Introduction

The first reported game of Australian Rules football, a ball sport that evolved loosely from Gaelic football, was played in Melbourne in 1858. It is played predominantly by males (although today there is increasing female participation) in a number of countries, although the highest participation rates are in the southern Australian states. The professional body responsible for overseeing the sport is the Australian football league (AFL). It is a contact sport and participants wear little if any protective equipment, although helmets are increasingly seen in use, particularly at junior levels. We identified 14 cases of sudden cardiac death in participants, some of whom had demonstrated symptoms prior to their fatal episode. The role of tailored pre-participation screening, as is the practice in parts of Europe and North America, with a view to reducing fatalities is perhaps worthy of consideration.

Methods

The National Coronial Information Database (NCIS) was searched using the key terms football, Australian Rules football and AFL, to identify sudden deaths in individuals less than 40 years of age who underwent medico legal autopsy at the Victorian Institute of Forensic Medicine between June 2001 and June 2015. Information was collated from postmortem reports and results of clinical follow up of surviving family members. Data examined include age, circumstances, cause of death, cardiac findings at autopsy, and the results of any genetic testing.

Results

There were 14 cases of sudden cardiac death identified (Table 1). All decedents were male with an age range of 13–36 and a mean and median age of 23 years. Conditions identified included coronary artery atherosclerosis, arrhythmogenic cardiomyopathy, anomalous coronary artery anatomy, myocarditis, and coronary atheroma in the setting of healed Kawasaki disease. In 5 cases the cause of death was undetermined raising the possibility of a channelopathy. Deaths occurred during play, at training, and on the sidelines. Relevant past histories included prior syncopal episodes (4), adult polycystic kidney disease with hypertension (1), childhood Kawasaki disease (1), asthma (2), and recent viral infection (1). In 7 cases referral was made to a cardiac genetics service, and in 1 to a family physician; in 1 family referral was declined and in 5 no referral was made. In 2 of the referred cases a potentially pathogenic mutation was identified and in 1 instance, while genetic testing was negative, a surviving sibling has been diagnosed with a cardiomyopathy. Clinical assessment is pending in the remaining cases (Table 2).

Table 1 Cases of sudden death while participating in Australian Rules football
Table 2 Cardiac findings at postmortem

Discussion

Reports examining deaths occurring in the setting of Australian Rules football competition are rare and in fact the authors could find only 2 such analyses in the scientific literature. McCrory et al. [1] examined deaths occurring over a 22 year period from 1968 to 1989 and identified 25 cases. There were 10 traumatic deaths (9 head injury and 1 blunt abdominal trauma) and 15 cardiac deaths. Diagnoses in the latter category included coronary artery atherosclerosis, hypertrophic cardiomyopathy (HCM), anomalous coronary artery anatomy, and commotio cordis. Young et al. [2] identified 8 cases of sudden cardiac death, all due to ischemic heart disease, in young Aboriginal males in the Northern Territory (of Australia) over a 15 year period.

In our study there were 14 cases of sudden cardiac death identified. All were male with an age range of 13–36 and a mean and median age of 23 years. This preponderance of males accords with the results of other authors who have scrutinized sudden cardiac deaths during sport [3]. This might reflect either a greater participation rate by males in high intensity sports (certainly the case with Australian Rules football) or perhaps, as suggested by some authors, a greater susceptibility of males to underlying cardiac disorders which can manifest as sudden cardiac death [4]. It is of interest that non cardiac, non-traumatic causes of death, such as asthma and ruptured cerebral aneurysms, which have been well documented in other studies of sudden death during sport [5], were not identified in our cohort.

The absence of any traumatic causes of death in our study is in contrast to 1 of the 2 other studies looking at deaths playing football [1].The risk of injury from contact to the head in Australian Rules is real and may encompass intracranial hemorrhage and diffuse cerebral edema with permanent neurological sequelae. The term second impact syndrome (SIS) is sometimes used to describe the scenario where an individual suffers a second head injury before the symptoms of the initial injury have resolved [6]. It tends self-evidently to occur in contact sports and cases have been described in American football and boxing [7, 8].While it has not been specifically described in Australian Rules, several of the cases identified by McCrory et al. may represent examples of the entity. Recently the existence of the syndrome as a distinc clinical entity has been questioned [6].

