabolic-androgenic steroid use among adolescents. Arch Pediatr Adolesc Med 1997; 151: 1197-1206. Australian Sports Medicine Federation. Survey or drug use in Australian sport. Sports Coach 1988: 9-10. Medical and nonmedical uses of anabolic-androgenic steroids. Council on Scientific Affairs. JAMA 1990; 264: 2923-2927. Wu Z, Bidlingmaier M, Dall R, Strasburger CJ. Detection of doping with human growth hormone. Lancet 1999; 353: 895. Sawka MN, Joyner MJ, Miles DS, et al. American College of Sports Medicine position stand. The use of blood doping as an ergogenic aid. Med Sci Sports Exerc 1996; 28: i-viii. Willey J. Insulin as an anabolic aid? The Physician and Sports Medicine 1997; 25: 103-104. Kennedy MC. Anabolic steroid abuse and toxicology. Aust N Z J Med 1992; 22: 374-381. Corrigan B. Anabolic steroids and the mind. Med J Aust 1996; 165: 222-226. Gillon R. Medical ethics: four principles plus attention to scope. BMJ 1994; 309: 184-188. Laseter JT, Russell JA. Anabolic steroid-induced tendon pathology: a review of the literature. Med Sci Sports Exerc 1991; 23: 1-3. Bhasin S, Storer TW, Berman N, et al. The effects of supraphysiologic doses of testosterone on muscle size and strength in normal men. N Engl J Med 1996; 335: 1-7. Kennedy MC, O'Sullivan AJ. Do anabolic-androgenic steroids enhance sporting performance? [editorial]. Med J Aust 1997; 166: 60-61. Franke WW, Berendonk B. Hormonal doping and androgenization of athletes: a secret program of the German Democratic Republic government. Clin Chem 1997; 43: 1262-1279. Farrell M, Hall W. The Swiss heroin trials: testing alternative approaches [editorial]. BMJ 1998; 316: 639. Fleming C. Abuse and trafficking in anabolic steroids -- United States and Canada. A report to the Sir Winston Churchill Memorial Trust. Australia 1997. Duda M. Do anabolic steroids pose an ethical dilemma for US physicians? Phys Sports Med 1986; 14: 173-175. Authors' details St Vincent's Hospital, Sydney, NSW. Michael C Kennedy, MD(UNSW), FRACP, Research Associate, Department of Clinical Pharmacology and Toxicology, and Consultant Physician, Manly. Manly, NSW. Judith R Kennedy, MA(ACU), MAPS, Psychologist. Reprints: Dr M C Kennedy, Manly Non-Invasive Cardiac Laboratory, Level 4, 22 Darley Road, Manly, NSW 2095. Email: drmkennATozemail.com.au

Michael C Kennedy · Judith R Kennedy

Sports Medicine Dehydroepiandrosterone and sport Dehydroepiandrosterone (DHEA) is a weak androgen, but is one of the main precursors of testosterone. Athletes use it for its androgenic and anticatabolic effects and it has been described as a "wonder drug", although there is little evidence to support these claims. There are no published studies of the long term effects of taking DHEA, particularly in the large doses used by athletes, or of its possible interactions with other agents. A Brian Corrigan MJA 1999; 171: 206-208 See also Kennedy Introduction - Physiology - DHEA and exercise - Medical use - Use by athletes - Screening for DHEA use - Long term effects - Acknowledgements - References - Authors' details - - More articles on Sports medicine Introduction In Australia, considerable interest in the use of dehydroepiandrosterone (DHEA) in sports has followed the positive drug tests of two sportsmen, one for DHEA and one for its metabolite, androstenediol. DHEA is a 19-carbon steroid, classified as an androgen,1 albeit a weak one. It is the major steroid hormone secreted by the adrenal glands2,3 and circulates in two forms. One is unconjugated DHEA; the other, present in a much higher concentration, is conjugated as its sulfate, DHEAS. The two are readily interconvertible.4-6DHEA is one of the main precursors in the biosynthesis of the male and female sex hormones.1 It is formed from the metabolism of cholesterol to pregnenolone and then to DHEA or DHEAS, and can be converted in the tissues to the far more potent androgens testosterone and dihydrotestosterone (Box 1).7 DHEA first burst into prominence nearly 20 years ago when, following animal experiments, it was described as a "wonder drug"8 and "the fountain of youth", with claims that it was an anti-aging, anti-obesity, and anticancer drug. At that time it was available in the United States only on prescription, but in 1985 the Food and Drug Administration (FDA) ordered manufacturers to stop marketing DHEA as a weight-loss product. In 1994, following intense lobbying by the healthfood industry, an Act of Congress allowed DHEA to be sold in the US as an over-the-counter dietary nutritional supplement.9 The effect of this Act was to shift the burden of proof onto the FDA to prove that a nutritional substance was harmful. The Act also stated that labelling was not to make any unsubstantiated health claims, but this failed to stop the profusion of advertisements on the Internet.10 The fond belief that, if labelled as having "no drug intent", DHEA would be used only as a food supplement, or that it would be used only in small doses, turned out to be just that -- a fond belief. The FDA still does not approve it for any medical indication.9,11 In Australia, DHEA is a banned drug, and a prohibited import under the Customs (Prohibited Imports) Regulations (Cwlth). It has no listed medical uses, and cannot be marketed. Physiology Circulating levels of DHEA and DHEAS peak in early adulthood, then progressively decline with age.6,12 DHEA has a short half-life of 25 minutes; DHEAS has a half-life of some 10 hours. Most DHEA circulates bound to albumin,13,14 with only minimal binding to sex hormone binding globulin (SHBG) and a smaller amount being free. In contrast, DHEAS is more strongly bound to albumin, only a small amount is free, and none appears bound to SHBG.13 Secretion of DHEA, but not of DHEAS, has a circadian rhythm.1,15,16 DHEAS is present at a plasma concentration much higher than any other adrenal steroid. Despite its abundance and rapid turnover rate, DHEA's physiological role remains uncertain.14,17,18 A DHEA deficiency state has never been described.19 For men or women who have either adrenal insufficiency or hypopituitarism, although gluco- and mineralocorticosteroid replacement is needed, 50 mg a day of DHEA is sufficient for replacement.12,20 DHEA and exercise Four studies have been published concerning the effect of physical exercise on DHEA levels. Two of these, involving trained sportsmen, found exercise produced a significant rise in DHEA levels.21,22 The third, with patients in a cardiac rehabilitation program,23 reported no effect. In the other,24 middle-aged women using a treadmill had raised serum DHEA and DHEAS levels. Medical use DHEA has been described in the treatment of many disorders, including cardiovascular disease,25 breast cancer,26 obesity,27 and as replacement therapy to improve the fall in DHEA levels that occurs in aging men and women.6,28,29 These are all controversial. DHEA is usually available in 25 mg or 50 mg tablets, which have an average absorption of 50% from the gut.28 It has also been used in an injectable ester form, intramuscular prasterone enanthate 200 mg (Gynodian Depot, Schering), and it has been given as a vaginal pessary. As with other sports drugs, such as steroids, tablets can be readily bought on the black market or on the Internet, but may prove to be counterfeit.30 Use by athletes The number of athletes who use DHEA as a supplement is unknown (Box 2).31 Athletes use DHEA for several reasons: as an anabolic agent to increase levels of androgens such as androstenediol and testosterone. Its effectiveness as an anabolic or energy-producing agent remains unproven. Nevertheless, an anabolic effect was supported in one study,18 when DHEA was given to healthy young men in a dose of 1600 mg a day orally for four weeks. Fat levels decreased and fat-free body mass increased by an average of 4.5 kg. However, in another study using better technology,32 a ninefold increase in DHEAS levels was induced in eight healthy young men given 1600 mg a day for four weeks in a double-blind crossover study. No effect on bodyweight, lean mass or cholesterol resulted; the authors concluded that "DHEA is not an important regulator of energy or protein metabolism in humans".32 There are no published data on what happens when athletes take long term supraphysiological doses of these agents, nor what might happen if older athletes, such as participants in the Master's Games, used DHEA to achieve the levels found in younger people. as an anticatabolic agent.33 One major proposed mechanism of DHEA's mode of action is to counteract the catabolic effect of corticosteroids, which may be elevated following stress and exhaustion due to sporting events or heavy training schedules.3 DHEA is a powerful antiglucocorticoid33-36 and could accelerate recovery from the stress. as a difficult-to-detect means to increase steroid levels. A positive drug test for anabolic steroids is based on the testosterone (T) to epitestosterone (E) ratio (epitestosterone is an inactive isomer of testosterone produced in the testes). The T/E ratio is around 1:1 in normal individuals, and it rises with exogenous steroid administration. The International Olympic Committee (IOC) uses a cut-off of 6:1 for drug testing; any test result above that is considered to be a positive that requires further investigation. As DHEA is a precursor in testosterone formation, it would increase the concentrations of both T and E, so that the T/E ratio would remain within the normal range. Although the T/E ratio does rise with DHEA use, it usually does so to only a modest degree, usually remaining below the IOC cut-off level.37 However, this is also obviously dependent on the dose and length of time of administration, so that, with a high enough dose, the ratio can be increased.38 Cases of a high T/E ratio have been known after excessive intake, but such an increase in the ratio is more likely to occur with androstenediol than with DHEA. as with most other steroids, DHEA is a neurosteroid39-41 capable