Sports medicine

Non-surgical intervention has many benefits. A recent article published in the Journal1 was widely reported in the popular press, with statements such as the following being quoted: public health messages encouraging people to eat healthy food and to exercise are unlikely to have long-term impact on their weight....

Daniel J Green PhD · Andrew J Maiorana PhD

There are many challenges in developing evidence-based physical activity guidelines for preschoolers that can ensure health benefits for children.Guidelines for the preschool years have recently been developed in several countries, but there are notable inconsistencies in the amount of physical activity regarded as sufficient for this age group.Given the currently high prevalence of childhood obesity, there is an....

Helen Skouteris PhD · Daniela Dell'Aquila BSocSci(Psych), PostGradDip(Psych) · Louise A Baur BSc(Med), PhD, FRACP · Genevieve M Dwyer MAppSc(Phty), PostgradCert (AdultEd · Marita P McCabe PhD · Lina A Ricciardelli PhD · Matthew Fuller-Tyszkiewicz PhD

Objectives: To examine the prevalence of overweight and obesity in Australian secondary school students and identify factors associated with excess adiposity....

on behalf of the NaSSDA Study Team*

Objectives: To highlight a fun activity — the sport of wife carrying — and to investigate factors associated with better performance.Design, setting and participants: Cross-sectional study based in Sonkajärvi, Finland (venue of the annual Wife Carrying World Championship race), of 172 couples participating in wife-carrying races, 1992–2010.Main outcome measure: Race finishing time.Results: The mean age for male participants was 32.6 (SD, 8.7) years and for female participants, 30.5 (SD, 9.2) years. The mean finishing time was 98 s. Finish times tended to be somewhat slower as the age of the male partner increased (P = 0.06), but not as the female partner’s age increased (P = 0.89). Race experience was not associated with faster times (P = 0.88). Estonians were almost 12 s faster than other nationalities, although this was not statistically significant (P = 0.25), probably due to the small number of Estonians. Men who engaged in endurance-type physical activities as hobbies (P = 0.003), or in both endurance- and strength-building activities (P = 0.001), were significantly faster than those who did neither. Among women, strength-building (P = 0.03) but not endurance-type (P = 0.36) physical activities were significantly associated with faster race times.Conclusions: Wife carrying can be a novel option for increasing physical activity levels, which improve health. Although some key data were unavailable, such as wife’s body weight, and injury rates, this study identified several factors associated with better performance in this sport.

I-Min Lee MB BS, ScD · Sylvia Titze MPH · Pekka Oja PhD

Clinical record A previously well 43-year-old Australian lawyer was hiking the Kokoda Track in Papua New Guinea in August 2008. She awoke with a headache on the second day and, suspecting dehydration, consumed about 7 L of fluid while hiking. By late afternoon she complained of increased headache and nausea, which was exacerbated by her lying supine. She developed seizures several hours after profuse vomiting. Temazepam and metoclopramide were administered rectally due to limited medical resources. Three doctors present provisionally diagnosed dilutional hyponatraemia but had no facilities for intravenous therapy. Arrangements were made for urgent repatriation by helicopter to Port Moresby but this was later abandoned due to bad weather. She deteriorated overnight, becoming unresponsive to painful stimuli and lapsing into coma. Her vomiting and convulsions continued. With no rescue imminent, salt solution approximating normal saline was administered rectally. There was some improvement in eye-opening and verbal responses on the Glasgow Coma Scale. Fortuitously, an American naval hospital ship anchored outside Port Moresby retrieved her via helicopter the following afternoon. Her plasma sodium on arrival to intensive care was 114 mmol/L. After she was intubated and treated with intravenous hypertonic saline, the patient made a good recovery. Exercise-associated hyponatraemia (EAH) is a modern, life-threatening condition first described in 19851 after introduction of guidelines promoting excessive fluid intake during exercise.2 EAH is defined as hyponatraemia occurring during or up to 24 hours after prolonged exercise (generally > 4 hours duration).3 This “conditioned overhydration” — drinking beyond thirst, variously influenced by misunderstanding of exercise physiology, media including sports-drink advertising,4 and forced rehydration protocols5 — has been reported among hikers,6 military personnel5 and long-distance sports participants.7 Despite being well documented in scientific literature, those most at risk are unaware of this preventable condition. EAH is common, with reported incidences of hyponatraemia (serum sodium concentration, < 135 mmol/L) and critical hyponatraemia (serum sodium concentration, < 120 mmol/L) during the 2002 Boston Marathon of 13% and 0.6%, respectively.7 At least eight fatalities have been documented8 — likely an underestimation given difficulties with postmortem diagnosis.9 The unexplained deaths in 2009 of four previously well hikers on the Kokoda Track in similar conditions provide urgency to the need to raise awareness of the association between overhydration and EAH. Extensive research confirms EAH is primarily dilutional secondary to overhydration,10 manifest as weight gain during exercise. That only a small proportion of individuals exposed to overhydration develop hyponatraemia suggests a role for associated underlying defects in free water excretion. These include exercise-induced non-osmotic antidiuretic hormone secretion,11 while the recent description of an activating mutation of the arginine vasopressin receptor 212 may explain the undetectable antidiuretic hormone levels found in other cases.13 Excessive-sweat sodium losses associated with subclinical cystic fibrosis have also been described.14 Identified risk factors for EAH8 include excessive drinking behaviour, weight gain during exercise, female sex, slow performance pace, high availability of drinking fluids, > 4 hours’ exercise duration and hot environmental conditions consistent with our scenario. Female sex hormones inhibit cellular sodium–potassium–ATPase function, which may explain the observed higher risk of EAH and cerebral oedema among women.8 Slow performance pace may reflect insufficient physical training and provides the opportunity for overhydration. Lessons from practice Military personnel, hikers and endurance sports participants are at risk due to overhydration during prolonged exercise. Non-specific symptoms are commonly mistaken for dehydration. Diagnosis requires a high degree of suspicion, and biochemical testing. Water should be consumed according to thirst and guided by weight comparison before and after exercise. Weight gain should be avoided, aiming for a 1%–2% weight loss during prolonged exercise. Education of at-risk groups is essential for prevention. Symptoms include lethargy, dizziness, headache, nausea and vomiting, with progression to confusion, ataxia, seizures and coma.3 Importantly, EAH cannot be easily distinguished clinically from heat exhaustion, with subsequent mistaken “rehydration” exacerbating the condition. EAH requires a high index of suspicion to facilitate timely evacuation for biochemical diagnosis and treatment. Specific clinical features include euvolaemia and polyuria. A recent review of 145 United States military cases identified that the training cadre often mistook EAH for dehydration, and treatment by aggressive water rehydration had fatal consequences in three cases.15 Overhydration was encouraged by well-meaning guides and colleagues in another near fatal case on the Kokoda Track reported in 2008.5 In this context, a prominent tour operator’s media assertion that “dehydration” in “the death zone”16 caused the recent deaths among young healthy Kokoda Track hikers may perpetuate a dangerous culture of conditioned overhydration. It is of grave concern that, in 2009, a second fatality occurred shortly after media speculation that dehydration was the cause of the first. Available evidence suggests that, in an environment of excess water (most trekkers carry > 4 L water per day), hikers on the Kokoda Track should be more concerned with severe EAH secondary to overhydration, rather than with dehydration. Initial treatment of EAH is fluid restriction to avoid exacerbation of hyponatraemia. Those with critical hyponatraemia or symptomatic, biochemically confirmed EAH require treatment with intravenous hypertonic saline (100 mL of 3% saline solution over 10 minutes) in a supervised environment. This is based on the assumption that the hyponatraemia is acute (< 48 hours) and that no cases of osmotic demyelination syndrome have been reported in treating EAH.3 No single preventive fluid intake regimen can be recommended to cover all activities. The Second International EAH Consensus Development Conference statement3 recommends drinking to thirst instead of a predetermined protocol. The aim should be never to gain weight during endurance exercise and to expect a small percentage weight loss (1%–2%) due to substrate use.3 Fluid intake requirements could be estimated for guided treks by comparison to baseline weight. Point-of-care electrolyte testing could be used. There is insufficient evidence to recommend salt tablet use.3 Importantly, there is no evidence that commercial sports drinks prevent hyponatraemia3 — in fact, given their sodium hypotonicity relative to normal saline (10–20 mmol/L v 145 mmol/L), excessive consumption could worsen hyponatraemia. At a public health level, education of those leading and participating in high-risk activities is critical. The number of EAH casualties at a New Zealand ultradistance event was reduced by spacing the distance between, and volume of fluid available at, drinking stations.17 EAH is a modern, life-threatening condition which is preventable through adherence to sensible fluid intake during prolonged exercise. Although American sports and military bodies have revised their guidelines, researchers have been critical of the sports-drink industry’s role in perpetuating a culture of overhydration.18 As medical practitioners, it is our responsibility to ensure the wider community is aware of the risks of conditioned overhydration during exercise in the face of lay misinformation and commercial interests.