When a player collapses and dies in the setting of a contact sport, it is not uncommon for the specter of commotio cordis to be raised. The term is applied in the setting of a blunt non penetrating blow to the chest, usually during athletic or recreational activity. It can cause death by means of induction of cardiac arrhythmias, particularly ventricular fibrillation [9]. Most reported cases have occurred in individuals playing baseball, ice hockey, and lacrosse and the critical risk factor is thought to be a blow of sufficient force to the precordial region during the vulnerable phase of ventricular repolarization (narrow 10–30 ms window just prior to T-wave peak; equivalent to less than 2 % of the cardiac cycle). The diagnosis can only ever be suspected, but with varying degrees of confidence depending on the history. The difficulty with contact sports, and particularly in the case of Australian Rules, is the fact that the affected individual has often had some form of contact to the body in the period immediately preceding their collapse. In two of our cases the possibility of the diagnosis was raised in information provided to the pathologist prior to autopsy. In one of our cases there was anomalous coronary artery anatomy and in the other, a SCN5A mutation was identified, raising the possibility of a cardiac channelopathy.

Cases of undiagnosed cardiomyopathy invariably feature prominently in series of sudden unexpected during sport [1, 5]. Thus it was perhaps surprising that no cases of hypertrophic cardiomyopathy (HCM) were identified in our series. There were, however, two cases of suspected arrhythmogenic right ventricular cardiomyopathy (ARVC), a form of dilated cardiomyopathy often associated with genetic defects in proteins of the myocyte desmosomal complex. In one instance the deceased male was found to be heterozygous for a novel transition (1114G>A) in exon 4 of the plakophilin-2 gene, a variant considered of uncertain significance by the clinical geneticists. In the second case, genetic testing was negative in the deceased but a surviving sibling has been diagnosed with ARVC on clinical grounds.

We identified two cases of deaths attributed to anomalous coronary artery anatomy, in accordance with the results from other studies [5]. There are a variety of described anomalies of coronary anatomy, of varying clinical significance. Our two cases comprised one example of origin of the left main coronary artery from the right sinus of Valsalva, and in the second case the right coronary arose from the left sinus with high take off. These anomalies can present difficulties in diagnosis clinically, and on occasions for the pathologist a dilemma in attributing significance. Notwithstanding the foregoing, they are usually effectively managed once identified [10]. One of our patients had experienced ante mortem symptoms and had been investigated for syncopal episodes. These were felt to be non-cardiac in nature and further investigations including ECG had not been performed.

The question of pre-participation screening for young competitive athletes is a thorny issue and is undertaken to varying degrees in Europe and North America [3, 4, 11, 12]. Organized screening of young sportspeople occurs on the largest scale in Italy where it is mandated by legislation. Approximately 10 % of Italy’s population is screened annually for this purpose. The program dates to 1982 when the Italian government instituted a nationwide program of pre-participation screening of athletes [13]. The results of the program were reviewed at 25 years and it was concluded that screening athletes by ECG was a clinically, cost effective means, with adequate sensitivity and specificity, by which potentially lethal arrhythmias and cardiomyopathies could be identified. It has led to a 90 % reduction in sudden unexpected death in competitive athletes. Perhaps not surprisingly, given the individuals now excluded, the most common causes of sudden cardiac death during sport in Italy today are coronary artery disease and anomalous coronary anatomy [14]. The Italian experience also emphasizes the importance of having ECGs reviewed by clinicians with specific expertise in managing competitive athletes, if misdiagnosis and inappropriate investigations are to be avoided [15].

The Australasian college of Sports Physicians has released guidelines suggesting that some form of pre-participation screening of competitive athletes is worthy of consideration [16]. This might take the form of routine history and examination with further testing such as ECG and echocardiography in appropriate circumstances. A number of professional football clubs are now offering varying degrees of cardiac screening to their playing staff. It is possible that some of the deaths in our series may have been prevented had the athlete been subjected to pre-participation screening.

Conclusions

Deaths occurring in the setting of competition in Australian Rules football are uncommon and are usually related to underlying cardiovascular disease. Perhaps surprisingly, given the high speed contact associated with the sport and the fact that competitors rarely wear any protective equipment, no traumatic deaths were identified in our study. It is also noteworthy that while other authors have identified hypertrophic cardiomyopathy (HCM) as a significant cause of mortality in competitive athletes, no cases of HCM were diagnosed in our, admittedly small, series. A final point of contention is the potential role, if any, of pre competition screening as a means of identifying at risk individuals and thus reducing the incidence of sudden unexpected death in young athletes.

Key points

  1. 1.

    Deaths in participants in Australian Rules football are uncommon and most often related to an underlying cardiac abnormality.

  2. 2.

    Medico legal autopsy often identifies information important to both the death investigation authority and to surviving family members.

  3. 3.

    Targeted genetic testing is a potentially useful tool but needs to be performed in a clinical environment with cardiological and clinical genetic support.

  4. 4.

    Pre participation screening could potentially reduce the number of fatalities associated with participation in Australian Rules football.