of producing marked psychological effects,28,42-44 such as euphoria or anxiety.45 Screening for DHEA use In Australia, DHEA is an illegal drug that may not be imported, prescribed or administered. However, it is still possible to order it from the Internet. In early 1997, the IOC specifically added it to the list of drugs proscribed because of its androgenic effects. Previously, it would have been banned as "a related substance". Few technical difficulties are associated with detecting DHEA in the urine, but its normal range and a legal level for detection purposes need to be established. In one report, the authors recommend a urinary concentration threshold of 300 mg per litre of DHEA glucuronide for drug-screening purposes.3 Similar figures have been obtained in Australia (Dr R Kazlauskas, Director, Australian Sports Drug Testing Laboratory, personal communication). A screening test might need to rely on urinary ratios between DHEA and other steroids, or else some form of carbon isotope ratio measurement might be developed.46 Long term effects The long term effects of DHEA are not known, although it does seem to be capable of interfering with many basic hormonal and endocrine systems, including breast, uterine and prostate tumours.47,48 Most of the theories concerning its anticipated effects have been extrapolated from epidemiological or animal studies. There have never been any properly conducted long term clinical trials of its efficacy or side effects in humans, and nothing is known about its interactions with other compounds. For these reasons, it should never be used as a long term treatment in young people such as athletes. Acknowledgements I would like to thank Dr John Carter and Dr Michael Kennedy; the Australian Sports Drug Agency, and the librarians at Concord Hospital, for all their help. References Williams JD. Textbook of endocrinology. Williams JD, Foster DW, editors. 8th ed. Philadelphia: WB Saunders, 1992; 579-581. Greenspan FS. Basic and clinical endocrinology. 3rd ed. New Jersey: Prentice-Hall, 1991; 469-471. Dehennin L, Ferry M, Lafarge P, et al. Oral administration of dehydroepiandrosterone to healthy men: alteration of the urinary androgen profile and consequences for the detection of abuse in sport by gas chromatography-mass spectrometry. Steroids 1998; 63: 80-87. Bird CE, Masters V, Clark AF. Dehydroepiandrosterone sulfate: kinetics of metabolism in normal young men and women. Clin Invest Med 1984; 7: 119-122. Haning RV Jr, Carlson IH, Flood CA, et al. Metabolism of dehydroepiandrosterone sulfate (DS) in normal women and women with high DS concentrations. J Clin Endocrinol Metab 1991; 73: 1210-1215. Herbert J. The age of dehydroepiandrosterone [editorial]. Lancet 1995; 345: 1193-1194. Labrie F, Belanger A, Simard J, et al. DHEA and peripheral androgen and estrogen formation: intracrinology. Ann N Y Acad Sci 1995; 774: 16-28. Kent S. DHEA: "miracle" drug? Geriatrics 1982; 37: 157-161. Skolnick AA. Scientific verdict still out on DHEA. JAMA 1996; 276: 1365-1367. Kreeger KY. Researchers ponder the benefits of DHEA on many fronts. The Scientist 1997; 11(9): 11,14. Dehydroepiandrosterone (DHEA). Med Lett Drugs Ther 1996; 38: 91-92. Young J, Couzinet B, Nahoul K, et al. Panhypopituitarism as a model to study the metabolism of dehydroepiandrosterone (DHEA) in humans. J Clin Endocrinol Metab 1997; 82: 2578-2585. Longcope C. Dehydroepiandrosterone metabolism. J Endocrinol 1996; 150 Suppl: S125-S127. Ebeling P, Koivisto VA. Physiological importance of dehydroepiandrosterone. Lancet 1994; 343: 1479-1481. Liu CH, Laughlin G, Fischer U, et al. Marked attenuation of ultradian and circadian rhythms of dehydroepiandrosterone in postmenopausal women: evidence for a reduced 17,20-desmolase enzymatic activity. J Clin Endocrinol Metab 1990; 71: 900-906. Baulieu EE. Dehydroepiandrosterone (DHEA): a fountain of youth? J Clin Endocrinol Metab 1996; 81: 3147-3151. Nestler JE, Kahwash Z. Sex-specific action of insulin to acutely increase the metabolic clearance rate of dehydroepiandrosterone in humans. J Clin Invest 1994; 94: 1484-1489. Nestler JE, Barlascini CO, Clore JN, et al. Dehydroepiandrosterone reduces serum low density lipoprotein levels and body fat but does not alter insulin sensitivity in normal men. J Clin Endocrinol Metab 1988; 66: 57-61. Regelson W, Loria R, Kalimi M. Dehydroepiandrosterone (DHEA) -- the "mother steroid". I. Immunologic action. Ann N Y Acad Sci 1994; 719: 553-563. Arlt W, Justl H-G, Callies F, et al. Oral dehydroepiandrosterone for adrenal androgen replacement: pharmacokinetics and peripheral conversion to androgens and estrogens in young healthy females after dexamethasone suppression. J Clin Endocrinol Metab 1998; 83: 1928-1932. Keizer H, Janssen GM, Menheere P, Kranenburg G. Changes in basal plasma testosterone, cortisol, and dehydroepiandrosterone sulfate in previously untrained males and females preparing for a marathon. Int J Sports Med 1989; 10 Suppl 3: S139-S145. Velardo A, Pantaleoni M, Valerio L, et al. Influence of exercise on dehydroepiandrosterone sulphate and delta 4-androstenedione plasma levels in man. Exp Clin Endocrinol 1991; 97: 99-101. Milani RV, Lavie CJ, Barbee RW, Littman AB. Lack of effect of exercise training on dehydroepiandrosterone-sulfate. Am J Med Sci 1995; 310: 242-246. Johnson LG, Kraemer RR, Haltom R, et al. Effects of estrogen replacement therapy on dehydroepiandrosterone, dehydroepiandrosterone sulfate, and cortisol responses to exercise in postmenopausal women. Fertil Steril 1997; 68: 836-843. Barrett-Connor E, Goodman-Gruen D. The epidemiology of DHEAS and cardiovascular disease. Ann N Y Acad Sci 1995; 774: 259-270. Bulbrook RD, Hayward JL, Spicer CC, et al. Relation between urinary androgen and corticoid excretion and subsequent breast cancer. Lancet 1971; 2: 395-398. Clore JN. Dehydroepiandrosterone and body fat. Obes Res 1995; 3 Suppl 4: 613S-616S. Morales AJ, Nolan JJ, Nelson JC, et al. Effects of replacement dose of dehydroepiandrosterone in men and women of advancing age. J Clin Endocrinol Metab 1994; 78: 1360-1367. Yen SSC, Morales AJ, Khorram O. Replacement of DHEA in aging men and women. Ann N Y Acad Sci 1995; 774: 128-142. Lifrak ET, Parker LN. Analysis of nonprescription capsules purported to contain an adrenal androgen. Am J Hosp Pharm 1985; 42: 587-589. Sturmi JE, Diorio DJ. Anabolic agents. Clin Sports Med 1998; 17: 261-282. Welle S, Jozefowicz R, Statt M. Failure of dehydroepiandrosterone to influence energy and protein metabolism in humans. J Clin Endocrinol Metab 1990; 71: 1259-1264. Loria RM. Antiglucocorticoid function of androstenetriol. Psychoneuroendocrinology 1997; 22 Suppl 1: S103-S108. Kalimi M, Shafagoj Y, Loria R, et al. Anti-glucocorticoid effects of dehydroepiandrosterone (DHEA). Mol Cell Biochem 1994; 131: 99-104. Regelson W, Kalimi M. Dehydroepiandrosterone (DHEA) -- the multifunctional steroid. II. Effects on the CNS, cell proliferation, metabolic and vascular, clinical and other effects. Mechanism of action? Ann N Y Acad Sci 1994; 719: 564-575. Fleshner M, Pugh CR, Tremblay D, et al. DHEA-S selectively impairs contextual-fear conditioning: support for the antiglucocorticoid hypothesis. Behav Neurosci 1997; 111: 512-527. Bosy TZ, Moore KA, Poklis A. The effect of oral dehydroepiandrosterone (DHEA) on the urine testosterone/epitestosterone (T/E) ratio in human male volunteers. J Anal Toxicol 1998; 22: 455-459. Bowers LD. Oral dehydroepiandrosterone supplementation can increase the testosterone/epitestosterone ratio. Clin Chem 1999; 45: 295-297. Baulieu EE. Neurosteroids of the nervous system, by the nervous system, for the nervous system. Recent Prog Horm Res 1997; 52: 1-32. Khorram O. DHEA: a hormone with multiple effects. Curr Opin Obstet Gynecol 1996; 8: 351-354. Dubrovsky B. Natural steroids counteracting some actions of putative depressogenic steroids on the central nervous system: potential therapeutic benefits. Med Hypotheses 1997; 49: 51-55. Corrigan AB. Anabolic steroids and the mind. Med J Aust 1996; 165: 222-226. Miller RA. DHEA -- brass ring or red herring? [editorial]. J Am Ger Soc 1977; 45: 1402-1403. Wang C, Alexander G, Berman N, et al. Testosterone replacement therapy improves mood in hypogonadal men -- a clinical research center study. J Clin Endocrinol Metab 1996; 81: 3578-3583. Imamura M, Prasad C. Modulation of GABA-gated chloride ion influx in the brain by dehydroepiandrosterone and its metabolites. Biochem Biophys Res Commun 1998; 243: 771-775. Magnay J. Days numbered for testosterone cheats. Sydney Morning Herald 1999; 16 July: 12. Armsey TD, Green GA. Nutrition supplements: science vs hype. Phys Sportsmed 1997; 25: 77-92. Dorgan JF, Stanczyk FZ, Longcope C, et al. Relationship of serum dehydroepiandrosterone (DHEA), DHEA sulfate and 5-androstene-3b,17b-diol to risk of breast cancer in postmenopausal women. Cancer Epidemiol Biomarkers Prev 1997; 6: 177-181. Authors' details Institute of Sports Medicine, Concord Hospital, Sydney, NSW. A Brian Corrigan, AM, FRACP, FRCP, Consultant Reprints will not be available from the author. Correspondence: Dr A B Corrigan, Lookout Avenue, Dee Why, NSW 2099. Email: abcATsouthernx.com.au Back to text2: DHEA use by Australian athletes In Australia, there have been two recent instances involving footballers. In the first, a player was given DHEA for presumed chronic fatigue syndrome, although there is no medical evidence that DHEA is of benefit in this condition. At the tribunal hearing, a complicated set of legal arguments resulted in the player being let off without any penalty. However, he was only to play again if he ceased his medication,which he has done, seemingly without any problems. In the second instance, a footballer used 50mg androstenediol capsules, allegedly because he believed that it was only a food supplement. On testing, a very high testosterone/epitestosterone ratio of 14.5 was found, and he was found guilty, and the maximum penalty imposed.