David A Pattison MB BS · Tomos E Walters MB BS, BMedSci · Eric Seal MB BS, FRACP, PhD

To the Editor: Dinh and colleagues present data on head injuries among cyclists admitted to the emergency department of Sydney’s Royal Prince Alfred Hospital (RPAH) from 1991 to 2010,1 and conclude with their opinion that legislation mandating the wearing of bicycle helmets should be maintained. However, their data provide poor evidence of the efficacy of helmets and of the effectiveness of legislation requiring helmet use. Almost all studies of helmet efficacy are case–control studies, which, to be of high quality, require a well defined and matched control group. In the study by Dinh et al, the control group was made up of patients who had been wearing a helmet. Many possible explanations for injury severity were not considered. For example, were the non-helmeted cyclists drinking alcohol or riding faster? Were they more likely to be risk-takers? Were the helmet wearers also wearing high-visibility vests or using lights at night? Case–control studies of this kind are a weak form of evidence (ranking just above anecdotal evidence and case studies) and cannot answer questions of causality. The two graphs presented by Dinh et al show that head injury rates among cyclists were very low and fairly stable over most of the time period examined. RPAH treats thousands of trauma patients each year. The study reported on 287 cyclists admitted in a 2.5-year period — an average of 115 per year. Of these, only 14 (eight helmeted; six not wearing helmets) incurred major trauma — about six per year. Given that helmet legislation was in place for the entire study period, these data add no evidence for its effectiveness. In public health terms, the risk of injury needs to be weighed against the benefits of increased physical activity, reduced chronic disease and reduced air pollution due to more people cycling. Because of the low absolute rate of cycling injuries, these benefits are nine to 20 times the size of the risk.2,3 Further, it is well documented that levels of cycling in Australia dropped by 30%–40% when helmet legislation was introduced. This had the unfortunate effect of making cycling less safe for the remaining cyclists because of the “safety in numbers” phenomenon.4 The poor uptake5 of the two public bicycle-hire schemes in Australia (in Melbourne and Brisbane) indicates that helmets are a significant barrier to short-trip and spontaneous cycling, with few potential or casual users carrying a bicycle helmet in case they decide to hire a bicycle. Dinh and colleagues obviously believe in the efficacy of the bicycle helmet, but this does not mean that mandating their use is the best public health policy response. When helmet legislation was introduced, we did not have the epidemics of diabetes and obesity that now threaten to bankrupt state health budgets. Strategies to increase levels of physical activity among the whole population are desperately needed, even if there is a small risk involved.