Research Rainfall, evaporation and the risk of non-contact anterior cruciate ligament injury in the Australian Football League John Orchard, Hugh Seward, Jeanne McGivern and Simon Hood MJA 1999; 170: 304-306 Abstract - Introduction - Methods - Results - Discussion - Acknowledgement - References - Authors' details - - More articles on Emergency medicine Abstract Objective: To determine if weather conditions affect the risk of anterior cruciate ligament (ACL) tear in Australian Football. Design: Prospective observational analytic study of football matches. Setting: The Australian Football League (AFL), a professional competition. Participants: All players in 2280 matches from 1992-1998. Main outcome measures: Surgically-proven ACL injury, not involving a direct contact mechanism, during a match; rainfall; water evaporation. Results: 59 ACL injuries not involving direct contact occurred during the study period, more commonly in cities north of Melbourne (χ2 = 17.0; df = 1; P < 0.001). Senior grade matches (relative risk [RR], 3.03; 95% confidence interval [CI], 1.52-6.03), high water evaporation in the month before the match (RR, 2.80; 95% CI, 1.53-5.10) and low rainfall in the year before the match (RR, 1.93; 95% CI, 1.12-3.34) were significantly associated with these injuries. Conclusion: Low water evaporation and high rainfall significantly lower the risk of ACL injuries in AFL footballers. The likely mechanism is a softening of the ground, which lowers shoe-surface traction. Consistent extra watering and covering of grounds during periods of high water evaporation may lower the rate of ACL injuries. Introduction Anterior cruciate ligament (ACL) injuries of the knee are the most costly injuries in football at both professional and amateur levels. Of the commonly occurring injuries, they are the most devastating for the player, as they usually require reconstruction and long term rehabilitation in order to retain normal knee function. In the Australian Football League (AFL), ACL injuries account for 12% of all missed playing time,1 which costs the competition over $1 million annually in injury payments alone. The rate of ACL injury in the AFL competition has increased over recent years.2 The exact numbers and costs of ACL injuries in amateur football are unknown. One report that tried to estimate the cost of sports injuries in Australia3 suggested that the cost of ACL injuries in all grades and codes of football was at least 10% of the nation's entire bill for sports injuries. It estimated 5000 football-related ACL injuries in Australia annually, directly costing $5000 each (not including lost work time and the increased susceptibility to later knee problems caused by these injuries).4 Recent studies have noted that there have been relatively more ACL injuries in the early months of the AFL season, in non-Victorian games, and in recent seasons of dry weather.2,5 Our aim was to examine the strength of the relationship of weather conditions to ACL injury. Methods We studied 2280 matches (all AFL home and away season, finals, reserve grade and Ansett Cup matches which occurred from 1992-1998 in the cities of Adelaide, Brisbane, Canberra, Darwin, Geelong, Hobart, Melbourne, Perth and Sydney), involving 2239 individual players. Approximately 75% of the matches were held in Melbourne, 5% to the south (Geelong and Hobart) and the remaining 20% in the northern cities. The occurrence of ACL injuries was determined by an ongoing injury surveillance program, which has attempted to determine the cause of every game missed through injury of listed players. The accuracy of this survey in determining the cause of missed games reached 100% in 1997, and has been greater than 90% in every year.1 In addition, a separate register for ACL injuries is held by the AFL. ACL injuries in the AFL are managed surgically and have the diagnosis proven at the time of simultaneous arthroscopy and reconstruction. The mechanism of injury was recorded by team doctors and divided into the categories of direct contact (where the player's knee or leg was contacted by another player) and no direct contact (which was subdivided into indirect contact and no contact). Daily weather variables were measured prospectively (but obtained by us retrospectively) by the Bureau of Meteorology at central locations in each city studied. No differentiation was made between rainfall in the differing suburbs of any city, except for Waverley Park (30 km from the centre of Melbourne), for which rainfall data were taken from the nearest centre (Moorabbin). Maximum and minimum temperature of the day of the match, rainfall, water evaporation and maximum wind gust were the raw weather variables considered. Water evaporation is a meteorological variable measuring the change of surface water into water vapour -- it is affected by temperature, sunshine, humidity and wind.6 Composite rainfall and evaporation variables were created (measuring the totals for the previous 7, 14, 28, 90 and 365 days), which were considered to have had potentially more effect on ground conditions than the weather only on the day of the match. Statistical analysis was carried out using SPSS for Windows.7 Chi-square and t tests (after variances assessed using Levene's test) were performed in the initial stages of the analysis. Multivariate analysis was performed using a logistic regression forward stepwise technique, with a significance of 0.05 to enter the equation. Continuous variables in the logistic regression were redefined into binary variables based on group median values, to calculate risk ratios adjusted for confounding. Results There were 111 surgically-proven ACL tears recorded in AFL players during the study period. Excluded from analysis were 33 injuries that did not occur in AFL matches (13 occurred during practice matches, 14 during training sessions and six in other league matches). Of the 78 injuries in AFL matches, 19 occurred through direct contact, 15 involved indirect contact (to another part of the body than the leg) and there was no contact involved in 44. Overall, games played north of Melbourne had a significantly higher rate of all ACL injuries (Table). However, injuries involving contact were not significantly associated with being north of Melbourne, although indirect-contact injuries were more common north of Melbourne. For the 59 ACL injuries that did not involve direct contact, the most predictive rainfall and evaporation variables for ACL injury were 28-day evaporation (t = - 3.8; df = 59; P < 0.001) and 365-day rainfall (t = 1.34; df = 2278; P = 0.18). Other significant associations were higher grade of match (t = 4.8; df = 59; P < 0.001), lower minimum temperature (t = - 3.7; df = 59; P < 0.001) and month (fewer injuries in winter) (t = 3.1; df = 2278; P = 0.002). Non-significant associations were night games (t = - 1.7; df = 59; P = 0.09) and wind speed (t = - 0.18; df = 2278; P = 0.86). Although 365-day rainfall was not significant according to the t test, this variable was entered into the logistic regression equation as significant. This is because of the confounding effect of evaporation -- venues with high evaporation also tend to have high rainfall. In a multivariate analysis including evaporation, variance in rainfall is more significant than when rainfall is considered alone. In contrast, night games and minimum temperature had less significance in the logistic regression model. All variables were considered in a logistic regression model with match grade, 28-day evaporation and 365-day rainfall qualifying to be entered into the equation. Senior grade matches had a 3.03-times risk of injury compared with reserve grade matches (95% confidence interval [CI], 1.52-6.03). Matches with high evaporation in the previous 28 days (> 48 mm) had a 2.80-times greater risk of injury (95% CI, 1.52-6.03). Matches with low rainfall (< 449 mm) in the previous year had a 1.93-times greater risk of injury (95% CI, 1.12-6.03). Figures 1 and 2 illustrate a strong association between the rate of ACL injuries not involving direct contact and 28-day evaporation and 365-day rainfall, respectively, for the matches in Melbourne over the study period. Discussion Risk factors for injury can be divided into intrinsic (personal) and extrinsic (environmental). Two intrinsic risk factors for ACL injury have been established: female sex8-11 and narrowed intercondylar notch.12-14 In a recent study, both factors were prospectively followed, and it was concluded that narrow intercondylar notch accounts for the increased number of ACL tears seen in female athletes. At this stage, narrowed intercondylar notch is not a reversible risk factor, but it can be measured at the time of injury and used to counsel athletes on the risk of recurrence, particularly to the contralateral knee. The most promising extrinsic risk factors postulated relate to the shoe-surface interface. It has been hypothesised for many years that increasing traction between a football boot and the playing surface would cause an increase in the rate of knee injuries.15 A recent study showed that American football boots, with a greater number of cleats and higher torsional resistance, were prospectively associated with an increased number of ACL injuries.16 Our results show that high water evaporation in the month before and low rainfall in the year before an AFL match confer an increased risk of ACL injury. This relationship is strong for most injuries not involving contact, but may not apply when the mechanism of injury involves a direct blow to the knee. The mechanism of this association is almost certainly through ground-related factors (either soil moisture content or amount and/or quality of grass). Increased speed of the game on dry grounds may also be relevant. These results are in keeping with the theory that excessive shoe-surface traction is a risk factor for ACL injury. Friction and torsional resistance from football boots has been shown to be higher in dry conditions on natural grass compared with wet conditions.17 In a recent review of non-contact ACL injuries in American Football, it was noted that almost all injuries on natural grass occurred in dry conditions,18 but that review did not measure or control for conditions on days when injury did not occur. We found that the long term effects of rainfall and water evaporation (over a period of months) are more relevant than the amount of rainfall and evaporation on the day or in the days leading up to a match. Further studies are required to determine the exact mechanism by which this relationship occurs and what the effects of intervention would be. The AFL has embarked on a study, beginning with the 1998 season, where matches have ground hardness readings taken with a Penetrometer, a device used in horse racing to measure track hardness. Penetrometer results are reliable and correlate with the speed of races.19 The preliminary results of the AFL study confirm that low rainfall and high evaporation are associated with hard (low) Penetrometer readings (< 4.7 cm).20 We did not study differences between ground conditions in coastal and inland locations, as (except for Canberra) all the major AFL venues are currently in coastal cities. Further study could include inland cities, which may experience different ground conditions due to much colder and drier winters. Irrespective of their mechanism of action, the effects of high water evaporation and low rainfall could be reversed on football grounds by consistently watering grounds during times of lower rainfall and covering them during times of increased sunshine. If grounds were prepared in this way to simulate the ground conditions typically experienced in a Melbourne winter, the number of ACL injuries would almost certainly be reduced. This is unlikely to lead to an increase in injuries of other types, as overall injury rates are consistently higher outside Victoria than in Victoria.1,5 In rugby league in the United Kingdom, injury rates increased across the board when the season was changed from winter to summer,21,22 suggesting harder grounds may be a universal risk factor for football injuries. In AFL, the main competing concern would be whether games played on consistently softer grounds would be a lesser spectacle for the attending and television public. In amateur football, similar reductions in ACL injuries could probably be achieved, without the standard of spectacle being an issue. The cost of manipulating ground conditions might seem initially prohibitive in this environment, but when the massive cost of ACL injury is considered, great overall savings could be made. In conclusion, low water evaporation and high rainfall significantly lower the risk of non-contact ACL injuries in AFL footballers. The mechanism is likely to be a softer surface, with lower shoe-surface traction and consequently less force transferred to the knee in movements such as pivoting. Consistent extra watering and covering of grounds during times of high water evaporation (sunny, windy periods with no rain) is likely to lower the rate of these devastating and costly injuries. Acknowledgement The Australian Football League funds the AFL Injury Surveillance System from which data for this study were derived. References Orchard J, Wood T, Seward H. AFL injury report 1997. Football Record 1998; 87: 54-61. Seward H. Can ACL injuries be prevented? In: Australian Conference of Science and Medicine in Sport. Canberra: Sports Medicine Australia, 1997. Egger G. Sports injuries in Australia: causes, costs and prevention. Sydney: National Better Health Program, 1990. Deacon A, Bennell K, Kiss ZS, et al. Osteoarthritis of the knee in retired, elite Australian Rules footballers. Med J Aust 1997; 166: 187-190. Orchard J, Seward H, Garlick D. Ground conditions and AFL injuries. In: Australian Conference of Science and Medicine in Sport. Canberra: Sports Medicine Australia, 1997. Lewis R, editor. Meteorological glossary. 6th ed. London: HMSO Publications, 1991. SPSS for Windows [computer program]. Version 6.0. Chicago, Ill: SPSS Inc, 1992. Arendt E, Dick R. Knee injury patterns among men and women in collegiate basketball and soccer. NCAA data and review of the literature. Am J Sports Med 1995; 23: 694-701. Ferretti A, Papandrea P, Conteduca F. Knee ligament injuries in volleyball players. Am J Sports Med 1992; 20: 203-207. Gray J, Taunton J, McKenzie D. A survey of injuries to the anterior cruciate ligament of the knee in female basketball players. Int J Sports Med 1985; 6: 314-316. Bjordal J, Arnoy F, Hannestad B, Strand T. Epidemiology of anterior cruciate ligament injuries in soccer. Am J Sports Med 1997; 25: 341-345. Souryal T, Moore H, Evans J. Bilaterality in anterior cruciate ligament injuries: associated intercondylar notch stenosis. Am J Sports Med 1988; 16: 449-454. Shelbourne K, Facibene W, Hunt J. Radiographic and intraoperative intercondylar notch width measurements in men and women with unilateral and bilateral anterior cruciate ligament tears. Knee Surg Sports Traumatol Arthrosc 1997; 5: 229-233. Shelbourne K, Davis T, Klootwyk T. The relationship between intercondylar notch width of the femur and the incidence of anterior cruciate ligament tears: a prospective study. Am J Sports Med 1998; 26: 402-408. Torg J, Quendenfeld T, Landau B. The shoe-surface interface and its relationship to football knee injuries. J Sports Med 1974; 2: 261-269. Lambson R, Barnhill B, Higgins R. Football cleat design and its effect on anterior cruciate ligament injuries: a three year prospective study. Am J Sports Med 1996; 24: 155-159. Heidt R, Dormer S, Cawley P, et al. Differences in friction and torsional resistance in athletic shoe-turf surface interfaces. Am J Sports Med 1996; 24: 834-842. Scranton P, Whitesel J, Powell J, et al. A review of selected noncontact anterior cruciate ligament injuries in the National Football League. Foot Ankle Int 1997; 18: 772-776. Neylan J, Stubbs A. Assessing racetrack conditions: a review of available devices. Canberra: Rural Industries Research & Development Corporation, 1998. Orchard J. Measurement of football ground hardness using the racetrack Penetrometer [abstract]. Med Sci Sports Exer. In press, 1999. Hodgson Phillips L, Standen P, Batt M. Effects of seasonal change in rugby league on the incidence of injury. Br J Sports Med 1998; 32: 144-148. Gissane C, Jennings D, White J, Cumine A. Injury in summer rugby league football: the experiences of one club. Br J Sports Med 1998; 32: 149-152. (Received 30 Jul, accepted 28 Nov, 1998) Authors' details Sports Medicine Unit, University of New South Wales, Kensington, NSW. John Orchard, MB BS, FACSP, Visiting Fellow. Australian Football League Medical Officers Association, Melbourne, VIC. Hugh Seward, MB BS, FACSP, President; Jeanne McGivern, MB BS, FRCS, Club Medical Officer; Simon Hood, BAppSci(PE), Research Officer. Reprints: Dr J Orchard, South Sydney Sports Medicine, 111 Anzac Parade, Kensington, NSW 2033. Email: johnorchardATmsn.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/> Back to text Back to text Back to text

John Orchard · Hugh Seward · Jeanne McGivern · Simon Hood

Rugby and spinal injury: what can be done? We cannot be complacent -- we must continue an expanding injury database MJA 1998; 168: 372-373 In the early 1980s, staff in Australian hospital spinal units became aware of a serious increase in the incidence of young football players in both codes of rugby -- union and league -- admitted with serious or permanent cervical spinal cord injury. By 1983 the two spinal units in Sydney were admitting 10 or more young players in a season.1 By 1984, I had introduced the Spinal Awareness and Prevention Program at the Royal North Shore Hospital, Sydney, for audiovisual presentation to schoolchildren in independent and public schools in New South Wales. Lecturers in this program, themselves disabled from spinal cord injury, highlighted how spinal cord injury could occur. By 1987, documentation from injured players had been presented in a report to the International Rugby Board, and changes to the scrum formation had been recommended. In 1987, in a review of 107 footballers in Australia who had suffered a spinal cord injury between 1960 and 1985, scrummaging in rugby union was identified as particularly dangerous, with illegal tackles (eg, "spear tackling" -- with a player being driven head-first into the ground, or a "stiff-arm" impact to a player's head and neck) identified as the most serious problem in rugby league.2 Administrators of both codes had already acknowledged these problems, particularly in "schoolboy" football. There were also lectures by sports medicine specialists to coaches and selectors of teams, with identification of the particular danger for young players in their mid teens beginning to participate in a contact sport. During the second half of the 1980s, coaches for both schoolboy and more senior grades of rugby union and rugby league were emphasising adequate preparation for the game and careful selection of players for particular positions of play, and encouraging the reporting of injuries. Some heads of independent schools in Sydney were initially reluctant to accept that many boys are genetically and psychologically destined to be unsuitable for participation in competitive contact sport! Some administrators were reluctant to consider changes of rules necessary to reduce the forces generated on the necks and shoulders of players involved in scrums and mauls and to ensure the absolute necessity of playing according to the rules. In 1997, Armour et al confirmed an increased frequency of serious spinal cord injuries in rugby union and league players over the 20-year period 1976 to 1995 in New Zealand.3 One hundred and forty-one players were admitted to New Zealand's two spinal injury units, and 47 remained permanently paralysed. The authors noted that, although studies of cervical spinal cord injury in rugby football had been presented to medical and rugby authorities within the previous five years, no action appeared to have been taken to reduce the unacceptable incidence of this grave injury. Professor Timothy Noakes, from Cape Town, South Africa, lamented in an editorial in the British Medical Journal in 1995 that "nearly 20 years after the BMJ first drew attention to the issue, we still do not know the true incidence of either spinal cord or cervical injuries in rugby players in any rugby-playing country".4 He emphasised that changes in rules of the game and player preparation could not be supported without sufficient accurate epidemiological data. More recently, Scher reported that the incidence of serious rugby spinal injuries in South Africa had not decreased over the past 10 years, with an average of 5.4 players per year admitted to one of the world's largest spinal cord injury centres, in Cape Town.5 Of interest, therefore, is the finding of Rotem et al, reported in this issue of the Journal, of a "small but significant decline in the number and approximate incidence of cases [of permanent neurological deficits leading to tetraplegia] associated with rugby union but no change in rugby league", from their survey of the spinal units at Royal North Shore Hospital and Prince Henry's Hospital.6 Further collection of data will allow a more detailed study of the statistics and will, one hopes, confirm the apparent trend towards reduction in injury incidence. In the 18 months since the New Zealand Rugby Union instituted compulsory nationwide safety seminars for coaches early in 1996, no cases of spinal cord injury from scrums have been reported in that country, although one player sustained tetraplegia in a tackle.3 During 1997, the spinal unit at Royal North Shore Hospital had no admissions of patients with serious cervical spinal cord injury from playing either rugby union or league (Dr Sue Rutkowski, Medical Director, personal communication), although this encouraging statistic could be a continuation of the variability seen in Rotem et al's study. In 1995, the National Health and Medical Research Council released a handbook7 with Guidelines for prevention and management of head and neck injuries in football. Compiled by medical specialists with knowledge and interest in neurotrauma from sporting injuries, this useful guide should be in the hands of all referees, umpires, coaches and players. The handbook highlights important first-aid principles and assessment of injured players before returning them to play, to prevent aggravation of a potentially serious injury. The laws for under-19 players, with the 1993 variations (such as rules eliminating "crotch binding" in scrums) introduced to rugby union in New South Wales, must also be maintained. The cost to the community of spinal cord injuries cannot be overemphasised. In Australia, 300 new patients with spinal cord injuries are expected every year; the lifetime cost is one million dollars for each paraplegic casualty and five million dollars for a tetraplegic casualty, as confirmed by awards in Australian courts. Our pessimism should be balanced by remembering Davidson's 1987 findings that, among 1444 schoolboys injured in interschool rugby from 1969 to 1986, there were two clinically "serious" injuries -- a skull fracture and a fracture dislocation of the cervical spine. The "severe" injury rate was 14 per 10 000 player-hours, or 0.12 per 100 player-games.8 Rotem et al have confirmed the impression of a reduction in the incidence of spinal cord injury in some contact sports following rule changes, as well as increasing our understanding of how cervical spinal cord injury occurs. Further epidemiological studies are essential for the adequate re-assessment of rule changes and of techniques to prepare players for contact sports. We must also further our knowledge of how injuries occur, and remain in close consultation with physicists, sports medicine clinicians and biomedical engineers. There must be no complacency in the future. Continuing vigilance is imperative to avoid the devastating personal and societal costs. John D Yeo, AO Associate Professor, and Consultant in Spinal Injuries Royal North Shore Hospital, Sydney, NSW Yeo JD, Walsh J. Prevention of spinal cord injuries in Australia. Paraplegia 1987; 25: 221-224. Taylor TKF, Coolican MRJ. Spinal cord injuries in Australian footballers, 1960-1985. Med J Aust 1987; 147: 112-118. Armour KS, Clatworthy BJ, Bean AR, et al. Spinal injuries in New Zealand rugby and rugby league -- a 20-year survey. N Z Med J 1997; 110: 462-465 . Noakes T, Jakoet I. Spinal cord injuries in rugby union players. BMJ 1995; 310: 1345-1346. Scher AT. Rugby injuries to the cervical spine and spinal cord -- a 10-year review. Clin Sports Med 1998; 17: 195-206. Rotem T, Lawson JS, Wilson SF, et al. Severe cervical spinal cord injuries related to rugby union and league football in New South Wales, 1984-1986. Med J Aust 1998; 168: 379-381. Newcombe R, et al. Football injuries of the head and neck. National Health and Medical Research Council Report, January 1995. Canberra: AGPS, 1995. Davidson RM. Schoolboy rugby injuries, 1969-1986. Med J Aust 1987; 147: 119-120. Lewis CS. The problem of pain. London: Collins Fontana Books, 1940: 141. - 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/>

John D Yeo

Severe cervical spinal cord injuries related to rugby union and league football in New South Wales, 1984-1996 Tai R Rotem, James S Lawson, Stephen F Wilson, Stella Engel, Sue B Rutkowski and Chris W Aisbett MJA 1998; 168: 379-381 For editorial comment see Yeo Correction note: This article was published online with a typographic error that was corrected on 15 June 1998: A P value of 0.06 was misprinted as 0.6. Jump to corrected par. Abstract - Introduction - Methods - Results - Discussion - Acknowledgement - References - Authors' details - - ©MJA1998 Abstract Objective: To determine the frequency and circumstances of serious cervical cord injuries associated with rugby union and league football in New South Wales. Design: Retrospective review of patients with rugby football-related cervical spinal cord injuries. Setting: The two central spinal units in NSW, from January 1984 to July 1996. Outcome measures: Admission to spinal units; injury resulting in permanent tetraplegia. Results: During the review period, 115 rugby football players (56 union and 59 league) were admitted to the spinal units because of cervical spinal cord injuries. 49 patients had resultant permanent neurological deficits (complete tetraplegia [quadriplegia]) -- 26 associated with rugby union and 23 with rugby league. Two patients died of injury sequelae within two weeks of admission. There was no significant change in the rate of football-related admissions to spinal units for either code. There was a small decline in the number (from 15 in 1984 to 1987 to 7 in 1992 to 1996) and incidence (from 1.2 to 0.5 per 10 000 participants) of patients with tetraplegia associated with rugby union. When this decline was tested as a trend over the years, it was found to be statistically significant (P = 0.06). No significant trend was found in the tetraplegia data associated with rugby league. Cervical spinal cord injuries leading to complete tetraplegia were most commonly associated with scrum-like plays in union and with tackles in league. Conclusion: Serious cervical spinal injuries associated with both codes of rugby continue to occur in NSW. Rugby football in its various forms is still an inherently dangerous game. Introduction Injury to the cervical spinal cord sustained while playing rugby union or league football has tragic personal consequences, with subsequent high demands on community resources.1 During the 1970s and early 1980s there was an approximately twofold increase in the incidence of such injuries in many countries,2-4 possibly because of the development of more powerful scrums and tackles (see Box for terms). In response, between 1984 and 1996, new rules were introduced intermittently, existing rules were more strictly enforced, and "safety" programs were offered -- these included exercises for strengthening players' neck muscles and the banning of players with long thin necks from taking dangerous positions, such as the front row of scrums. We report the findings of a survey of rugby union- and league-related cervical spinal cord injuries in New South Wales (NSW) for the period 1984 to 1996. Methods We retrospectively reviewed the medical records of all patients admitted to the two central spinal units in NSW (at the Royal North Shore Hospital and Prince Henry Hospital, Sydney) because of cervical spinal cord injuries associated with rugby union and rugby league football from January 1984 to December 1996. Patients transferred from outside NSW were excluded from the analysis. Almost all patients (more than 95%) with spinal injuries that occur in NSW are admitted to these two units. Additional information about the circumstances of the injuries, including eyewitness reports of the events leading to them, was obtained from the NSW Sporting Injuries Committee -- a statutory authority which administers an insurance scheme for people permanently injured while playing sports. We also estimated the number of participants in rugby union and league football in NSW per year in the review period, based on the Committee's data5 plus surveys of NSW schoolboy football participants.6 As some of these data were incomplete and there was some duplication, these estimates are broad approximations only. Statistical analysis The number of cervical spinal cord injury cases is small, so any statistical analysis necessarily lacks power. To develop valid conclusions from this study, we analysed cases of cervical spinal cord injuries according to: total number of admissions to the two spinal units; permanent neurological deficits (ie, complete tetraplegia); and trends during the review period. When there are large numbers of participants and the risk of cervical spinal cord injury to any particular player is very low over a short time period -- and the injury is permanent and will not allow a return to the game -- the number of injuries in each year is assumed to follow a Poisson distribution. In the absence of data on hours of playing football or training for football, we assumed that the total number of hours devoted to the game for each code and grade did not vary from year to year. The null hypothesis for each test we performed was that there was no change in aggregated risk of cervical spinal injury against the alternative that the risk had decreased. All tests were based on the null-hypothesis assumption that the best estimate of annual rate of injuries was the average rate of injuries. We then fitted a simple linear regression, of time, to a probability transformation of the injury data. The number of injuries for each year was converted to the probability of observing, at most, that number of injuries in a particular year. These values were then converted to their corresponding standard normal score. The tests were based only on the regression slopes, which were tested to see if they were negative. The critical level of significance for these tests was 0.1. All calculations were performed using Microsoft Excel. The function POISSON was used to calculate the cumulative probabilities; the function NORMINV was used to calculate the standard normal scores; the function LINEST was used to calculate the slope and its standard error; and the function TDIST (one-tailed 11 degrees of freedom) was used to obtain the significance of the results. The Random Number Generator was used in a small simulation study to confirm the size of the testing procedure. Results During the 13-year period of the review, 117 rugby football players (56 union and 59 league players, plus one "backyard" and one "touch" player) were admitted to the spinal units because of cervical spinal cord injuries. The injuries were associated with permanent neurological deficits which led to complete tetraplegia (quadriplegia) in 26 union and 23 league players and in both the "backyard" and the "touch" football players. (The touch and backyard football players were not included in this analysis because they were not playing according to official union or league rules [Table 1].) The 23 "unspecified" admissions shown in Table 1 could not be included in the formal analysis because the football code was omitted from their clinical records. Two patients died of pneumonia within 14 days of sustaining the cervical spinal cord injuries. The age range of the injured players from both codes was 15-37 years (median, 22 years); all were male. The number of patients admitted per year to the spinal units because of cervical spinal cord injuries varied widely: from one to nine per year for league and one to eight per year for union. The number of players who had permanent tetraplegia varied from none to five per year for league and none to six for union (Table 1). Incidence and trends There were about 106 000 participants in rugby league and about 31 000 in rugby union in NSW during each year of the review.5,6 Trends in rates of admissions and incidence of permanent neurological deficits per 10 000 participants are shown in Table 2. Using the data shown in Table 1, there was no decline in the number (and hence the rate) of admissions for union (P = 0.21) or league (P = 0.33) players. There was a small but significant decline for union in the number and hence the incidence (P = 0.06) of players with permanent neurological deficits, but no significant decline for league (P = 0.16). Type of play associated with severe cervical spinal cord injuries Although detailed self-reports and eyewitness accounts of the events surrounding the injuries were available for 43 of the 49 patients with complete tetraplegia, no consistent patterns of play or events could be identified other than that the injury occurred in scrum-like plays (scrums, mauls and rucks; n = 23) or tackles (n = 26). Repeatedly, eyewitnesses observed that a player was found paralysed on the ground, without an obvious causal explanation, while the general play moved on. This lack of a specific, out-of-the-ordinary event was supported by two video recordings of cervical spinal cord injuries that occurred during scrums. The injuries were most common in scrum-like plays in union and in tackles in league. The most common level of spinal cord damage was C4-5 (Table 3). Discussion Despite its limitations as a retrospective study (such as the use of records created for other purposes), the findings of this review are disturbing. While for union players there was a small reduction in both the number and incidence of those with permanent neurological deficits leading to tetraplegia, there were no such changes for league players. Nor were there any changes for either code in the number of players admitted or rates of admission to spinal units. While any fall in the number and incidence of permanent neurological deficits among union players is pleasing and may well be a consequence of rule changes and safety measures,7 the unchanged rate of admissions to spinal units suggests that such improvements may not be sustained. In those players admitted to spinal units who do not experience permanent neurological deficits, the injuries can be regarded as "near misses" (ie, possible damage to the vertebral column without spinal cord injury).7 While evacuation procedures for suspected cervical and other spinal cord injuries may vary, such "near misses" included in the admission rates offer a useful indicator of the risks of such injuries associated with rugby union and league football.8 Our observation that cervical spinal cord injuries are more common in scrum-like plays in union and tackles in league is similar to recent findings in New Zealand.7 However, there is insufficient information in this review and in the New Zealand7 and other reviews9 of rugby football-associated spinal cord injury upon which to base sound recommendations for detailed changes to the rules or other safety measures. These reviews confirm the obvious -- that both rugby union and league are inherently dangerous games. There appear to be several options: Maintain the status quo and accept that each year several union and league players in NSW (and elsewhere) will suffer cervical spinal cord injuries which will leave them permanently paralysed below the neck; For rugby union, change the rules so as to substantially reduce the number of scrum-like plays and change the organisation of the scrum; For rugby league, introduce changes to the rules aimed at substantially altering the nature of the tackle. Acknowledgement This study was conducted with a grant from the NSW Sporting Injuries Committee. Disclaimer of conflict of interest: Apart from providing access to their own case files, the NSW Sporting Injuries Committee was in no way involved with the collection or analysis of data and did not have the right to disapprove or influence the contents of the manuscript. References Yeo JD. Prevention of spinal cord injuries in an Australian study (NSW). Paraplegia 1993; 31: 759-763. Taylor TKF, Coolican MRJ. Spinal cord injuries in Australian footballers, 1960-1985. Med J Aust 1987; 147: 112-118. Silver JR. Injuries of the spine sustained during rugby. BMJ 1984; 288: 37-43. Silver JR, Stewart D. The prevention of spinal injuries in rugby football. Paraplegia 1994; 32: 442-453. NSW Sporting Injuries Scheme. Annual reports of the NSW Sporting Injuries Committee. Sydney 1984 to 1995. Sydney: NSW Sporting Injuries Committee, 1984-1995. Northern Sydney Area Health Service. NSW Youth Sports Injury Report. July 1997. Sydney: Northern Sydney Area Health Service, 1997. Armour KS, Clatworthy BJ, Bean AR, et al. Spinal injuries in New Zealand rugby and rugby league -- a twenty-year survey. N Z Med J 1997; 110: 462-465. Noakes T, Jakoet I. Spinal cord injuries in rugby union players: How much longer must we wait for proper epidemiological studies? BMJ 1995; 310: 1345-1346. Kew T, Noakes TD, Kettles AN, et al. A retrospective study of spinal cord injuries in Cape Province rugby players, 1963-1989. S Afr Med J 1991; 80: 127-133. (Received 18 Sep 1997, accepted 27 Jan 1998) Authors' details School of Health Services Management, Faculty of Medicine, University of NSW, Sydney, NSW. Tai R Rotem, BSocSci, Research Fellow; James S Lawson, MD, MHA, Professor; Chris W Aisbett, BSc, Visiting Fellow. Department of Aged Care and Rehabilitation, Royal North Shore Hospital, Sydney, NSW. Stephen F Wilson, MB BS, FAFRM(RACP), Senior Staff Specialist. Department of Rehabilitation, Prince Henry Hospital, Sydney, NSW. Stella Engel, DPRM, FAFRM(RACP), Director. Spinal Injuries Unit, Royal North Shore Hospital, Sydney, NSW. Sue B Rutkowski, MB BS, Director. Reprints will not be available from the authors. Correspondence: Professor J S Lawson, School of Health Services Management, Faculty of Medicine, University of NSW, Sydney, NSW 2052. - 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/>