Chris E Rissel · Paul Martin

To the Editor: The benefits of bicycle helmet use have been the subject of recent discussion, with calls from some experts to review laws mandating the wearing of helmets.1 The objective of this brief report is to summarise long-term trends in cyclist head injuries seen at an inner-city major trauma centre and determine the odds of any skull fracture or intracranial bleed associated with not wearing a helmet. This was a retrospective study conducted at the Royal Prince Alfred Hospital (RPAH, Sydney, New South Wales), covering several local government areas that have the highest bicycle-use rates in NSW,2 where the law for mandatory helmet wearing was enacted in 1991. Patient data were obtained through the hospital trauma registry, which contains data on all patients admitted to the hospital with trauma. These data included information on helmet use routinely abstracted from ambulance and medical notes. Inclusion criteria were cyclists admitted from 1991 to 2009, who were over 16 years of age and involved in an incident on a public road. We excluded patients transferred from other hospitals. Head Abbreviated Injury Scale (AIS) scores (AIS 1990, 1998 and 2005 versions3) were used, with a head AIS score ≥ 3 indicating severe head injury, such as significant intracranial bleeding or depressed or comminuted skull fracture. Injuries with an AIS score of 2 included isolated concussion and simple skull fractures. To investigate the association between helmet use and head injury, we reviewed the medical charts of all cyclists admitted with trauma from 2008 to June 2010. We compared mechanism of injury (fall off bike without collision versus collision with another vehicle or object), anatomical injury (skull fracture or intracranial bleed), helmet use and the type of road where the incident occurred (state or regional roads versus local roads), according to NSW Roads and Traffic Authority classifications. Data were analysed using Stata software, version 10.1 (StataCorp, College Station, Tex, USA). Percentages were calculated with 95% confidence intervals, and categorical data were compared using χ2 tests. Mean ages were compared using the Student t test, and a logistic regression model was used to obtain odds ratios for any skull fracture or intracranial bleed associated with not using a helmet, after adjusting for mechanism of injury and road type. The study was approved by the Sydney South West Area Health Service RPAH Ethics Review Committee (RPAH Zone). There were 979 patients who met our inclusion criteria. The long-term trend in the number of cyclists sustaining severe head injuries remained low (range, 0–3 per year) (Box 1). Cyclists as a percentage of total admissions for trauma increased from 1.3% in 2005 (29/2258 [95% CI, 0.9%–1.8%]) to 3.9% in 2009 (122/3104 [95% CI, 3.3%–4.7%]). Trends in helmet use and severe head injury are summarised in Box 2. Severe head injury rates as a percentage of total cyclists admitted decreased from 10.3% (3/29 [95% CI, 3.6%–26.4%]) in 2005 to 2.5% (3/122 [95% CI, 0.8%–7.0%]) in 2009, a relative reduction of 76%. Helmet use in admitted cyclists from 1991 to 2009 ranged from 85% to 100%. Information was available about the location of the fall and helmet use for 287 of the 313 cyclists identified from 2008–2010 (Box 3). Their mean age was 36 years (95% CI, 34–37 years) and 81% were men. Non-helmet wearers had five times higher odds of intracranial bleeding or skull fracture compared with helmet wearers after adjusting for road type and mechanism of injury (odds ratio, 5.3 [95% CI, 1.7–17.1]; P = 0.005). The increase in admissions for bicycle injury is consistent with recently reported population trends.4 In addition, the number of cyclists sustaining severe head injuries has remained consistently low over the long term, with an apparent decline in the rate of severe head injuries in admitted patients since 2005. The odds reduction for skull fractures and intracranial bleeds in those wearing helmets is within the range reported in a Cochrane review of helmet use.5 The benefits of helmet use need to be placed in the context of lifetime costs of severe traumatic brain injury, estimated to be around $4.8 million per incident case.6 It is the opinion of the trauma service at RPAH, based on these findings, that mandatory bicycle helmet laws be maintained, and enforced as part of overall road safety strategies. 1 Trends in cyclist admissions and head injuries in admitted cyclists, RPAH, Sydney, New South Wales, 1991–2009 AIS = Abbreviated Injury Scale. RPAH = Royal Prince Alfred Hospital. 2 Trends in bicycle helmet use and severe head injury as a percentage of total cyclist trauma admissions, RPAH, Sydney, New South Wales, 1991–2009 AIS = Abbreviated Injury Scale. RPAH = Royal Prince Alfred Hospital. 3 Head injury in helmet and non-helmet users among 287 cyclists admitted to Royal Prince Alfred Hospital with trauma, 2008 to June 2010 Helmet (n = 241) No helmet (n = 46) Significance† Age, years (95% CI) 36 (34–38 years) 33 (29–37 years) P = 0.14 Men (%; 95% CI) 196 (81%; 76%–86%) 39 (85%; 71%–92%) P = 0.60 Fall off bicycle* (%; 95% CI) 83 (34%; 29%–41%) 13 (28%; 17%–43%) P = 0.75 State/regional road (%; 95% CI) 63 (26%; 21%–32%) 11 (24%; 14%–38%) P = 0.75 Skull fracture or intracranial bleed (%; 95% CI) 8 (3%; 2%–6%) 6 (13%; 6%–36%) P = 0.005 * Without direct collision with another vehicle, object or person. † Two-tailed P < 0.05 significant.

Michael M Dinh · Susan Roncal · Timothy C Green · Elizabeth Leonard · Amanda Stack · Chris Byrne · Jeffrey Petchell

To the Editor: Sikic and colleagues state that the 1990 legislation making helmets compulsory for bicyclists in Victoria was associated with a decrease in non-fatal head injuries and fatalities.1 However, of the three citations given to support this statement (references 8–10 in Sikic et al),1 one is a study performed before the helmet law was introduced, another is an editorial, and the third makes the common error of attributing to helmet use the effects of economic recession and road safety campaigns. These together reduced all road deaths in Australia by about a third.2 Careful analysis takes account of such factors. Western Australia and New Zealand offer good datasets of injuries to cyclists and control groups through the period of increasing helmet use and enforcement: neither dataset shows evidence that mass helmet use reduced the occurrence of serious head injuries to cyclists.3 With fewer serious crashes, there were fewer serious head injuries, and a general reduction in severity of injury in road accidents for all road users. These observations make it hard to accept that cycle helmets reliably confer significant protection. Sikic et al further state that “Wearing an approved safety helmet substantially reduces the risk of serious head injury in cyclists who fall or are involved in collisions with motor vehicles”,1 citing case–control studies. Such studies are known to have serious weaknesses when applied to voluntary behaviour in a socially disparate population.4,5 Risk assessments do not justify helmet laws for cyclists alone. Analysis of Australian Government data (1988–1990) showed that cyclists faced a lower risk of death per hour than car occupants (0.41 v 0.46 fatalities per million hours of use).6 Wider risk assessment based on European data confirms that cycling risks are in the same range as for walking and driving.7 Sikic et al ask for further research to identify factors other than helmet wearing that contribute to preventing cycling injuries. One important factor is already well known: an increase in cyclists on the roads means less risk per cyclist.8 Considerable experience is now available to show that mass helmet use has not been effective in preventing serious head injuries in cycling populations.3 Enforced helmet laws in Australia may deter people from cycling9 and getting the major health benefits of moderate exercise.10

Malcolm J Wardlaw

In reply: The main conclusion of our population-based study1 was that a consistent increase in bicycle-related injuries occurred over the study period. Our study was not designed to analyse the effect of helmet wearing. The potential benefits of helmet wearing were identified in the discussion as a means of reducing the increasing burden of injury. There has been opposition to legislation enforcing helmet wearing in Australia.2 The response to this opposition has been adequately addressed by Canadian researchers.3,4 In addition, a number of Cochrane systematic reviews have arrived at different conclusions to Wardlaw.5,6 Although there are no randomised controlled trials, the weight of evidence would suggest that wearing helmets reduces head injuries in the bicycle-riding population and the imposition is worth the inconvenience to bicycle riders.

Antonina A Mikocka-Walus · Francis T McDermott · Peter A Cameron

Objectives: To describe rates of occurrence of falls, injuries and fatalities to horse-racing jockeys in Australia.Design and setting: Retrospective analysis of data on race-day falls from stewards’ reports provided by the Principal Racing Authority of each state and territory of Australia, August 2002 – July 2006.Main outcome measures: Fall, injury and fatality incidence rates; comparison with overseas rates.Results: There were 3360 jockey falls from 748 367 rides. Falls occurred at a rate of 0.42 per 100 rides in flat races and 5.26 per 100 rides in jumps races. In flat racing, 54.6% (1694/3101) of falls occurred before the start of the race and 11.1% (344/3101) of falls occurred post-race. The 34.3% (1063/3101) of falls that occurred during flat races resulted in 61.7% (516/836) of the injuries sustained. In jumps racing, most falls occurred at a jump and 9.7% (25/259) of jockeys who fell were transported to hospital and/or declared unfit to ride. There were five fatalities resulting from falls during the study period, all in flat racing. Fall and injury rates were comparable with those found in the United Kingdom, Ireland, France and Japan.Conclusions: Being a jockey carries a substantial risk of injury and death. Although rates of injury in Australia are not exceptional by international standards, there can be improvement to safety standards in the Australian racing industry.