Tai R Rotem · James S Lawson · Stephen F Wilson · Stella Engel · Sue B Rutkowski · Chris W Aisbett

Medical planning for the Sydney 2000 Olympic and Paralympic Games Your country will need you MJA 1997; 167: 593-594 - - - ©MJA1997 Introduction Planning for an Olympic Games is in one sense unique. It involves deploying resources (human, logistic and material) on a scale almost unprecedented in peacetime. This is for a transient spectacle that rarely returns to the same country, an event equivalent to holding 28 World Championships simultaneously in one city. It is incumbent on planners for the Sydney 2000 Olympic Games to draw on the wealth of experience already available, both in Australia and other countries. This includes at least 18 scientific manuscripts published (or in press) on activities of the Medical Program at the 1996 Atlanta Olympics;1-19 three of these articles1-3 appear in this issue of the Journal (see Brennan et al., Eaton et al., and Keim and Williams). The International Olympic Committee (IOC) has entrusted the task of staging the Sydney 2000 Olympic Games to the Sydney Organising Committee for the Olympic Games (SOCOG), together with the New South Wales (NSW) Government and the City of Sydney. SOCOG's Medical Program is responsible for facilitating the health and wellbeing not only of the members of the Olympic Family (athletes, officials, administrators, staff and volunteers), but also of hundreds of thousands of spectators at the 35 competition venues. The NSW Department of Health, in collaboration with SOCOG, will administer services relating to public health, medical disaster planning, hospitals and health care interpreters. The Ambulance Service of NSW and St John Ambulance are also key participants. Under the aegis of the IOC Medical Commission, SOCOG, through the Chief Medical Officer, is also responsible for administering both the IOC's doping control program, as well as the gender verification program for women competitors. The Olympic Games are centre-stage for scrutinising the abuse of illegal performance-enhancing drugs, and Australia has a proud record to maintain in the fight against doping. The Australian Sports Drug Agency (ASDA) conducts over 3000 tests annually, either in competition or unannounced. ASDA will provide some training services for the extra personnel needed for the Games. Sydney is also fortunate in already having the Australian Sports Drug Testing Laboratory (ASDTL), the first such facility in the southern hemisphere with IOC accreditation. In conjunction with Sports Medicine Australia, SOCOG will help to organise the 5th IOC Congress on Sport Sciences, to be held in Sydney in November 1999. The Olympic Games provide the opportunity for elite sports medicine research. SOCOG will facilitate a series of biomechanics research projects to be carried out at the Games under the auspices of the IOC Medical Commission. Such projects serve to illustrate that performance can be enhanced by means other than doping. What personnel and resources are needed? We anticipate that planning and implementing the Sydney 2000 Olympic Games Medical Program will require about 4500 volunteers from a variety of health care backgrounds to supplement the handful of salaried SOCOG staff. We also envisage that much of the equipment and consumables will be made available through donation or sponsorship. Volunteers will need not only to have first-rate professional skills, but to be able to work in newly assembled teams in an exciting, if at times stressful and unfamiliar, environment. We hope that many who volunteer for the Olympic Games will also assist at the less "glamorous" Paralympic Games. This large and extraordinary event will involve over 4000 athletes with disabilities participating over 10 days of elite competition. Those who give their time to work with the Paralympic Games will be rewarded with a unique and inspirational experience. From 1998 to 2000, a series of "test events" will be held to evaluate venues and logistics, albeit on a small scale. We plan to begin the call for Medical Program volunteers in mid 1998, with the support of the relevant professional colleges, societies, associations and health authorities. What lessons can we learn from previous Olympic Games? Although many aspects of Olympic medical programs remain constant, operational and logistic factors may vary substantially. For example, compared with Atlanta, Sydney enjoys much closer collaboration between the organising committee and government and also between the Olympic and Paralympic organising committees. Hospital and ambulance services in Atlanta were provided via a series of private hospitals, one of which (Crawford Long Hospital) was chosen for athlete care (as described by Keim and Williams,3). In Sydney, a single State-run ambulance service and designated public hospitals will be involved. Surprisingly for such a large event, in Atlanta there were only 306 ambulance transfers and fewer than 70 hospital admissions from Olympic venues (and similar numbers in Barcelona in 1992). However, the potential impact of the Games on the provision of normal hospital and ambulance services needs to be, and is being, considered during planning. Another major difference between Atlanta and Sydney is the Olympic Village Polyclinic. This will provide general and sports medical care for up to a month for the 15 300 Village residents (athletes and team officials) plus several thousand SOCOG support staff (equivalent to the population of a medium-sized country town). In Atlanta, the Polyclinic was housed in the Student Health Center of the Georgia Institute of Technology together with an adjacent Sports Performance Centre, as the Village used campus dormitories for accommodation (see Eaton et al.,2). In contrast, in Sydney all Polyclinic services will be in one building. We will not have the luxury of a dedicated health care facility, as the Polyclinic is destined to become a primary school for the new Sydney suburb of Newington. This poses interesting challenges in design and fit-out which need to be addressed in detail now. The operational aspects of public health programs, emergency medical care and disaster preparedness in Atlanta are well summarised by Brennan et al.1). We face similar organisational challenges in Sydney, except for the lower likelihood of heat-related illnesses, as our Games will be held in spring. We must prepare for the possibility of a disaster (natural or man-made) either within a venue or outside (as happened in Atlanta, with the Centennial Park bombing, and more recently in Israel, at the Maccabiah Games, where a bridge used by competitors collapsed). The Medical Program in Atlanta was well run, thanks to careful planning, good management and the selfless involvement of thousands of volunteers. Sydney has considerable expertise in medical management of mass gatherings (e.g., the annual City-to-Surf run and the 1988 Bicentennial celebrations). Preparations for the Sydney 2000 Olympic Games began even before the successful bid was announced in 1993, and detailed operational planning is now well under way. In cooperation with government, in consultation with a variety of agencies and individuals, and hopefully with the enthusiastic support of health care professionals from Sydney and throughout Australia, we will achieve the same success at both the Olympic and Paralympic Games in 2000. Daniel Stiel Chief Medical Officer Patsy Trethowan Manager Medical Program Nicki Vance Manager Doping Control Program Sydney Organising Committee for the Olympic Games Brennan RJ, Keim ME, Sharp TW, et al. Medical and public health services at the 1996 Atlanta Olympic Games: an overview. Med J Aust 1997; 167: 595-598. Eaton SB, Woodfin BA, Askew JL, et al. The Polyclinic at the 1996 Atlanta Olympic Village. Med J Aust 1997; 167: 599-602. Keim ME, Williams D. Hospital use by Olympic athletes during the 1996 Atlanta Olympic Games. Med J Aust 1997; 167: 602-605. Anderson GV Jr, Feliciano DV. The Centennial Olympic Park bombing: Grady's response. J Med Assoc Ga 1997; 86: 42-46. Cantwell JD. Role of the cardiologist in the 1996 Olympic Games. Am J Cardiol 1995; 75: 1081-1082. Cantwell JD, James B. Connolly; First modern Olympic champion. J Med Assoc Ga 1995; 84: 41-45. Cantwell JD. An explosion in Centennial Olympic Park! Atlanta Med 1996; 70: 41-43. Cantwell JD. The five Olympic passions in sports and medicine. Atlanta Med 1996; 70: 43-44. Cantwell JD. The Olympic medical experience: an overview. J Med Assoc Ga 1997; 86: 13-14. Cantwell JD. Cardiovascular events in the 1996 Olympic Games. Am J Cardiol. In press. Cohen RW. Doping control in the '96 Olympics. J Med Assoc Ga 1997; 86: 33-36. Elsas LJ, Hayes RP, Muralidharan K. Gender verification at the centennial Olympic games. J Med Assoc Ga 1997; 86: 50-54. Henderson JM. The Olympics in Columbus: a first and a legacy. J Med Assoc Ga 1997; 86: 37-40. Mulherin WB. Soccer at Sanford. J Med Assoc Ga 1997; 86: 25-27. Nettles JL. Reflections on the Olympics: the memories linger. J Med Assoc Ga 1997; 86: 18-19. Sparling PB. Environmental conditions during the 1996 Olympic Games: a brief follow-up report. Clin J Sport Med. 1997; 7: 159-161. Wilkes JS, et al. The Olympic medical experience: venue and command center perspective. J Med Assoc Ga 1997; 86: 47-49. Woodfin BA, Eaton SB, Askew JL. Medical care at the 1996 Olympic Village. J Med Assoc Ga 1997; 86: 15-17. - ©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.

Daniel Stiel · Patsy Trethowan · Nicki Vance

Medical and public health services at the 1996 Atlanta Olympic Games: an overview Richard J Brennan, Mark E Keim, Trueman W Sharp, Scott F Wetterhall, R Joel Williams, Edward L Baker, John D Cantwell and Scott R Lillibridge Planning for the 2000 Sydney Olympic Games may benefit from the experience of the 1996 Atlanta Olympics. Excellent health promotion and prevention activities before and during the Games resulted in fewer medical and public health problems than anticipated. Despite this, there was room for improvement in the level of communication and cooperation between the many service providers to ensure the most appropriate and efficient responses. MJA 1997; 167: 595-598 Introduction - Medical care at the Olympic venues - Prehospital care - Hospital emergency departments - Public health - Disaster preparedness - Conclusion - References - Authors' details - - - ©MJA1997 Introduction The 1996 summer Olympic Games in Atlanta was the largest event in sporting history. With the influx of over 10 000 athletes from 197 countries and an estimated 2.2 million visitors, there were concerns that the city's health services and infrastructure would be strained excessively. Experience at previous Olympics and other mass gatherings had shown that issues of medical care for athletes and visitors, emergency services, public health and disaster preparedness would need to be addressed.1-6 Major anticipated medical problems included heat-related illness, foodborne and waterborne illness, and sexually transmitted disease. With 35 heads of state expected to attend, as well as many other world political and business leaders, disaster preparedness planning had to include the consequences of a terrorist attack with conventional, chemical, biological or nuclear weapons. We review the medical and public health preparation and services provided for the Atlanta Olympics, with emphasis on aspects relevant to the forthcoming Sydney Olympics. Medical care at the Olympic venues Responsibility for providing medical and first aid services for spectators and athletes was assumed by the Atlanta Committee for the Olympic Games (ACOG). Services were provided at all 35 Olympic sporting venues, at the Olympic Village (athletes' residences) and at Centennial Olympic Park (a community park open to the public). Services were staffed with the help of 4000 medical volunteers, including Red Cross personnel, emergency medical technicians, paramedics, nurses and almost 700 physicians from across the United States (US). A venue medical officer coordinated services at each site. Separate medical services and clinics were provided for athletes and spectators. For athletes, in addition to the Polyclinic at the Olympic Village, there was a medical clinic at each sports venue, coordinated by the athlete medical director. Medical care for spectators was provided by: First responders -- Red Cross volunteers, trained in first aid and basic life support, and stationed in the crowd. Advanced life support teams -- teams of two volunteers, at least one of whom was a paramedic, who could be alerted by first responders. They were able to provide advanced medical care on scene, including defibrillation and endotracheal intubation. First aid stations and clinics -- at each venue, staffed by physicians, nurses, paramedics and emergency medical technicians. Medical care included minor suturing, short-term intravenous therapy and basic analgesia. Clinics were equipped with cardiac monitors and defibrillators with pacing capabilities to facilitate management of cardiac and other medical emergencies before hospital transfer. Not all presenting patients required physician assessment, but all those who were reviewed by a physician had a medical encounter form completed to assist with public health surveillance. During the Olympics, more than 30 000 people sought medical assistance at first aid stations and clinics, and 10 723 were examined by physicians. The most common indication for physician examination was injury (34%); heat-related illness was diagnosed in 10%. The busiest medical facility was the Polyclinic at the Olympic Village, where 2474 Olympic staff and athletes were assessed, with many of those from other countries having routine dental and eye examinations (see Eaton et al., page 599 ). Prehospital care Ambulance services for patients who could not be managed at the Olympic venues were provided under agreements with ACOG by the 37 licensed emergency medical services (EMS) -- private ambulance companies -- that service the Atlanta metropolitan area. In addition, some emergency medical technicians used bicycles and motorised golf carts for rapid movement around heavily congested venues and pedestrian areas. A medical helicopter service was on stand-by. Each of the 37 EMS providers in Atlanta services a different metropolitan region. To facilitate the sometimes poor communication and coordination between these providers and regions, the State Emergency Medical Services Advisory Council issued them with uniform recommendations. These included uniform operational plans and procedures developed for the Olympics, agreements on enhanced lines of communication, protocols for management of heat-related illness, and guidelines for response to a mass casualty incident. A major issue for the emergency medical services was to provide quality care to athletes, spectators and visitors without depleting services to the general population. Most EMS providers cancelled employee leave. ACOG and the Atlanta Police Department developed a traffic plan that outlined expedient ambulance routes, and real-time traffic information was provided to the services. During the Games, emergency medical technicians from Atlanta Fire Services (the main first responders within the City of Atlanta) responded to 2163 emergency calls, an increase of 16.2% over usual. Interestingly, average response times did not increase. Use of medical golf carts in the "Olympic Ring", where most Olympic venues were located, was very successful in overcoming the problems of traffic congestion; average response time was an impressive 2.1 minutes for the 414 calls received (Don Hiett, Atlanta Fire Department, personal communication). One patient was successfully resuscitated after a cardiac arrest. Hospital emergency departments Most Atlanta hospitals began serious preparation many months before the Olympics. Staff were educated on heat-related illness, mass casualty incidents, patient overflow plans, traffic projections, and busy event days. Most medical facilities reviewed their disaster response plans and scheduled extra staff to work during the Olympic period. To optimise coordination of emergency and hospital services in case of a disaster, a baseline survey of Atlanta hospital resources was conducted a week before the Games. This determined staffed in-patient beds, emergency department capacities and specialty services. During the Olympic period, hospitals were asked to telephone or fax information on beds and other resources to the central coordinating centre, which generated an Olympic Bed Report twice daily. Most hospitals cooperated, with 68%-92% responding on each occasion (Ruth De Loor, RN, Area Emergency Manager, National Disaster Medical System Coordinator, Atlanta Veterans Administration Medical Center, personal communication). However, the efficiency and accuracy of this system could have been improved by computerised, real-time monitoring of bed status. Ensuring reliable communications among EMS providers, hospitals and coordinating centres was a major consideration. Extra radios were provided to EMS workers by state and federal sources. A communications protocol was distributed to hospital emergency departments in the week before the opening ceremonies. The major means of communication between hospitals and Emergency Operations Centers were routine telephone and fax lines, but about two-thirds of hospitals also had VHF radios as a back-up. Neither the four metropolitan nor the four non-metropolitan sentinel hospitals had a significant increase in emergency department presentations during the Olympics. The number of patients presenting with unintentional injuries and vomiting without diarrhoea increased slightly. The number seen for heat-related illness in metropolitan hospitals peaked at 18 on the second day of Olympic competition, 20 July. There were no increases in numbers of patients presenting with infectious diseases or with sexually transmitted diseases (STDs). Olympic athletes were referred to a single hospital near the Olympic Village, Crawford Long Hospital of Emory University. During the Games, 43 sought hospital care and 22 of these required inpatient admission (see Keim and Williams). Public health Public health services during the Olympic Games were coordinated by the Division of Public Health within the Georgia State Department of Human Resources. Services addressed the major public health concerns of heat-related illness, infectious diseases, food and beverage safety, and environmental health. Surveillance systems were set up to detect emerging outbreaks of infectious disease and unusual disease and injury patterns, and to measure health service use during the Games. Surveillance: Two complementary public health surveillance systems were established specifically for the Games. Surveillance inside Olympic venues was coordinated by ACOG with the assistance of the Centers for Disease Control and Prevention (CDC). Every physician encounter at Olympic venue clinics and first aid stations was documented, and records were faxed to the Olympic Medical Data Center for compilation and analysis. Daily and cumulative summaries were submitted to the ACOG medical coordinator and to state and federal health officials. Rates of illness could be determined for each venue, as attendance figures provided denominators, allowing health and medical interventions to be targeted. For example, the highest rates of heat-related illness were documented at the beach volleyball venue (24 cases/100 000 attendees) and the Horse Park (19.7 cases/100 000 attendees). This information allowed ACOG and public health officials to increase public awareness announcements at these venues, encouraging spectators to drink more fluids, to seek shade and to recognise the symptoms of heat-related illness.7 No unusual disease outbreaks or illness patterns were detected at Olympic venues. Surveillance outside the Olympic venues was coordinated by the State Division of Public Health. The pre-existing passive system for notification of infectious diseases and other significant conditions was augmented by: Active surveillance of medical presentations at eight sentinel hospitals (four in metropolitan Atlanta and four in other cities hosting Olympic events), with daily data transmitted electronically to the Division of Public Health. Daily reports from the Georgia public health laboratory and the state's busiest private laboratory. Encouragement to physicians and other health care providers to report unusual medical presentations directly to the state Division of Public Health. These data were compiled, summarised and reported daily to ACOG and to state and federal health officials. Heat-related illness: Atlanta's hot, humid summer weather, combined with overcrowding on the streets, on public transport and at Olympic venues, made prevention of heat-related illness a major challenge of the Olympics.7,8 An extensive media public awareness campaign was supplemented by pamphlets sent to ticket purchasers informing them of preventive measures. The Georgia State Division of Public Health, the Red Cross and the Salvation Army combined to provide shelter, water, wide-brimmed hats, fans, sunscreen and prevention information to pedestrians along corridors to Olympic venues. In addition, water misters attached to high velocity evaporative fans were placed at 25 of the most crowded sites to help cool spectators and pedestrians. State health officials distributed guidelines on recognition and management of heat-related illness to EMS providers and hospitals. Heat-related illness was less common than anticipated, diagnosed in only 10% of patients examined by physicians at Olympic venue clinics and first aid stations. This may have reflected the cooler than expected weather: average air temperatures and relative humidities during the 17 days of Olympic competition were 23.4¡C and 83% (0700), 29.4¡C and 63% (1300) and 27.7¡C and 67% (1900),9 and the temperature range was 20¡C to 37¡C (Southeast Regional Climate Center, personal communication). In addition, the impressive promotion and preventive activities probably contributed to the control of heat-related illness. Food safety and environmental health: The enormous influx of visitors made food safety and prevention of foodborne illness critically important. About 150 food and drug inspectors from throughout Georgia and other areas of the US were employed to inspect and monitor food vendors, who were required to comply with strict state health and safety regulations and to have an official licence. General environmental health services, such as water testing, sanitation services and solid waste disposal, were augmented by local and state public health officials. On the first day of Olympic competition, two unlicensed food vendors were detected in the Olympic Village, and were implicated in the development of diarrhoeal disease by two residents. However, food safety precautions were in general highly successful. According to the Department of Human Resources, the Atlanta Olympic Games were the first in the modern era to have no major outbreak of foodborne disease. A mosquito infestation at the Olympic Village was investigated by state environmental health officers and control measures recommended to ACOG. Infectious diseases: A large international gathering such as the Olympic Games may allow intercontinental transmission of microorganisms, which may be drug-resistant. 4 During a previous international sporting event in the US, a measles outbreak was traced to a visiting athlete.5 At the Atlanta Olympics, the active surveillance for unusual presentations and infectious disease outbreaks was designed to allow same-day medical and public health interventions. In addition, physicians and public health workers initiated a safe-sex campaign to limit the spread of STDs. Posters, pamphlets and buttons in 17 languages were used to communicate a "safe sex" message, and 50 000 condoms in Olympic colours were distributed at the Polyclinic. The surveillance system detected no outbreaks of any of the 40 diseases notifiable in the US, nor any increase in STD incidence in the Atlanta metropolitan area. Disaster preparedness Disaster planning was a key component of Oympic preparations. The City of Atlanta and the State of Georgia are prone to natural disasters, such as hurricanes and tornadoes; Hurricane Bertha had threatened the Georgia coast in the week before the Games, and state Disaster Medical Assistance Teams had been placed on alert. However, of greater concern was the potential for a major terrorist attack. The recent bombings in Oklahoma City and at the World Trade Center had shown that the US was prone to major terrorist incidents, while the 1995 sarin gas attack in Tokyo showed that terrorists had access to new weapons. Local agencies and institutions within Atlanta worked extensively on disaster planning. As well as revising disaster plans, many medical institutions developed educational programs to address mass casualty incidents. Over 1700 emergency room staff and prehospital personnel were trained in management of patients exposed to chemical, biological or nuclear agents, and disaster drills were conducted. However, the City of Atlanta and each of the seven counties within metropolitan Atlanta had separate disaster plans, and no centralised coordinating body was established to optimise use of the limited resources. State disaster preparedness was coordinated by the Georgia Emergency Management Agency and the Department of Human Resources. State officials, recognising they lacked the resources to deal with a major terrorist event, especially involving a chemical, biological or nuclear agent, officially requested assistance from federal agencies, including the US National Disaster Medical System. Urban Search and Rescue teams were brought to Atlanta from around the US to assist with extrication and care of victims of, for example, a building collapse. Five-member Disaster Medical Assistance Teams were stationed at key points around the city to facilitate a rapid medical response. The Marines deployed a highly skilled 300-member Chemical-Biological Incident Response Force. Forensic and laboratory services were provided by units from the Federal Bureau of Investigation, the US Army and the US Navy, Environmental Protection Agency, and CDC. In addition, members of these units were stationed at a specially convened Science and Technology Center at CDC to provide expert public health and emergency medical, toxicological and scientific consultation. The responsibilities of US federal government agencies in domestic disaster response are outlined in the Federal Response Plan. 10 For the Olympic Games, a supplementary document, the Federal Consequence Management Response Plan ,11 was developed. ACOG also developed a separate medical disaster plan to address incidents within Olympic venues and the Olympic Village. If a disaster within the Olympic "fence" exceeded the capabilities of ACOG, local, state and federal resources were to be mobilised. The bombing at Centennial Olympic Park on 27 July resulted in two deaths and 111 victims presenting to city hospitals. Most injuries were relatively minor, with only 24 victims requiring inpatient admission. The incident was handled with local resources, and the FBI was the only federal agency to respond. Although the medical care provided to the victims of the bombing was excellent, the incident demonstrated the difficulties of effecting a rapid disaster response despite extensive preparations. Coordination of EMS activities was suboptimal, as excessive numbers of ambulances were dispatched before adequate assessment of the scene, potentially depleting EMS services to other areas of the city and contributing to vehicular congestion around the scene. Fortunately, this lack of coordination had negligible effects on patient care and outcomes (Denis Lockeridge, District III EMS Co-ordinator, personal communication). Conclusion During the Olympics, the sheer volume of people visiting the host city poses significant challenges to medical and public health communities. Meeting these challenges requires the contributions of multiple agencies and service providers. Although there were several significant problems of communication and cooperation between providers at the Atlanta Olympics, the overall provision of medical and public health services was of the highest order. Excellent health promotion and prevention activities before and during the Games resulted in fewer medical and public health problems than had been anticipated. As Sydney prepares for the year 2000 Olympics, Australian health officials could do well to learn from the Atlanta experience. References Baker WM, Simone BM, Niemann JT, Daly A. Special event medical care: The 1984 Los Angeles summer Olympics experience. Ann Emerg Med 1986; 15: 185-190. Weiss BP, Mascola L, Fannin SL. Public health and the 1984 summer Olympics: The Los Angeles County experience. Am J Public Health 1988; 78: 686-688. Thompson JM, Savoia G, Powell G, et al. Level of medical care required for mass gatherings: the XV winter Olympic Games in Calgary, Canada. Ann Emerg Med 1991; 20: 385-390. Stienbecker RS, Steinberg JP, Schwartz B, et al. Evaluation of travelers returning from the 1992 Olympics in Barcelona, Spain: did they acquire resistant pneumococci and meningococci? Clin Infect Dis 1995; 220: 731-732. Ehresmann KR, Hedberg CW, Grimm MB, et al. An outbreak of measles at an international sporting event with airborne transmission in a domed stadium. J Inf Dis 1995; 171: 679-683. Leonard RB. Medical support for mass gatherings. Emerg Med Clin North Am 1996; 14: 383-397. Centers for Disease Control and Prevention. Prevention and management of heat-related illness among spectators and staff during the Olympic Games -- Atlanta, July 6-23, 1996. Morb Mortal Wkly Rep 1996; 45: 631-633. Sparling PB. Expected environmental conditions for the 1996 summer Olympic Games in Atlanta. Clin J Sport Med 1995; 5: 220-222. Sparling PB. Environmental conditions during the 1996 Olympic Games. Clin J Sport Med . In press. Federal Emergency Management Agency. Federal Response Plan. Washington, DC: Federal Emergency Management Agency, 1992. Federal Emergency Management Agency. Federal Consequence Management Response Plan -- 1996 Summer Olympic Games. Washington, DC: Federal Emergency Management Agency, 1996. (Received 8 Jul, accepted 28 Jul, 1997) Authors' details Centers for Disease Control and Prevention, Atlanta, Georgia, USA. Richard J Brennan, MPH, FACEM, Visiting Scientist, Emergency, Refugee and International Health, National Center for Environmental Health; Scott F Wetterhall, MD, Medical Epidemiologist, Office of Program Planning and Evaluation; R Joel Williams, DVM, MS, Epidemiology Intelligence Service Officer, National Center for Infectious Diseases; Edward L Baker, MD, Director, Public Health Practice Program Office; Scott R Lillibridge, MD, Associate Director, Emergency, Refugee and International Health, National Center for Environmental Health. Division of Emergency Medicine, Emory University School of Medicine, Atlanta, Georgia, USA. Mark E Keim, MD, Fellow in Disaster Medicine. Headquarters, United States Marine Corps, Washington, DC, USA. Trueman W Sharp, MD, MPH, Preventive Medicine Officer. 1996 Centennial Olympic Games, Atlanta, Georgia, USA. John D Cantwell, MD, Chief Medical Officer. Reprints: Dr R J Brennan, Center of Excellence in Disaster Management and Humanitarian Assistance, 1 Jarrett White Road (MCPA-DM), Honolulu, HI 96814, USA. E-mail: brennanrATwebsite.tamc.amedd.army.mil - ©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.