Peta L Hitchens BAppSci(Equine), MVPHMgt · C Leigh Blizzard PhD · Graeme Jones MMedSc, MD, FRACP · Lesley M Day BSc(Hons), MPH, PhD · James Fell BEd, MPhil, PhD

Objective: To characterise injuries sustained in basketball and netball that result in hospital admission and to compare the profiles of injury between the two sports.Design and setting: Population-based retrospective descriptive epidemiological study using data from the National Hospital Morbidity Database, July 2000 to June 2004.Participants: Patients discharged from a public or private hospital with basketball or netball codes as the “activity when injured”.Results: There were 5090 basketball-related hospital admissions (mean patient age, 22.2 [SD, 10.7] years; 71.5% male) and 4596 netball-related admissions (mean patient age, 26.3 [SD, 10.9] years; 88.9% female). Fractures were the most common injury (46.8% [2384] of basketball-related and 29.5% [1358] of netball-related admissions), with the forearm and hand or wrist the most common fracture sites. The participant-based forearm fracture hospitalisation rate (5 + years age group) peaked in the 5–14-years age group. Anterior cruciate ligament rupture was the most common diagnosis, accounting for 760 (16.5%) netball-related admissions (mean [SD] age, 26.7 [8.4] years) and 354 (7.0%) basketball-related admissions (mean age, 25.5 [7.9] years). Achilles tendon injury accounted for 732 (15.9%) netball-related admissions (mean age, 35.2 [7.5] years) and 381 (7.5%) basketball-related admissions (mean age, 35.8 [7.8] years).Conclusions: The high rates of anterior cruciate ligament rupture and Achilles tendon injury resulting in hospital admission and their long-term consequences impact extensively on the individual and the community. The common injuries sustained in basketball and netball were strongly age-related.

Louise Flood MB BS · James E Harrison MB BS, MPH, FAFPHM

An otherwise healthy 28-year-old man had a cardiac arrest after a day of motocross racing. He had consumed excessive amounts of a caffeinated “energy drink” throughout the day. We postulate that a combination of excessive ingestion of caffeine- and taurine-containing energy drinks and strenuous physical activity can produce myocardial ischaemia by inducing coronary vasospasm. Clinical recordA 28-year-old male amateur motocross rider was admitted to Port Macquarie Base Hospital in August 2007 after having an out-of-hospital cardiac arrest. He had collapsed shortly after participating in a motocross race. An off-duty paramedic and nurse had been on hand, and effective cardiopulmonary resuscitation was commenced promptly. Paramedics arrived after about 20 minutes of resuscitation. The patient’s initial cardiac rhythm was recorded as ventricular fibrillation (Box 1). He was restored to sinus rhythm after receiving two 150 J biphasic direct-current shocks. Adrenaline 1 mg and atropine 1 mg were both given as adjuvants. He was intubated by paramedics and transported to hospital. Later, the patient recalled feeling well earlier in the day, until after his second race, when he developed dull constant retrosternal chest pain. He described this as being mild in intensity, with no radiation or associated symptoms. It settled within 30 minutes of sitting down to rest. He went on to participate in (and win) one more race that afternoon. He collapsed at about 3 pm, approximately 20 minutes after the last race. There had been no symptoms immediately preceding the collapse that he could recall. The patient had been well in the week preceding these events. He denied having any previous episodes of chest pain or syncope. He had a large breakfast on the morning of the motocross race and had remained adequately hydrated throughout the day. Further, he had consumed 7–8 cans of a caffeinated “energy drink” between 8 am and his collapse 7 hours later. He was otherwise fit and well and taking no regular medication. There was no family history of premature coronary disease, sudden cardiac death or unexplained syncope. He was a smoker with a six pack-year history of smoking. He denied alcohol misuse or illicit drug use. On arrival at hospital, the patient was intubated and sedated. He was haemodynamically stable, and physical examination was unremarkable. An initial electrocardiograph (ECG) showed sinus rhythm and elevated anteroseptal ST segments with reciprocal inferior ST depression. Chest x-ray showed a normal cardiac silhouette and no signs of pulmonary venous congestion. Computed tomography scans of the chest and brain were unremarkable, specifically excluding aortic dissection. Abnormal findings from laboratory tests included an elevated level of troponin I (0.24 mmol/L; reference range [RR], < 0.05 mmol/L) and a lowered potassium level (3.0 mmol/L; RR, 3.6–5.4 mmol/L). Results of a urinary screen for drugs of misuse, including amphetamines and cocaine, were negative. Screening for anabolic steroids was not performed. The provisional diagnosis was of anteroseptal ST elevation myocardial infarction. The patient was given thrombolysis with 50 mg of tenecteplase and commenced on an infusion of intravenous heparin. He was given loading doses of 300 mg of both aspirin and clopidogrel, and 25 mg of metoprolol, all by nasogastric tube. Hypokalaemia was corrected via intravenous infusion. The patient was transferred to a tertiary referral centre for cardiac catheterisation. On arrival there, an ECG showed evolving ischaemic changes across the anterolateral leads (Box 2). A troponin I peak level of 12.2 mmol/L was measured; his potassium level had normalised at 4.0 mmol/L. Echocardiography showed mild left ventricular enlargement and low-normal systolic function with a hypokinetic anteroseptal segment. Coronary angiography, performed on the same day, gave normal results. No attempts were made during angiography to induce vasospasm. The patient was cooled for 24 hours and extubated without difficulty. He was discharged after 6 days. At discharge, he was taking atenolol 50 mg, aspirin 100 mg, spironolactone 25 mg and perindopril 2.5 mg. On follow-up 2 months later, the patient reported that he had remained well and symptom-free. Echocardiography showed preserved global left ventricular function with a limited residual area of akinesis of the anteroseptal wall. He continued taking aspirin, perindopril and atenolol (reduced to 25 mg). He was advised not to compete in motocross races for 6 months, after which a stress echocardiogram was performed; this was negative for exercise-induced ischaemia. DiscussionWe postulate a possible role of excessive consumption of caffeinated energy drinks in triggering the life-threatening cardiac events described in this case. Although sudden cardiac death is an uncommon occurrence in people under the age of 40 years, when it does happen it is most often associated with the presence of structural heart disease, most frequently premature coronary atherosclerosis. Other common associations are hypertrophic obstructive cardiomyopathy and myocarditis.1,2 However, autopsy review studies have found that some 10%–12% of subjects in this age group have no obvious cardiac abnormalities on postmortem examination.1,2 Of identified causes in this group, many are familial sudden cardiac deaths or disorders of conduction, such as Wolff–Parkinson–White syndrome.3 Our patient had electrocardiographic and echocardiographic features indicative of transmural ischaemia localised to the anterior territory. This is suggestive of a regional rather than a global process, and suggests an ischaemic event rather than a primary arrhythmia. However, the angiogram did not show any significant coronary lesions. Although non-stenotic atherosclerotic plaques may rupture or denude and cause infarction through the formation of superimposed thrombi, which may have then been dissolved by the administration of thrombolytics, we believe that — considering this man’s relative youth — there is a distinct possibility that the underlying abnormality was coronary vasospasm. An arrhythmia, possibly triggered by the ingestion of stimulants in the presence of hypokalaemia and physical exertion, was a differential diagnosis. However, this would not account for the regional abnormality seen. The cause of this patient’s hypokalaemia is unclear, but may have been related to electrolyte losses from excessive sweating during exertion. This effect may have been exacerbated by the diuretic effect of caffeine. The role of illicit stimulants, especially cocaine, in causing coronary vasospasm in young people is well established.4 However, this patient denied cocaine use and returned a negative result on his drug test, making this an unlikely cause. The energy drink consumed by our patient contains 80 mg of caffeine (equivalent to one cup of espresso) per can. He drank seven or eight cans within 7 hours — up to 640 mg of caffeine in total. The drink also contains high doses of taurine (an amino acid) and glucuronolactone (a glucose metabolite), neither of which are considered to have significant toxicity, although there is a paucity of data.5,6 Caffeine is a naturally occurring xanthine derivative related to theophylline; it has a number of potential pharmacological actions on the cardiovascular system. Its primary mechanism of action is thought to be through competitive inhibition of adenosine receptors.7 It also induces catecholamine release, and causes a rise in intracellular calcium in myocytes through release of calcium from the sarcoplasmic reticulum, leading variably to smooth muscle contraction and relaxation.8-10 The role of caffeine in triggering arrhythmia is well established.8 There have been a number of case reports on hospitalisations or deaths due to caffeine toxicity, although the mechanism usually seems to be tachyarrhythmia and involves far higher doses than in this case.11,12 The median lethal dose in rats is 200–400 mg/kg.13 A 1997 case report described a young woman who suffered a myocardial infarction due to caffeine toxicity; however, this involved an oral dose of 20 g.14 In-vitro studies have shown that taurine has an inotropic effect on cardiac muscle similar to that of caffeine, and potentiates caffeine-induced muscle contracture. Few taurine toxicity studies have been performed, and there are insufficient data to suggest what an unsafe level of taurine consumption might be, if any.9,14 Both taurine and caffeine have been shown in vitro to have physiological effects on intracellular calcium concentration within vascular smooth muscle, and they could conceivably induce coronary vasospasm. In-vivo studies have demonstrated a capacity for caffeine to decrease myocardial blood flow during exercise.15 We postulate that, in physiologically predisposed individuals, a combination of excessive ingestion of caffeine- and taurine-containing energy drinks and strenuous physical activity can induce myocardial ischaemia by coronary vasospasm, with potentially fatal results. Caffeine has been removed from the list of prohibited substances in sport but remains on a monitoring program run by the World Anti-Doping Agency.16 Anecdotal reports suggest that the many caffeinated energy drinks now on the market are widely used by amateur and professional athletes to enhance their performance. We are concerned that a combination of exercise and the caffeine contained in these drinks may have the potential to trigger serious cardiovascular events. We accept that this is a single case, which does not and cannot establish causality. However, in the context of concerns reported in the media in recent years relating to similar events overseas, and in the presence of a plausible pharmacological mechanism, we believe that the potential dangers of these caffeinated energy drinks should be highlighted, and monitoring for future adverse events should be conducted. 1 Patient’s initial cardiac rhythm, showing ventricular fibrillation 2 Patient’s electrocardiograph on arrival at tertiary referral centre, showing evolving ischaemic changes across the anterolateral leads