Richard J Brennan · Mark E Keim · Trueman W Sharp · Scott F Wetterhall · Edward L Baker · John D Cantwell · Scott R Lillibridge

The Polyclinic at the 1996 Atlanta Olympic Village S Boyd Eaton, Blane A Woodfin, James L Askew, Blaise M Morrisey, Louis J Elsas, Jay L Shoop, Elizabeth A Martin and John D Cantwell The Polyclinic, staffed mainly by volunteers, successfully provided primary health care during 16 519 patient encounters, 64% involving athletes. However, the profile of patient needs held some surprises. MJA 1997; 167: 599-602 Introduction - Planning, physical facilities and staff - Administration - Special services - Clinical services - Ancillary services - Further considerations - Use profile - Conclusions - Authors' details - - - ©MJA1997 The best way to pay tribute to an illustrious past obviously lies in learning lessons from it to prepare for the future. Baron Pierre de Coubertin (instigator of the modern Olympic Games and first President of the International Olympic Committee) Introduction This report describes the challenges and experiences of operating the Olympic Village Polyclinic, the health centre for athletes and staff during 33 days of preparation for and competition in the 1996 Olympic Games. In Coubertin's spirit, we hope the analysis will be useful to medical care planners for future events, including the Sydney Olympic Games in 2000. Planning, physical facilities and staff The Polyclinic's mission was to care for athletes (3100 women and 7750 men) and Olympic "family" (4500 administrators, coaches, officials, physicians and trainers) living in the Olympic Village. Other personnel (4000 volunteers, 3600 contracted service employees and 1800 security forces) were also given emergency and, when expedient, routine services. The planning committee had 25 members, comprising administrators, trainers, dentists, nurses, optometrists, podiatrists and physicians, and began work in 1992. Several members had been observers at the Barcelona Olympic Games (1992) and the Lillehammer Winter Games (1994) and operated a small polyclinic during the 1994 Goodwill Games in St Petersburg. The Polyclinic was established in the Student Health Center of the Georgia Institute of Technology, under a contract between the Atlanta Committee for the Olympic Games (ACOG) and the Institute. The Health Center is a two-storey building with a floorspace of about 2300m2 renovated in 1994-1996. Personnel from the Health Center formed the nucleus of the clerical and administrative staff, while shifts of volunteers helped meet the demands of 24-hour operation. Overall, 18% of staff were employed (39% of clerical and administrative staff) and 82% were volunteers. The physical facilities and staff of the Polyclinic are shown along with patient numbers in Box 1. Administration Patient reception and medical record storage were adjacent, and cross-trained staff could work in either area. Incoming telephone and facsimile lines were also housed there, but use greatly exceeded expectations and hampered other operations. The admitting area was often congested by non-patients. Patient registration and other paperwork were handled manually, as computerised filing was unavailable. The process would have been improved by optical scanning of bar-coded accreditation, automated generation of encounter forms and computerised generation of epidemiological data. Special services Sports medicine: Physical and massage therapy and athletic training were housed in a separate facility about 750 m from the Polyclinic and handled by athletic trainers and physical therapists supervised by the Village Medical Director. Patients could be referred by team or Polyclinic physicians or could self-refer. In the latter case, they were assessed by an athletic trainer or physical therapist, and any whose condition was in doubt were sent to the Polyclinic for evaluation. There were about 2000 visits for massage therapy and 3000 for physical therapy with, to our knowledge, no inappropriate treatment. Doping control: Two rooms were maintained so athletes unable to void after evening competition could be observed in a central location; these were used nearly every day. Gender verification: This program, mandated by the International Olympic Committee (IOC), was segregated from the rest of the Polyclinic, with a separate entrance so that large numbers of athletes could be processed without congesting clinical areas. All women athletes participated, except those competing in equestrian events (which are mixed-sex) and those who had been gender-certified at previous Olympic competitions. Height and weight were recorded, a photo-identification card was made, and a series of buccal smears were obtained for DNA extraction; the process required about 10 minutes. About two-thirds of gender testing was done over the six days around Opening Ceremonies, when the unit operated from 0800 to 2200. It processed 837 athletes on the peak day. Specimens, identified by number, were sent by bonded courier to the Emory University Genetics Laboratory, in Atlanta, for analysis. A few participants were found to have SRY DNA (generally about one woman in 500 has a Y chromosome) and were further evaluated by a medical geneticist and a female gynaecologist, with prompt, confidential examinations to avoid stigmatisation. No men masquerading as women were encountered, and all participants were cleared for competition. However, in future Games, it may be more efficient for gender verification to be housed at the Accreditation Center rather than at a medical facility. Clinical services Dentistry: A team of volunteer dentists (including an oral surgeon), dental assistants and hygienists served about 910 patients, taking over 500 dental radiographs and performing about 400 fillings (290 amalgam, 110 composite), 84 extractions, 62 endodontal procedures and 14 oral surgical operations. Eye services: Each shift included two optometrists, an ophthalmologist and an optician. The 790 patients were provided with 620 pairs of spectacles and 50 sets of contact lenses. Beyond vision correction, clinical problems included corneal abrasions, conjunctivitis, pterygium, pingueculitis, glaucoma and blepharitis. Three chalazion excisions and one repair of a post-traumatic cicatricial ectropion were performed. Primary care: Patients with general medical complaints were treated by internists (primary care physicians) and family practitioners, assisted by registered nurses. Sprains and strains were the most common conditions (Box 2); those involving athletes were referred to orthopaedic surgeons. Exotic infectious disease was less common than anticipated, with eight cases of malaria (seven had been previously diagnosed), three of hepatitis and one of filariasis. Nine patients requested HIV tests, yielding no positive results. An unexpected amount of time was required for telephone consultation with National Olympic Committee team physicians, most of whom requested notification before their country's participants were evaluated or treated. Establishing these contacts was often difficult. Another time-consuming activity involved patients initially sent to primary care but ultimately referred to specialty care. A triage physician stationed in the admitting area would have improved patient flow. Orthopaedics: 222 patients (70% of them athletes) were treated. Knee injuries were especially common (about 70), equalling in frequency the next three most numerous injuries (hand/wrist, ankle, and shoulder). Orthopaedic supports, especially knee braces, were in short supply; a larger stock (starting each day with 6-8 in each size) would have been desirable. Twelve arthroscopic procedures, chiefly meniscectomies and cruciate ligament reconstructions, were performed off site by Polyclinic orthopaedic surgeons during the Games. Other specialty care: Unexpectedly few gynaecology patients (25) were treated, despite a record number of women athletes and staff. A contributing factor may have been the presence of some male gynaecologists; several patients refused services on learning the physician on duty was a man. One athlete was unexpectedly found to be pregnant. Similarly, surprisingly few patients availed themselves of the psychiatry/sports psychology service, and no visits were related to the Centennial Park bomb explosion. However, the encounters that occurred emphasised the service's importance. One athlete became overwhelmed by the prospect of Olympic competition, deciding to return home prematurely, but after psychological intervention successfully advanced to the quarter-finals. In another case, emergency treatment was needed for an acute psychotic breakdown. Podiatrists saw over 200 patients and dispensed modified orthotic devices for 65. Dermatologists treated 112 patients, while nearly 240 additional patients with skin disorders were treated by primary care physicians. Otolaryngologists saw 110 patients; two rooms were originally designated for otolaryngology, but one was sufficient, and the other was used for eye services. Emergency medicine: 24-hour emergency care was provided. Each shift comprised one emergency physician and two ambulance-based paramedics, with two registered nurses during the day, but only one at night. A night-time clerical support person would have been very helpful. Patient numbers ranged from 4 to 22 (night) to 3 to 9 (day). Chest pain, lacerations, abdominal pain, multisystem trauma, head injuries, and seizures were common presenting complaints. Heat-related conditions, often problems at outdoor events, were uncommon (29 cases). Communication with National Olympic Committee team physicians, competition venues, referral hospitals, the medical command centre, and especially with ambulance crews, was a vital emergency physician function. About 125 patients were transported from the Village to one of two nearby Olympic-affiliated hospitals. Of these, about a third were dispatched directly from the pick-up point, while the rest were first evaluated at the Polyclinic. About 70% of patients sent to area hospitals were discharged after evaluation. Ancillary services Pharmacy: Pharmacists were present 18 hours per day; emergency call-back was available but unnecessary, as drugs in the emergency room were adequate for night-time needs. All drugs in the IOC-approved drug formulary were stocked, while restricted and prohibited drugs were stored separately and flagged in the pharmacy computer to prevent inappropriate dispensing. Just over 3600 prescriptions were filled, with a one-day high of 219. Ibuprofen, amoxycillin, naproxen, acetaminophen, cimetidine, clotrimazole, diazepam, terfenadine, guaiphenesin/dextromethorphan and phenol/menthol lozenges were most commonly dispensed, but 282 different preparations were ordered at least once. Clinical laboratory services: Laboratory services were available from 0700 to 2300 during the first 10 days and around the clock thereafter, requiring 10 technicians to work overlapping shifts. About 500 patients were referred for 937 tests, including complete blood counts (213), biochemical profiles (129), urinalyses (114), group A streptococcal screens (42), and erythrocyte sedimentation rates (33). A fifth of all ordered tests were performed at a nearby laboratory (e.g., stool sample culture/sensitivity or "ova/parasites", thyroid profiles and microscopy of malaria smears). Imaging services: In preparation for the Games, the Health Center's radiography room was updated to allow digital acquisition and processing of radiographs. Sponsoring manufacturers provided ultrasound equipment and a mobile magnetic resonance imaging (MRI) unit (placed in a nearby car park). Teleradiography links were established with two Atlanta hospitals. Imaging included 744 radiography examinations on 634 patients (about 60% athletes), with 50 examinations on the peak day; 204 MRI studies (mostly musculoskeletal); and 112 ultrasound studies (about half musculoskeletal). Further considerations Language services were provided by translators, generally via "speaker" telephones; 31 languages were available and service was always provided within 45 seconds. Although translators were not specially trained in medical terminology, it was always possible to obtain adequate histories and other necessary clinical data. As the security cordon around the Village complicated resupply, an individual was assigned logistical responsibility. He became familiar with the elaborate (and frequently changing) protocols for moving supplies and equipment into the Village after "lock-down", and developed a good relationship with logistics and security officials. Thus incorporated into the system, the Polyclinic was able to procure necessary matŽriel despite the burdensome bureaucracy, even when unanticipated needs arose. The possibility of terrorism was considered during planning. Polyclinic personnel received instruction on bomb blast injuries and care of chemical/biological warfare victims. The pharmacy stocked pralidoxime chloride and atropine for treating nerve gas poisoning. A facility was prepared for hosing down individuals contaminated with gas or radio activity. Atlanta's chiropractic community offered to provide services in the Village. This proposal was referred to the IOC Medical Commission, which, in keeping with previous Olympic practice, ruled against accepting the offer. Use profile Use of the Polyclinic followed the Seoul/Barcelona pattern: operations began 13 days before Opening Ceremonies and extended for three days after Closing Ceremonies. The slow first week was invaluable; equipment was tested, personnel became familiar with the system, supply deficiencies were corrected and unexpected problems were addressed. Thereafter, volume increased to a plateau extending from before Opening Ceremonies to the end of the first week's competition. Use gradually declined until Closing Ceremonies, and then fell rapidly. Demand for MRI and ultrasound imaging increased steadily. Conclusions Most Polyclinic staff were volunteers, who provided commitment and enthusiasm, as well as expertise. However, most were unable to serve throughout the Games, which meant personnel varied from day to day, introducing confusion and inefficiency during the early stages and hindering effective communication. However, although using fully contracted staff may have avoided these problems, we believe the esprit de corps provided by volunteers far outweighed the inconveniences. Interaction with public health officers was more important than originally anticipated, requiring near-daily communication between Polyclinic physicians and the public health team, chiefly about potentially communicable diseases. Athletes, and especially Olympic "family", could be regarded as taking advantage of the opportunity to obtain free eyeglasses and dental fillings. Perhaps providing these has become an unstated obligation of the host city; clarification with the IOC Medical Commission is probably in order. No amount of preparation can anticipate all contingencies, so a flexible outlook is essential. While the 1996 Polyclinic usually adjusted appropriately, triage was a failure. The need for a physician to direct patient flow became apparent immediately, but schedules could not be revised to allow this. In contrast, the eyecare team was able to successfully reorganise procedures for spectacle delivery when it became apparent that the original plan was inadequate. While aspects of its organisation and function could have been improved, the Polyclinic achieved its most important objective - providing medical services during 16 519 overall encounters, 10 641 (64%) of which involved athletes. With respect for the sentiments of Baron de Coubertin, and in the Olympic spirit, we hope this report will help health care personnel charged with like responsibilities in the future to approach the optimum more closely. (Received 25 Mar, accepted 26 Sep, 1997) Authors' details Olympic Village, Atlanta, Georgia, USA. S Boyd Eaton, MD, Polyclinic Medical Director; Blane A Woodfin, MD, Village Medical Director; James L Askew, MD, Village Medical Coordinator; Blaise M Morrisey, MHA, Polyclinic Administrator; Louis J Elsas, MD, Gender Verification Director; Jay L Shoop, ATC, Sports Medicine Director; Elizabeth A Martin, PT, Medical Services Program Director; John D Cantwell, MD, Chief Medical Officer, Atlanta Committee for the Olympic Games, Atlanta, Georgia, USA. Reprints: Dr S B Eaton, Suite 110, 3193 Howell Mill Road NW, Atlanta, Georgia, 30327 USA. E-mail: sboydeatonATaol.com - ©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.