Adam J Berger MB BS, BSc(Med) · Kevin Alford MB BS, FRACP, DDU

The mark, especially the “high mark” and “spectacular grab”, distinguishes Australian Rules football from more earthbound varieties.1 Photographs taken at a recent South Australian National Football League match revealed a high mark where hyperextension of the proximal interphalangeal joint of the right index finger occurred. Interview with the player and examination of the affected digit 4 days after the match revealed no injury to the finger, although some bruising of the right thenar web space and mild tenderness of the first metacarpophalangeal joint were evident. A previous report concluded that virtually all pure hyperextension injuries of the proximal interphalangeal joint result in rupture of the distal end of the volar plate,2 but fracture dislocation appears to depend on joint angle at the time of injury.3 A review of published literature and photographic libraries failed to reveal a similar incident. Further research is required to characterise the biomechanical forces necessary to cause digital injury in sports requiring barehanded capture of a travelling ball.

Robert J Douglas

To the Editor: Snowboarding is increasing in popularity, but Australian snowboarders have been shown to have 2.4 times as many fractures as skiers, with 35% of upper limb injuries being fractures.1 The most common site of injury is the wrist, accounting for 21.6% of all snowboarding injuries.2 It has been suggested that the use of wrist guards could reduce the risk of injury, particularly as snowboarding injuries tend to be impactive rather than torsional.3,4 However, concern has been raised that use of wrist guards will redistribute the impact of the force to more proximal areas of the arm, causing elbow injuries.5 We conducted a case–control study at the Mount Buller Medical Centre, Victoria, during the 2004 and 2005 ski seasons to assess: the association between wrist guard use and wrist fracture in snowboarders in Australia; and the association between wrist guard use and the severity of wrist and elbow injury. Cases were defined as any snowboarder seen at the clinic with a fractured wrist (n = 119). Controls (n = 375) were snowboarders — identified by their boots — who attended the clinic, either as companions to case participants or other patients, or as patients presenting for a reason other than wrist fracture. Study participants completed a questionnaire about wrist guard use and snow-sport behaviour. The site and severity of fractures were recorded by clinic staff. Logistic regression was used to determine adjusted odds ratios for risk factors against the main outcome measure of wrist fracture and injury in snowboarders with and without wrist guards. Characteristics strongly associated with wrist fracture were being of school age (odds ratio [OR], 2.37; P < 0.001) and being a novice at snowboarding (OR, 3.41; P < 0.001) (Box). After adjustment for all significant variables — sex, age, days of snowboarding and snowboarder ability — the odds of having worn wrist guards were lower in snowboarders with a wrist fracture (cases) than in those without such a fracture, but the difference did not reach significance (adjusted OR, 0.58; 95% CI, 0.32–1.04; P = 0.07). Full analysis of all factors considered is available from the authors. Among the sample of 494 snowboarders, 15 had elbow injuries, comprising: five with soft tissue injuries (4/86 wearing wrist guards v 1/391 not wearing wrist guards; adjusted OR, 17.6; 95% CI, 1.93–160.2; P = 0.01); and 10 with elbow fractures or dislocations (3/86 wearing wrist guards v 77/391 not wearing wrist guards; adjusted OR, 1.84; 95% CI, 0.46–7.30; P = 0.39). The association between wrist guard use and increased soft tissue elbow injuries, but not elbow fractures and dislocations, supports the value of wearing wrist guards to reduce overall injury severity. Despite a lack of overall statistical significance, the clinical context and consistency in direction of the findings suggest that snowboarders who wear wrist guards in Australian snow conditions could benefit from a reduction in wrist fracture injury of approximately 42%. This is consistent with reports from other countries that show a protective effect of wrist guards of 52% to 87%, with the greatest benefit in novice snowboarders.4 We suggest that wrist guard use should be strongly recommended for novices, and should be mandatory for school-aged snowboarders. Local schools in the Mansfield district, near Mt Buller, have adopted a policy of “no wrist guard = no snowboard”, and we hope that other schools visiting Mt Buller, and indeed other ski resorts in Australia, will follow this lead. Characteristics associated with wrist fracture among snowboarders Characteristic Cases (n = 119) Controls (n = 375) Odds ratio (95% CI) P for difference Wearing wrist guards today No 100 (84%) 299 (80%) 1.00* Yes 18 (15%) 75 (20%) 0.72 (0.41–1.26) 0.25 Missing data 1 (0.8%) 1 (0.3%) Age (years) 0–19 72 (61%) 149 (40%) 2.37 (1.55–3.63) < 0.001 > 19 46 (39%) 226 (60%) 1.00* Missing data 1 (0.8%) Ability of snowboarder Novice 60 (50%) 112 (30%) 3.41 (1.79–6.49) < 0.001 Intermediate 43 (36%) 173 (46%) 1.58 (0.82–3.04) 0.17 Advanced 14 (12%) 89 (24%) 1.00* Missing data 2 (2%) 1 (0.3%) * Reference category.

Graham M Slaney · Judith C Finn · Angus Cook · Philip Weinstein

To the Editor: A 20-year-old sub-elite Australian Rules football player presented with pain and tenderness in the lower third of the sternum. He had been involved in a moderate body collision with an opposing player about 3 weeks before presentation, and had continued to train and play despite sternal discomfort. He described no other symptoms. On examination, there was no obvious sternal deformity. There was mild to moderate tenderness over the lower third of the sternum, and minimal sternal discomfort on lateral chest compression. Chest auscultation was clear. Plain chest and sternal x-rays were normal. A technetium-99m HDP bone scan showed increased tracer uptake in the lower sternum, consistent with an undisplaced oblique sternal fracture (Box). Management of the player’s injury and his fitness to train and play were discussed informally with medical and paramedical practitioners. Their opinions ranged from an immediate return to competition to 12 weeks of complete rest. After discussions within the player’s club, he was placed on a training regimen that avoided all upper body clashes and stresses, and he was rested from match play. He was regularly reassessed for symptoms and made an uneventful return to full competition 6 weeks after his initial injury. He remained asymptomatic and competitive for the remainder of the season and at 1-year review. The usual cause of sternal fracture is blunt anterior chest trauma, with about 90% of sternal fractures caused by trauma resulting from the forces associated with motor vehicle accidents.1 Sternal fracture is rarely encountered in Australian Rules football and such a case has not previously been described in the literature. The Australian Football League Injury Report database revealed only four cases of sternal fracture over the period 1992–2006, accounting for a total of 18 missed games (range, 1–11 games) (John Orchard, Conjoint Senior Lecturer, Sports Medicine Program, University of New South Wales, personal communication, May 2007). Patients suspected of suffering a sternal fracture should be investigated with appropriate chest x-rays. If these are inconclusive, it is now suggested the patient should be further investigated with sternal ultrasound, which has recently been demonstrated to be superior to bone scan in identifying sternal fractures,2 and without the associated radiation exposure. Patients with an acute suspected sternal fracture should also undergo electrocardiography. If the electrocardiogram is normal and there is no evidence of intrathoracic injury on radiological investigation, the patient can safely be discharged.3 Chest pain is the predominant persisting symptom after sternal fracture.4 Conservative management with rest, analgesia and/or anti-inflammatories, and, if required, appropriate padding and taping5 should result in full recovery and an uneventful return to competition. Bone delay views from dynamic localised technetium-99m HDP bone scan There is a band of low to moderate tracer uptake running in a slightly oblique line across the lower sternum (arrow), suggesting a sternal fracture.

Robert J Douglas

Financial motivation can encourage greater sports injury prevention efforts A landmark study published recently in the BMJ has shown that the rate of catastrophic spinal injury in rugby union in New Zealand has halved.1 For the period 2001–2005, the rate was 1.3 spinal injuries per 100 000 players per year, compared with 2.7 per 100 000 players per year in the period 1996–2000, which was typical of the previous 25 years.1 This drop coincided with the introduction of “RugbySmart” (http://www.rugbysmart.co.nz), a 10-point annual injury prevention program that was made compulsory from 2001 for all coaches and referees in New Zealand.1,2 While the observational study does not claim that the drop in catastrophic spinal injuries can be unequivocally attributed to RugbySmart, an accompanying editorial in the BMJ stated: “The beauty of the RugbySmart programme is that it can do no harm, and according to the results of this study may do great good”.3 What is the current state of play with respect to catastrophic spinal injuries in rugby in Australia? Although comparisons of spinal injury rates between New Zealand and Australia are difficult,1 recently published rates in Australia are substantially higher (between 3.24 and 6.85 injuries per 100 000 players per year). New Zealand is in a much better position to accurately determine incidence rates because compensation for all injuries (both sporting and from other causes) is available through a universal, government-funded scheme operated by the Accident Compensation Corporation (ACC).6 From 2005, the Australian Rugby Union (ARU) instituted a similar (but less extensive) program called “SmartRugby” for its referees and coaches. Tests of its effectiveness have not been reported, but it should be noted that the ARU does not have nearly the same financial motivation as the ACC to make it successful. In New Zealand, the ACC compensates for all catastrophic spinal injuries with lifetime medical care and annual replacement of 80% of wages, which can be up to NZ$14 million per case.2 In Australia in 2005, the maximum compensation paid to a rugby player rendered quadriplegic was A$300 000, accurately described by Carmody et al as “grossly inadequate”.4 This is particularly so when compared with a median payout of A$7.6 million for quadriplegia in recent negligence cases in Australia.7 Orchard and Finch argued in 2002 that, from a public health viewpoint, New Zealand’s system of maintaining a government body that monitors, compensates and seeks to prevent sports injuries is superior to Australia’s lack of any comparable system.6 Noakes and Draper suggested that New Zealand’s drop in spinal injuries “would not have been possible if the New Zealand government did not provide a national insurance policy that also covers sports injuries”.3 The ACC can also claim other successes in preventing sports injuries that we have not yet achieved in Australia. Mouthguard use in rugby in New Zealand has increased from 67% to 93%, reducing rugby-related dental claims to the ACC by 43%.8 A similar analogy can be used — in Australia there is no organised body paying dental claims, so there is no strong financial motivation to encourage increased mouthguard usage. The ACC is already in the position where it is evaluating New Zealand’s national sports injury prevention programs (in many sports) for cost-effectiveness, in terms of reducing injuries and claim payments.9 By comparison, in Australia there is generally no monitoring of sports injury rates, let alone well coordinated national sports injury prevention programs in place. If a national body was created in Australia to take on this role, even if it was not fully funded out of general revenue like the ACC, at the very least it could insist that federal government funding for sports be tied to minimum standards of monitoring injury rates and instituting injury prevention programs. Reducing work-related and traffic accidents have been listed as two of the top 10 public health achievements of the 20th century.10 These achievements would not have been possible without major bodies having responsibility for monitoring injury rates and instituting preventive measures. New Zealand is already showing that this model works equally well for sports injuries, so why should it not be applied in Australia? A new federal government body would cost money to establish and maintain, but the New Zealand experience suggests that subsequent savings may soon cover the costs of establishment and operation.2 In conclusion, the following matters deserve our urgent attention in Australia: The creation of a federal government body either primarily responsible for monitoring and preventing sports injuries or, at the very least, delegating these responsibilities to sporting bodies in a coordinated fashion. This body should compensate for injury, either (1) totally, as is the case in New Zealand; or (2) partially, in conjunction with sporting bodies, private insurers, public hospitals and Medicare. The minimum compensation for complete quadriplegia occurring in sport in Australia should be increased at least tenfold, both (1) to bring compensation for sporting quadriplegia more into line with compensation for quadriplegia arising from other causes; and (2) to give compensating and sporting bodies a much stronger financial motivation for prevention, as is the case in New Zealand.

John W Orchard MD, PhD, FACSP · Stephen R Leeder PhD, FRACP, FAFPHM · Gary E Moorhead BA(Hons), MEd · Jessica J Coates LLB(Hons), BEc · Peter D Brukner MB BS, FACSP

To the Editor: We report two cases of previously well male bodybuilders who presented with severe extrapyramidal reactions after intramuscular injection of the antipsychotic fluphenazine decanoate, in the mistaken belief that it was an anabolic steroid. The first patient, aged 31 years, obtained fluphenazine decanoate from a gym contact. He injected 50 mg intramuscularly on alternate days (Days 1, 3 and 5) to a total of 150 mg, then presented to two local hospitals on Days 7 and 11 with difficulty swallowing, generalised muscle stiffness and lethargy. He withheld the history of fluphenazine use, and was diagnosed with tonsillitis. On Day 14, he presented to our emergency department (ED) with marked dystonia, immobility, and inability to speak or swallow food. On examination, he was afebrile and haemodynamically stable. He was given a trial dose of benztropine 2 mg, but improvement was slight and, given the absence of relevant history, benztropine was not repeated. The neurology team raised the possibility of a conversion disorder, but the psychiatry team, noting the patient’s attempts to speak and an absence of recent stressors, believed that further investigation into an organic cause was required. When the patient’s wife learned that he had used fluphenazine and alerted the neurology team to this use, he was started on regular benztropine and his condition improved over the next 3 days. The dose of benztropine was reduced on discharge, but his dystonia recurred and required readmission to hospital for further treatment. The second, unrelated patient, also aged 31 years, openly admitted purchasing fluphenazine decanoate from “a friend of a friend”. After injecting two 50 mg depots, he had multiple presentations to three EDs, where he was treated for dystonia with immediate doses and then regular low doses of benztropine. On admission to our hospital 19 days after injection, he was afebrile and haemodynamically stable, with marked dystonia. His initial creatine kinase level was elevated (553 U/L; normal, < 204 U/L), but subsequently normalised and was not accompanied by autonomic dysfunction. His condition improved with regular oral diazepam and benztropine, but symptoms recurred when he inappropriately reduced his benztropine dose after discharge. On subsequent review, both patients’ dystonia was resolving, but they had significant akathisia. Inadvertent and inappropriate use of a long-acting phenothiazine not only required prolonged anticholinergic therapy for these men, but we believe placed them at risk of neuroleptic malignant syndrome. We have found no previous similar reports in the medical literature, but are aware anecdotally of at least one other case of a patient treated recently at a district hospital. The anabolic steroid nandrolone decanoate is referred to colloquially on numerous websites and by our patients as “deca” (from the Organon brand name Deca-Durabolin). We believe our patients and their supplier(s) have mistaken the “decanoate” in fluphenazine decanoate for the pharmacologically active component of the drug.

Elizabeth A S Giugni · Rachel S Boddy · Natalie G Limet

To the Editor: Safe sports participation has become a key national issue, especially in view of the potential for concerns about safety to inhibit sports participation,1 in a nation where obesity rates are rising2 and more exercise is recommended. Australians participate in many sports, but the safety of the football codes is especially criticised by the media and the community because of the intense focus on injuries to players at the elite level. This is particularly the case for Australian Football (AF) and its elite game, the Australian Football League (AFL). National reports released in 2006 have identified AF as the sport most associated with injury admissions to hospital3 and with private health insurance claims.4 These have sparked media commentary about the safety of AF. Response to these injury reports prompted an unprecedented media release5 from the country’s peak sports medicine body, Sports Medicine Australia, detailing issues with the report figures, urging caution in their interpretation and supporting the efforts of the football codes in improving participant safety. The modified version of the game (Auskick), which is played by children, has been shown to be safer,6 but there is a progression to adult rules by the under-15 age group, and the umbrella of safety provided by modified rules is eventually gone, raising the question of how safe the non-modified version is. Recently released AFL figures suggest that injury rates at the elite level are at a historical low,7 but the report provided insufficient information to assess whether this represents a significant decline since 1997, and the data are already one season behind. Equivalent information for the more than 450 000 adult, non-elite participants is not available. Published literature related to injury prevention highlights a dearth of knowledge relating to the causes of injuries in non-elite participants and a very small evidence base for ways to prevent injuries in AF. With AF played almost exclusively in Australia, the onus to provide evidence for improving the safety of participation clearly falls on the stakeholders of the sport here. Gains in reducing both the public health impact of football injuries and the fear of injury associated with participation will only come from substantial investment in large-scale trials at the non-elite level, and a multidisciplinary approach to safety and injury issues across all levels of play. This will require active and committed collaboration of key stakeholders such as clinicians, allied health practitioners, researchers, clubs, sports administrators, coaches and the participants themselves.