Blane A Woodfin · James L Askew · Blaise M Morrisey · Louis J Elsas · Jay L Shoop · Elizabeth A Martin · John D Cantwell

Hospital use by Olympic athletes during the 1996 Atlanta Olympic Games Mark E Keim and Dianne Williams Only 43 athletes presented to the hospital at the Atlanta Olympics; their conditions fell within the range routinely seen in modern hospitals. MJA 1997; 167: 603-605 Introduction - Hospital preparation - Presentations - Investigations - Course in the Emergency Department - Course during hospitalisation - Planning for future Games - References - Authors' details - - - ©MJA1997 Introduction The Centennial Anniversary Olympic Games in Atlanta, Georgia, in the summer of 1996 was the largest gathering of athletes for any event in history. Over 10 000 athletes from 197 countries converged on Atlanta. Support services, including medical care, were provided by the Atlanta Committee for the Olympic Games (ACOG). Primary medical and dental care was provided by the Polyclinic in the Olympic Village (a closed compound on the campus of the Georgia Institute of Technology) (see Eaton et al.). Medical evaluation or treatment beyond the scope of non-emergency outpatient care was referred to a nearby hospital, Crawford Long Hospital of Emory University. This 600-bed hospital is located within five blocks of the Olympic Village and within three kilometres of the Olympic Stadium. It was selected by ACOG as exclusive provider of outpatient emergency medical services and hospitalisation for athletes. ACOG also made agreements with local ambulance providers for emergency medical services and transport of athletes to the hospital. Crawford Long Hospital sought advance information on athletes' medical needs at the Olympics, but little has been published on this topic. Only recently have articles on public health and spectator medical care at the Los Angeles, Calgary and Barcelona Games been published.1-4 To our knowledge, no reports have focused on the specific medical needs of athletes at the Olympics. Therefore, we conducted a retrospective review of the hospital records of all Olympic athletes presenting to hospital in the period around the 1996 Atlanta Olympics (July 14 to August 7, 1996). Hospital preparation Armed security was provided for athletes by the hospital security force, which comprises fully deputised public law enforcement officers with full jurisdiction to arrest and detain suspected law violators. The watch around the hospital perimeter and on all hospital property was increased. In the Emergency Department, athletes were evaluated in private rooms with an armed sentry outside the door at all times. During hospitalisation, athletes were housed on a single floor with access restricted by armed security. The placement of sentries in the outpatient diagnostic centre during athlete outpatient visits was not documented. The hospital organised interpreting services with a language translation telephone service provided by IBM, as well as with local multilingual volunteers. Presentations Forty-three Olympic athletes presented to the hospital between 14 July and 7 August 1996; 31 of these presented to the Emergency Department (about 0.31% of all Olympic athletes), with 14 subsequently admitted to hospital. Another eight were admitted after direct referral by team or Polyclinic doctors, and four were referred for outpatient diagnostic services -- bone radioscintigraphy, computed tomography, and magnetic resonance imaging. Numbers of presentations per day ranged from zero to six, peaking on 24 July. No athletes presented after the bombing of the Centennial Olympic Park on 27 July, which killed two people and injured 111. Further, Crawford Long Hospital received few victims despite its proximity to the Park, due in part to a community triage system designed to keep facilities in reserve in case of a secondary attack on athletes. The presenting athletes comprised 16 women (37%) and 27 men (63%), with age range 16-36 years (mean, 24.7 years). Hospital presentations according to competitive event are shown in Box 1; the highest numbers were for participants in boxing, wrestling and track events (five each). The most frequent countries of origin were Australia (four) and Russia, South Africa and South Korea (three each). Fifteen patients (35%) required interpreters. Twenty-two athletes arrived by ambulance. Venues most often needing ambulance transport were boxing (four athletes), track-and-field and cycling (three each), and judo (two). Twenty-two athletes underwent some degree of formal medical evaluation before arriving at Crawford Long Hospital; three of these were evaluated in hospital emergency departments closer to the venue where the injuries occurred, but were then transferred by ambulance to Crawford Long Hospital. No extra security was arranged for this transfer. Most complaints (30; 70%) were described as caused by a sport-associated injury. For 20, the injury occurred during competition and, for seven, during training (time of others was unknown). Ten cases were associated with exacerbation of pre-existing illness or injury, most commonly degenerative disc disease (four), followed by patellar tendinitis and jaw fracture (two each). However, 24 athletes denied any significant past medical history. Investigations Most diagnostic work-ups in the Emergency Department and in hospital were routine. Laboratory studies included 22 complete blood counts, 17 urinalyses, 27 biochemical profiles, microscopy of one malaria smear, and serological tests for dengue fever virus and ehrlichiae. Other investigations included 29 radiographs, six computed tomography (CT) scans of the head, one magnetic resonance imaging (MRI) study of the knee, one bone radioscintigraphy (BRS) study of the leg, three electrocardiograms, one echocardiogram, one pelvic ultrasound examination, and one radionuclide heart scan. In addition, outpatient radiological studies were provided for four athletes: CT scan of the spine for one athlete with back pain (showing no abnormalities), MRI of the ankle for another (showing a tarso navicular fracture), and BRS of the leg for two (showing stress fractures of the femur and tibia, respectively). Course in the Emergency Department Primary diagnoses of the 31 athletes who presented to the Emergency Department are shown in Box 2. Most conditions were trauma-related (23; 74%); none were considered life-threatening. The most common primary diagnosis was concussion (four). Sixteen (52%) were discharged home, while one left without being evaluated after having been referred for an orthopaedic brace. (The athlete did not require medical evaluation but requested only the brace. Hospital policy required evaluation by a physician before goods or medications could be dispensed.) Course during hospitalisation Diagnoses on discharge for the 22 athletes admitted to hospital are shown in Box 3. These athletes spent a total of 37 days at Crawford Long Hospital. Two had same-day surgery (knee arthroscopies) without an overnight stay, and 14 had one-day stays. The longest stay was five days (one patient with malaria with thrombocytopenia, and another with a radius fracture requiring open reduction and internal fixation). There were no complications during hospitalisation. Apart from one appendicectomy, all surgical procedures were orthopaedic (including knee arthroscopy, open reduction and internal fixation of radius, subtotal meniscectomy, three tendon repairs [two patellar and one Achilles], and a closed-reduction of the mandible with wiring). Only one athlete required overnight cardiac monitoring, and none required critical-care facilities. All but one of the hospitalised athletes were discharged home. The exception, who was admitted with fever and a thigh abscess, checked out of the hospital against medical advice after a one-day stay. Planning for future Games The medical and surgical needs of athletes at the Atlanta Olympics fell within the range encountered routinely in modern hospitals. The secondary care of athlete patients required no extraordinary equipment or facilities. However, the situation generated some special needs which warrant consideration by future planners of medical care for Olympic athletes. These include the need for:* A comprehensive memorandum of agreement with ambulance services to allow for a catchment area that includes all athlete activities, including leisure activities, throughout their stay; * A continuous chain of security that includes prehospital transport, outpatient studies, emergency department and inpatient hospitalisations; * An easily accessible language translation service; * Ready availability of hospital-based clinicians, including emergency medicine specialists, orthopaedic surgeons, internists (general physicians), radiologists, neurosurgeons, oral surgeons, cardiologists, general surgeons, and anesthetists; * A small outpatient dispensary as a back-up to provide athletes with medical equipment and supplies not readily available at primary medical facilities; and * A hospital emergency contingency plan that includes response to an attack against athletes and is coordinated with the community response. References Baker WM, Simone BM, Niemann JT, Daly A. Special event medical care: the 1984 Los Angeles summer Olympics experience. Ann Emerg Med 1986; 15: 185-190. Steinbecker RS, Steinberg JP, Schwartz B, et al. Evaluation of travelers returning from the 1992 Olympics in Barcelona, Spain: did they acquire resistant pneumococci and meningococci? Clin Inf Dis 1995; 220: 731-732. Thompson JM, Savoia G, Powell G, et al. Level of medical care required for mass gatherings: the XV winter Olympic Games in Calgary, Canada. Ann Emerg Med 1991; 20: 385-390. Weiss BP, Mascola L, Farnin SL. Public health and the 1984 summer Olympics: The Los Angeles County experience. Amer J Pub Hlth 1988: 78; 686-688. (Received 8 Jul, accepted 26 Sep, 1997) Authors' details Division of Emergency Medicine, Emory University School of Medicine, Atlanta, Georgia, USA. Mark E Keim, MD, Disaster Medicine Fellow. Crawford Long Hospital of Emory University, Atlanta, Georgia, USA. Dianne Williams, RN, MSN, Emergency Department Director of Nursing. Reprints: Mark E Keim, MD, Division of Emergency Medicine, 69 Butler Street, SE, Atlanta, GA 30303, USA. E-mail: mkeimATemory.edu - ©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.

Mark E Keim · Dianne Williams