Belinda J Gabbe · Caroline F Finch · Peter A Cameron

Objective: To review whether watching football increases the population cardiac event risk in New South Wales.Design: Analysis of hospital admissions for acute myocardial infarction, other cardiovascular disease, and other acute injuries at the time of two stressful sporting events in NSW in 2005: the Sydney Swans playing in the Australian Football League (AFL) Grand Final, and the Socceroos’ penalty shoot-out in their World Cup qualifying match against Uruguay.Results: There were no increases in any of the studied admission events at the time of, or in the days immediately following, these football matches.Conclusions: Australians appear to be resistant to acute stressors associated with watching sporting events, possibly due to higher rates of motivational deficiency disorder (MoDeD) than in European populations.

Adrian E Bauman PhD, FAFPHM · Hidde P van der Ploeg PhD · Tien Chey MAppStats · Gary Sholler FRACP

Sports participation among children is declining. Sport and physical activity are important in childhood for optimising bone mass and reducing obesity and insulin resistance. Physical activity reduces cardiovascular risk factors in adults, and can improve survival in patients with cardiac failure. Musculoskeletal injury is the most common complication of sports participation in adults — not cardiac events. Some of the decline in function which occurs with ageing can be positively affected by regular physical activity.

Carolyn R Broderick MB BS, FACSP, GDSSc · Gregory J Winter FACSP, FRACGP, MSpMed · Roger M Allan FRACP, FCSANZ, FACC

Neville R Blomeley President, Sports Doctors Australia, and Medical Director, Optima Sports Medicine, 6/66 Station Road, Indooroopilly, QLD 4068. drnbauscareindATbigpond.com Comment: I would like to draw readers’ attention to a very enthusiastic and active group of sports medicine practitioners that was not mentioned in the editorial by Orchard and Brukner,1 which introduced the Sports Medicine Practice Essentials series. Sports Doctors Australia comprises general practitioners and others from areas such as orthopaedics, rehabilitation, accident and emergency, and sports dentistry. Virtually all fellows of Sports Doctors Australia (SDrA) have obtained a postgraduate degree in sports medicine from an Australian university (most commonly a masters degree from the University of New South Wales). We are committed to delivering excellent care in all areas of sports medicine to the general public as well as to elite athletes. Because of our wider background in general medicine, we are in an ideal position to provide overall care to teams and individual athletes. Many of our fellows are, or have been, very successful team doctors for national teams. A number of fellows are active in clinical research and have academic appointments with university medical schools. Our main aim is not to obtain specialist status (as it is for members of the Australasian College of Sports Physicians), but to provide excellence in sports medicine care for athletes at all levels, and to provide sports medicine education to other doctors, medical students and the general public.

Neville R Blomeley

Effectively managing on-field emergencies is the most important role of the doctor on the sidelines. Pre-event preparation is essential and should include a formulated plan for dealing with emergencies and access to emergency equipment such as a stretcher and a bag and mask. Game day injuries should be assessed by adhering as closely as possible to a normal clinical consultation, with a proper history and examination being performed for all injuries. The athlete with an on-field head injury should be treated as having a concomitant cervical spine injury until proven otherwise. Athletes with any symptoms after head injury should be comprehensively and continuously assessed. Return-to-play decisions are made by balancing the risk of injury recurrence, the potential severity of injury recurrence and the benefits of returning to the field (which are higher at elite than amateur level). There is currently a shortage of doctors willing to cover sports events in Australia, which is partially explained by inadequate remuneration, inadequate facilities provided at venues, inadequate training opportunities in sports medicine, and fear of the medicolegal consequences in taking on the role as a team doctor.

Geoffrey M Verrall MB BS, FACSP · Peter D Brukner MB BS, FACSP · Hugh G Seward MB BS, FACSP, FASMF

Magnetic resonance imaging and arthroscopy of the hip have shown that labral injuries, chondral injuries, rim lesions, synovitis and tears of the ligament teres are common causes of hip, groin and low-back pain. Hip arthroscopy is used both as a diagnostic and therapeutic tool; it has been shown to be of benefit in recent traumatic labral injury, but disappointing in the management of chronic hip pain (which may be associated with degenerative change, and chondral lesions of the acetabulum). The McConnell multimodal physiotherapy regimen is effective in treating patellofemoral pain. Anterior cruciate ligament rupture is three to five times more common in women, but neuromuscular training appears to decrease its incidence. Patellar tendon and hamstring grafts appear to be equally effective in anterior cruciate ligament reconstruction. Articular cartilage defects remain a significant problem, and the efficacy of treatments such as autologous chondrocyte implantation is still unclear.

Peter D Brukner MB BS, FACSP · Kay M Crossley BAppSci(Physio), PhD · Hayden Morris MB BS, FRACS · Simon J Bartold BSc, FASMF, FAAPSM · Bruce Elliott PhD, FAAKPE, FISBS

C Scott Masters,* Michael J Yelland† * Vice-President, Australian Association of Musculoskeletal Medicine, Caloundra Sports Medicine Centre, 39 Minchinton Street, Caloundra, QLD 4551. † Associate Professor of Primary Health Care, Griffith University, QLD. scotty1ATozemail.com.au To the Editor: Paoloni and Orchard provided a concise summary of the evidence for injections for soft-tissue injuries,1 but omitted some important references on the mechanism of action of corticosteroids and on prolotherapy. An important action of corticosteroids is blocking of transmission in nociceptive C-fibres.2 Given the lack of evidence of inflammation in chronically painful tendinopathies,3 this is a more probable mechanism of action than the suppression of inflammation. Paoloni and Orchard correctly report that steroids have only a temporary effect in suppressing soft tissue pain. However, in low back pain, if their use is preceded by manual therapy and exercises they have the potential to give more prolonged relief of pain and disability.4 A recent Swedish randomised controlled trial (RCT) of polidocanol prolotherapy injections for chronic Achilles tendinopathy showed reduced pain and normalisation of ultrasound abnormalities.5 Similarly, a New Zealand case series of glucose prolotherapy injections showed very positive results for the same condition.6 An Australian RCT into prolotherapy for chronic low back pain (average duration, 14 years) showed sustained reductions in pain and disability with glucose prolotherapy injections, although similar results were obtained with saline injections.7 A pilot study of glucose prolotherapy in 24 elite male kicking-sport athletes with chronic groin pain (mean duration, 15.5 months) who had failed physical therapy reported a pain-free state and return to sports in 82% at an average follow-up of 17.2 months.8 This evidence would suggest there is a role for this glucose prolotherapy in managing soft-tissue pain, especially as musculoskeletal pain is one of the major presentations to primary practice in Australia. Training primary care physicians in prolotherapy injection techniques should be a priority in medical education.

C Scott Masters · Michael J Yelland